Peripheral AFFERENT NEURONS which are sensitive to injuries or pain, usually caused by extreme thermal exposures, mechanical forces, or other noxious stimuli. Their cell bodies reside in the DORSAL ROOT GANGLIA. Their peripheral terminals (NERVE ENDINGS) innervate target tissues and transduce noxious stimuli via axons to the CENTRAL NERVOUS SYSTEM.
A class of nerve fibers as defined by their nerve sheath arrangement. The AXONS of the unmyelinated nerve fibers are small in diameter and usually several are surrounded by a single MYELIN SHEATH. They conduct low-velocity impulses, and represent the majority of peripheral sensory and autonomic fibers, but are also found in the BRAIN and SPINAL CORD.
Cells specialized to transduce mechanical stimuli and relay that information centrally in the nervous system. Mechanoreceptor cells include the INNER EAR hair cells, which mediate hearing and balance, and the various somatosensory receptors, often with non-neural accessory structures.
Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.
Act of eliciting a response from a person or organism through physical contact.
An increased sensation of pain or discomfort produced by mimimally noxious stimuli due to damage to soft tissue containing NOCICEPTORS or injury to a peripheral nerve.
Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.
An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.
Cellular receptors which mediate the sense of temperature. Thermoreceptors in vertebrates are mostly located under the skin. In mammals there are separate types of thermoreceptors for cold and for warmth and NOCICEPTORS which detect cold or heat extreme enough to cause pain.
Presence of warmth or heat or a temperature notably higher than an accustomed norm.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
A subgroup of TRP cation channels named after vanilloid receptor. They are very sensitive to TEMPERATURE and hot spicy food and CAPSAICIN. They have the TRP domain and ANKYRIN repeats. Selectivity for CALCIUM over SODIUM ranges from 3 to 100 fold.
Slender processes of NEURONS, including the AXONS and their glial envelopes (MYELIN SHEATH). Nerve fibers conduct nerve impulses to and from the CENTRAL NERVOUS SYSTEM.
A voltage-gated sodium channel subtype that is expressed in nociceptors, including spinal and trigeminal sensory neurons. It plays a role in the transmission of pain signals induced by cold, heat, and mechanical stimuli.
Specialized afferent neurons capable of transducing sensory stimuli into NERVE IMPULSES to be transmitted to the CENTRAL NERVOUS SYSTEM. Sometimes sensory receptors for external stimuli are called exteroceptors; for internal stimuli are called interoceptors and proprioceptors.
Amount of stimulation required before the sensation of pain is experienced.
The sensation of cold, heat, coolness, and warmth as detected by THERMORECEPTORS.
A class of nerve fibers as defined by their structure, specifically the nerve sheath arrangement. The AXONS of the myelinated nerve fibers are completely encased in a MYELIN SHEATH. They are fibers of relatively large and varied diameters. Their NEURAL CONDUCTION rates are faster than those of the unmyelinated nerve fibers (NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.
Any of several BRASSICA species that are commonly called mustard. Brassica alba is white mustard, B. juncea is brown or Chinese mustard, and B. nigra is black, brown, or red mustard. The plant is grown both for mustard seed from which oil is extracted or used as SPICES, and for its greens used as VEGETABLES or ANIMAL FEED. There is no relationship to MUSTARD COMPOUNDS.
Drugs that act on neuronal sensory receptors resulting in an increase, decrease, or modification of afferent nerve activity. (From Smith and Reynard, Textbook of Pharmacology, 1991, p367)
The three membranes that cover the BRAIN and the SPINAL CORD. They are the dura mater, the arachnoid, and the pia mater.
Scales, questionnaires, tests, and other methods used to assess pain severity and duration in patients or experimental animals to aid in diagnosis, therapy, and physiological studies.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The semilunar-shaped ganglion containing the cells of origin of most of the sensory fibers of the trigeminal nerve. It is situated within the dural cleft on the cerebral surface of the petrous portion of the temporal bone and gives off the ophthalmic, maxillary, and part of the mandibular nerves.
The branch of pharmacology dealing especially with the action of drugs upon various parts of the nervous system.
Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.
Calcitonin gene-related peptide. A 37-amino acid peptide derived from the calcitonin gene. It occurs as a result of alternative processing of mRNA from the calcitonin gene. The neuropeptide is widely distributed in neural tissue of the brain, gut, perivascular nerves, and other tissue. The peptide produces multiple biological effects and has both circulatory and neurotransmitter modes of action. In particular, it is a potent endogenous vasodilator.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
The minimum amount of stimulus energy necessary to elicit a sensory response.
A broad group of eukaryotic six-transmembrane cation channels that are classified by sequence homology because their functional involvement with SENSATION is varied. They have only weak voltage sensitivity and ion selectivity. They are named after a DROSOPHILA mutant that displayed transient receptor potentials in response to light. A 25-amino-acid motif containing a TRP box (EWKFAR) just C-terminal to S6 is found in TRPC, TRPV and TRPM subgroups. ANKYRIN repeats are found in TRPC, TRPV & TRPN subgroups. Some are functionally associated with TYROSINE KINASE or TYPE C PHOSPHOLIPASES.
Ion channels that specifically allow the passage of SODIUM ions. A variety of specific sodium channel subtypes are involved in serving specialized functions such as neuronal signaling, CARDIAC MUSCLE contraction, and KIDNEY function.
A family of proton-gated sodium channels that are primarily expressed in neuronal tissue. They are AMILORIDE-sensitive and are implicated in the signaling of a variety of neurological stimuli, most notably that of pain in response to acidic conditions.
Nerve structures through which impulses are conducted from a peripheral part toward a nerve center.
An increased response to stimulation that is mediated by amplification of signaling in the CENTRAL NERVOUS SYSTEM (CNS).
Sensing of noxious mechanical, thermal or chemical stimuli by NOCICEPTORS. It is the sensory component of visceral and tissue pain (NOCICEPTIVE PAIN).
A voltage-gated sodium channel subtype found in the neurons of the NERVOUS SYSTEM and DORSAL ROOT GANGLIA. It may play a role in the generation of heat and mechanical pain hypersensitivity.
Rapidly decreasing response to a drug or physiologically active agent after administration of a few doses. In immunology, it is the rapid immunization against the effect of toxic doses of an extract or serum by previous injection of small doses. (Dorland, 28th ed)
A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include PAIN; PARESTHESIAS; PARESIS; or HYPESTHESIA.
An absence of warmth or heat or a temperature notably below an accustomed norm.
An alcohol produced from mint oils or prepared synthetically.
A major nerve of the upper extremity. In humans the fibers of the radial nerve originate in the lower cervical and upper thoracic spinal cord (usually C5 to T1), travel via the posterior cord of the brachial plexus, and supply motor innervation to extensor muscles of the arm and cutaneous sensory fibers to extensor regions of the arm and hand.
The functions of the skin in the human and animal body. It includes the pigmentation of the skin.
Inflammation caused by an injurious stimulus of peripheral neurons and resulting in release of neuropeptides which affect vascular permeability and help initiate proinflammatory and immune reactions at the site of injury.
Inflammation of the DENTAL PULP, usually due to bacterial infection in dental caries, tooth fracture, or other conditions causing exposure of the pulp to bacterial invasion. Chemical irritants, thermal factors, hyperemic changes, and other factors may also cause pulpitis.
The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors.
The process by which cells convert mechanical stimuli into a chemical response. It can occur in both cells specialized for sensing mechanical cues such as MECHANORECEPTORS, and in parenchymal cells whose primary function is not mechanosensory.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
A subclass of ADENOSINE RECEPTORS that are generally considered to be coupled to the GS, STIMULATORY G-PROTEIN which causes up regulation of CYCLIC AMP.
Biological actions and events that constitute the functions of the NERVOUS SYSTEM.
A condition where damage to the peripheral nervous system (including the peripheral elements of the autonomic nervous system) is associated with chronic ingestion of alcoholic beverages. The disorder may be caused by a direct effect of alcohol, an associated nutritional deficiency, or a combination of factors. Clinical manifestations include variable degrees of weakness; ATROPHY; PARESTHESIAS; pain; loss of reflexes; sensory loss; diaphoresis; and postural hypotension. (From Arch Neurol 1995;52(1):45-51; Adams et al., Principles of Neurology, 6th ed, p1146)
Neurons in the SPINAL CORD DORSAL HORN whose cell bodies and processes are confined entirely to the CENTRAL NERVOUS SYSTEM. They receive collateral or direct terminations of dorsal root fibers. They send their axons either directly to ANTERIOR HORN CELLS or to the WHITE MATTER ascending and descending longitudinal fibers.
Agents, usually topical, that relieve itching (pruritus).
A class of drugs that act by inhibition of sodium influx through cell membranes. Blockade of sodium channels slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, and reduces conduction velocity.
Drugs that act principally at one or more sites within the peripheral neuroeffector systems, the autonomic system, and motor nerve-skeletal system. (From Smith and Reynard, Textbook of Pharmacology, 1991, p75)
The lateral of the two terminal branches of the sciatic nerve. The peroneal (or fibular) nerve provides motor and sensory innervation to parts of the leg and foot.
The 5th and largest cranial nerve. The trigeminal nerve is a mixed motor and sensory nerve. The larger sensory part forms the ophthalmic, mandibular, and maxillary nerves which carry afferents sensitive to external or internal stimuli from the skin, muscles, and joints of the face and mouth and from the teeth. Most of these fibers originate from cells of the TRIGEMINAL GANGLION and project to the TRIGEMINAL NUCLEUS of the brain stem. The smaller motor part arises from the brain stem trigeminal motor nucleus and innervates the muscles of mastication.
An antigen solution emulsified in mineral oil. The complete form is made up of killed, dried mycobacteria, usually M. tuberculosis, suspended in the oil phase. It is effective in stimulating cell-mediated immunity (IMMUNITY, CELLULAR) and potentiates the production of certain IMMUNOGLOBULINS in some animals. The incomplete form does not contain mycobacteria.
The medial terminal branch of the sciatic nerve. The tibial nerve fibers originate in lumbar and sacral spinal segments (L4 to S2). They supply motor and sensory innervation to parts of the calf and foot.
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
The inferior (caudal) ganglion of the vagus (10th cranial) nerve. The unipolar nodose ganglion cells are sensory cells with central projections to the medulla and peripheral processes traveling in various branches of the vagus nerve.
A protein-tyrosine kinase receptor that is specific for NERVE GROWTH FACTOR; NEUROTROPHIN 3; neurotrophin 4, neurotrophin 5. It plays a crucial role in pain sensation and thermoregulation in humans. Gene mutations that cause loss of receptor function are associated with CONGENITAL INSENSITIVITY TO PAIN WITH ANHIDROSIS, while gene rearrangements that activate the protein-tyrosine kinase function are associated with tumorigenesis.
The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included.
The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium.
An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.
The founding member of the glial cell line-derived neurotrophic factor family. It was originally characterized as a NERVE GROWTH FACTOR promoting the survival of MIDBRAIN dopaminergic NEURONS, and it has been studied as a potential treatment for PARKINSON DISEASE.
Use of electric potential or currents to elicit biological responses.
The TEMPERATURE at the outer surface of the body.
Sensation of making physical contact with objects, animate or inanimate. Tactile stimuli are detected by MECHANORECEPTORS in the skin and mucous membranes.
The outermost of the three MENINGES, a fibrous membrane of connective tissue that covers the brain and the spinal cord.
A purinergic P2X neurotransmitter receptor involved in sensory signaling of TASTE PERCEPTION, chemoreception, visceral distension, and NEUROPATHIC PAIN. The receptor comprises three P2X3 subunits. The P2X3 subunits are also associated with P2X2 RECEPTOR subunits in a heterotrimeric receptor variant.
NERVE GROWTH FACTOR is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
The observable response an animal makes to any situation.
An intense itching sensation that produces the urge to rub or scratch the skin to obtain relief.
Proteins that share the common characteristic of binding to carbohydrates. Some ANTIBODIES and carbohydrate-metabolizing proteins (ENZYMES) also bind to carbohydrates, however they are not considered lectins. PLANT LECTINS are carbohydrate-binding proteins that have been primarily identified by their hemagglutinating activity (HEMAGGLUTININS). However, a variety of lectins occur in animal species where they serve diverse array of functions through specific carbohydrate recognition.
Compounds capable of relieving pain without the loss of CONSCIOUSNESS.
A richly vascularized and innervated connective tissue of mesodermal origin, contained in the central cavity of a tooth and delimited by the dentin, and having formative, nutritive, sensory, and protective functions. (Jablonski, Dictionary of Dentistry, 1992)
A subgroup of TRP cation channels named after melastatin protein. They have the TRP domain but lack ANKYRIN repeats. Enzyme domains in the C-terminus leads to them being called chanzymes.
Compounds that bind to and stimulate ADENOSINE A1 RECEPTORS.
The process by which PAIN is recognized and interpreted by the brain.
Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.
The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.
An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order TETRAODONTIFORMES, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction.
A nerve originating in the lumbar spinal cord (usually L2 to L4) and traveling through the lumbar plexus to provide motor innervation to extensors of the thigh and sensory innervation to parts of the thigh, lower leg, and foot, and to the hip and knee joints.
A class of disabling primary headache disorders, characterized by recurrent unilateral pulsatile headaches. The two major subtypes are common migraine (without aura) and classic migraine (with aura or neurological symptoms). (International Classification of Headache Disorders, 2nd ed. Cephalalgia 2004: suppl 1)
A subgroup of TRP cation channels that contain 3-4 ANKYRIN REPEAT DOMAINS and a conserved C-terminal domain. Members are highly expressed in the CENTRAL NERVOUS SYSTEM. Selectivity for calcium over sodium ranges from 0.5 to 10.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
A heterogenous group of transient or low voltage activated type CALCIUM CHANNELS. They are found in cardiac myocyte membranes, the sinoatrial node, Purkinje cells of the heart and the central nervous system.
A water-soluble extractive mixture of sulfated polysaccharides from RED ALGAE. Chief sources are the Irish moss CHONDRUS CRISPUS (Carrageen), and Gigartina stellata. It is used as a stabilizer, for suspending COCOA in chocolate manufacture, and to clarify BEVERAGES.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A protein kinase C subtype that was originally characterized as a CALCIUM-independent, serine-threonine kinase that is activated by PHORBOL ESTERS and DIACYLGLYCEROLS. It is targeted to specific cellular compartments in response to extracellular signals that activate G-PROTEIN-COUPLED RECEPTORS; TYROSINE KINASE RECEPTORS; and intracellular protein tyrosine kinase.
A vesicular glutamate transporter protein that is predominately expressed in the DIENCEPHALON and lower brainstem regions of the CENTRAL NERVOUS SYSTEM.
The process in which specialized SENSORY RECEPTOR CELLS transduce peripheral stimuli (physical or chemical) into NERVE IMPULSES which are then transmitted to the various sensory centers in the CENTRAL NERVOUS SYSTEM.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Chemical compounds which yield hydrogen ions or protons when dissolved in water, whose hydrogen can be replaced by metals or basic radicals, or which react with bases to form salts and water (neutralization). An extension of the term includes substances dissolved in media other than water. (Grant & Hackh's Chemical Dictionary, 5th ed)
A highly reactive aldehyde gas formed by oxidation or incomplete combustion of hydrocarbons. In solution, it has a wide range of uses: in the manufacture of resins and textiles, as a disinfectant, and as a laboratory fixative or preservative. Formaldehyde solution (formalin) is considered a hazardous compound, and its vapor toxic. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p717)
Injuries to the PERIPHERAL NERVES.
Oils derived from plants or plant products.
Disorders of sensory information received from superficial and deep regions of the body. The somatosensory system conveys neural impulses which pertain to proprioception, tactile sensation, thermal sensation, pressure sensation, and pain. PERIPHERAL NERVOUS SYSTEM DISEASES; SPINAL CORD DISEASES; and BRAIN DISEASES may be associated with impaired or abnormal somatic sensation.
A species of the genus MACACA which typically lives near the coast in tidal creeks and mangrove swamps primarily on the islands of the Malay peninsula.

Adenoviral gene transfer into the normal and injured spinal cord: enhanced transgene stability by combined administration of temperature-sensitive virus and transient immune blockade. (1/1699)

This study characterized gene transfer into both normal and injured adult rat dorsal spinal cord using first (E1-/E3-) or second (E1-/E2A125/E3-, temperature-sensitive; ts) generation of replication-defective adenoviral (Ad) vectors. A novel immunosuppressive regimen aimed at blocking CD4/CD45 lymphocytic receptors was tested for improving transgene persistence. In addition, the effect of gene transfer on nociception was also evaluated. Seven days after treatment, numerous LacZ-positive cells were observed after transfection with either viral vector. By 21 days after transfection, beta-galactosidase staining was reduced and suggestive of ongoing cytopathology in both Ad-treated groups, despite the fact that the immunogenicity of LacZ/Adts appeared less when compared with that elicited by the LacZ/Ad vector. In contrast, immunosuppressed animals showed a significant (P < or = 0.05) increase in the number of LacZ-positive cells not displaying cytopathology. In these animals, a concomitant reduction in numbers of macrophages/microglia and CD4 and CD8 lymphocytes was observed. Only animals that received LacZ/Adts and immunosuppression showed transgene expression after 60 days. Similar results were observed in animals in which the L4-L5 dorsal roots were lesioned before transfection. Gene transfer into the dorsal spinal cord did not affect nociception, independent of the adenovirus vector. These results indicate that immune blockade of the CD4/CD45 lymphocytic receptors enhanced transgene stability in adult animals with normal or injured spinal cords and that persistent transgene expression in the spinal cord does not interfere with normal neural function.  (+info)

Uninjured C-fiber nociceptors develop spontaneous activity and alpha-adrenergic sensitivity following L6 spinal nerve ligation in monkey. (2/1699)

We investigated whether uninjured cutaneous C-fiber nociceptors in primates develop abnormal responses after partial denervation of the skin. Partial denervation was induced by tightly ligating spinal nerve L6 that innervates the dorsum of the foot. Using an in vitro skin-nerve preparation, we recorded from uninjured single afferent nerve fibers in the superficial peroneal nerve. Recordings were made from 32 C-fiber nociceptors 2-3 wk after ligation and from 29 C-fiber nociceptors in control animals. Phenylephrine, a selective alpha1-adrenergic agonist, and UK14304 (UK), a selective alpha2-adrenergic agonist, were applied to the receptive field for 5 min in increasing concentrations from 0.1 to 100 microM. Nociceptors from in vitro control experiments were not significantly different from nociceptors recorded by us previously in in vivo experiments. In comparison to in vitro control animals, the afferents found in lesioned animals had 1) a significantly higher incidence of spontaneous activity, 2) a significantly higher incidence of response to phenylephrine, and 3) a higher incidence of response to UK. In lesioned animals, the peak response to phenylephrine was significantly greater than to UK, and the mechanical threshold of phenylephrine-sensitive afferents was significantly lower than for phenylephrine-insensitive afferents. Staining with protein gene product 9.5 revealed an approximately 55% reduction in the number of unmyelinated terminals in the epidermis of the lesioned limb compared with the contralateral limb. Thus uninjured cutaneous C-fiber nociceptors that innervate skin partially denervated by ligation of a spinal nerve acquire two abnormal properties: spontaneous activity and alpha-adrenergic sensitivity. These abnormalities in nociceptor function may contribute to neuropathic pain.  (+info)

The effects of inflammation and inflammatory mediators on nociceptive behaviour induced by ATP analogues in the rat. (3/1699)

1. We have studied the behavioural effects of intraplantar injections of adenosine 5'-triphosphate (ATP) and related compounds in freely moving rats and investigated whether these nociceptive effects are augmented in the presence of inflammatory mediators. 2. We find that in normal animals ATP and analogues produce dose-dependent nocifensive behaviour (seen as bursts of elevation of the treated hindpaw), and localized thermal hyperalgesia. The rank order of potency was: alpha,beta-methyleneadenosine 5'-triphosphate (alpha,beta-methylene ATP) > 2-methylthioadenosine triphosphate (2-methylthio ATP) > ATP. After neonatal treatment with capsaicin, to destroy small calibre primary sensory neurones, nocifensive behaviour was largely absent. 3. The effects of ATP analogues were assessed in three models of peripheral sensitization: 2 h after dilute intraplantar carrageenan (0.25% w v(-1)); 24 h after irradiation of the hindpaw with ultraviolet (U.V.) B; immediately following prostaglandin E2 (PGE2) treatment. In all models the effect of alpha,beta-methylene ATP was greatly augmented. After carrageenan, significant hindpaw-lifting behaviour activity was induced by injection of only 0.05 nmol of alpha,beta-methylene ATP, some 100 times less than necessary in normal skin. 4. Our data suggest that it is much more likely that endogenous levels of ATP will reach levels capable of exciting nociceptors in inflamed versus normal skin. Our data also suggest the involvement of P2X3 receptor subunits in ATP-induced nociception.  (+info)

The distribution of neurons expressing calcium-permeable AMPA receptors in the superficial laminae of the spinal cord dorsal horn. (4/1699)

The superficial dorsal horn is a major site of termination of nociceptive primary afferents. Fast excitatory synaptic transmission in this region is mediated mainly by release of glutamate onto postsynaptic AMPA and NMDA receptors. NMDA receptors are known to be Ca2+-permeable and to provide synaptically localized Ca2+ signals that mediate short-term and long-term changes in synaptic strength. Less well known is a subpopulation of AMPA receptors that is Ca2+-permeable and has been shown to be synaptically localized on dorsal horn neurons in culture (Gu et al., 1996) and expressed by dorsal horn neurons in situ (Nagy et al., 1994; Engelman et al., 1997). We used kainate-induced cobalt uptake as a functional marker of neurons expressing Ca2+-permeable AMPA receptors and combined this with markers of nociceptive primary afferents in the postnatal rat dorsal horn. We have shown that cobalt-positive neurons are located in lamina I and outer lamina II, a region strongly innervated by nociceptors. These cobalt-positive neurons colocalize with afferents labeled by LD2, and with the most dorsal region of capsaicin-sensitive and IB4- and LA4-positive afferents. In contrast, inner lamina II has a sparser distribution of cobalt-positive neurons. Some lamina I neurons expressing the NK1 receptor, the receptor for substance P, are also cobalt positive. These neurons are likely to be projection neurons in the nociceptive pathway. On the basis of all of these observations, we propose that Ca2+-permeable AMPA receptors are localized to mediate transmission of nociceptive information.  (+info)

Role of protein kinase A in the maintenance of inflammatory pain. (5/1699)

Although the initiation of inflammatory pain (hyperalgesia) has been demonstrated to require the cAMP second messenger signaling cascade, whether this mechanism and/or other mechanisms underlie the continued maintenance of the induced hyperalgesia is unknown. We report that injection of adenylyl cyclase inhibitors before but not after injection of direct-acting hyperalgesic agents (prostaglandin E2 and purine and serotonin receptor agonists) resulted in reduction in hyperalgesia, evaluated by the Randall-Selitto paw-withdrawal test. In contrast, injection of protein kinase A (PKA) inhibitors either before or after these hyperalgesic agents resulted in reduced hyperalgesia, suggesting that hyperalgesia after its activation was maintained by persistent PKA activity but not by adenylyl cyclase activity. To evaluate further the role of PKA activity in the maintenance of hyperalgesia, we injected the catalytic subunit of PKA (PKACS) that resulted in hyperalgesia similar in magnitude to that induced by the direct-acting hyperalgesic agents but much longer in duration (>48 vs 2 hr). Injection of WIPTIDE (a PKA inhibitor) at 24 hr after PKACS reduced hyperalgesia, suggesting that PKACS hyperalgesia is not independently maintained by steps downstream from PKA. In summary, our results indicate that, once established, inflammatory mediator-induced hyperalgesia is no longer maintained by adenylyl cyclase activity but rather is dependent on ongoing PKA activity. An understanding of the mechanism maintaining hyperalgesia may provide important insight into targets for the treatment of persistent pain.  (+info)

Alteration of descending modulation of nociception during the course of monoarthritis in the rat. (6/1699)

Diffuse noxious inhibitory controls (DNIC), which involve supraspinal structures and modulate the transmission of nociceptive signals, were investigated at different stages during the development of adjuvant-induced monoarthritis in the rat. After behavioral evaluation, recordings of trigeminal convergent neurons were performed in anesthetized animals with acute (24-48 hr) or chronic (3-4 weeks) monoarthritis of the ankle. Inhibitions of C-fiber-evoked neuronal responses during and after the application of noxious conditioning stimuli to the ankle were measured to evaluate DNIC. The conditioning stimuli consisted of mechanical (maximal flexion and graded pressures) and graded thermal stimuli and were applied alternately to normal and arthritic ankles. Behaviorally, the two groups of animals exhibited a similar increased sensitivity to mechanical stimuli applied to the arthritic joint (i.e., an increased ankle-bend score and a decreased vocalization threshold to pressure stimuli). However, they showed different electrophysiological profiles. In the animals with acute monoarthritis, the DNIC-induced inhibitions produced by mechanical or thermal stimulation of the arthritic joint were significantly increased at all intensities compared with the normal joint. In contrast, in the chronic stage of monoarthritis, the DNIC-induced inhibitions triggered by thermal or pressure stimuli were similar for both ankles, except with the most intense mechanical stimuli. This discrepancy between the behavioral and electrophysiological findings suggests that inputs activated during chronic monoarthritis may fail to recruit DNIC and may thus be functionally different from those activated in the acute stage of inflammation.  (+info)

Activity-dependent slowing of conduction differentiates functional subtypes of C fibres innervating human skin. (7/1699)

1. The effects of impulse activity on conduction in cutaneous C fibres have been examined in 46 microneurographic recordings from 11 normal subjects and 11 diabetic patients with normal nerve conduction. A tungsten microelectrode was inserted into a cutaneous nerve, usually the superficial peroneal close to the ankle, and intraneural microstimulation was used to identify an area of skin innervated. Three minute trains of 0.25 ms stimuli at 1, 2 and 4 Hz were then delivered to the surface of the skin, separated by intervals of 6 min with stimulation at 0.25 Hz. Slowing and block of conduction were measured from the nerve responses for up to seven C units per stimulation sequence. 2. Three types of C unit were distinguished by their responses to repetitive stimulation: type 1 units slowed progressively during the 3 min trains; slowing of type 2 units reached a plateau within 1 min; while type 3 units hardly slowed at all. Data from normal and diabetic subjects did not differ and were pooled. After 3 min at 2 Hz, the percentage increases in latency were for type 1, 28.3 +/- 9.7 (n = 63 units, mean +/- s.d.); for type 2, 5.2 +/- 1.6 (n = 14); and for type 3, 0.8 +/- 0.5 (n = 5), with no overlap. After 3 min at 4 Hz, 58 % of type 1 units (but no type 2 or 3 units) blocked intermittently. Recovery of latency after stimulation was faster for type 2 than for type 1 units, but conduction velocities of the three types were similar. 3. Type 1 units were identified as nociceptors and 7 type 2 units were identified as 'cold' fibres, activated by non-noxious cold, with no overlap in modality. None of the units tested was activated by weak mechanical stimuli or reflex sympathetic activation. 4. Spike waveforms were averaged for 18 type 1, 10 type 2 and 6 type 3 units. All units had predominantly triphasic action potentials with a major negative peak, but those of type 3 units were on average both smaller and briefer than those of type 1 and type 2 units. 5. It is concluded that repetitive electrical stimulation reliably differentiates nociceptive from cold-specific C fibres innervating human hairy skin, as has previously been shown for the rat. Cold fibres can propagate impulses continuously at much higher rates than nociceptive fibres. The nature of the type 3 units is unclear.  (+info)

Ketamine-induced peripheral analgesia in rats. (8/1699)

AIM: To examine whether ketamine may directly act at peripheral nociceptors to produce analgesia. METHODS: Wistar rats were anesthetized with urethane. As a nociceptive flexion reflex (FR), C responses from the posterior biceps semitendinosus (PBST) muscle was evoked by electrical stimulation (2 ms, 80 V, 2-3 pulses, 0.5 Hz) via a pair of stainless steel needles inserted subcutaneously applied to the two toes of ipsilateral hindpw. RESULTS: Subcutaneous injection of ketamine (36 mmol.L-1, 5 microL) into the ipsilateral hindpaw produced an inhibition of C responses. At 9 min after application of ketamine, injection of naloxone (1%, 5 microL) into the same area annulled ketamine-induced inhibition. CONCLUSION: Ketamine as a dissociate anesthetic acts on peripheral nociceptors to produce analgesia, which is related to activity of peripheral opioid receptors.  (+info)

Hyperalgesia is often seen in people with chronic pain conditions, such as fibromyalgia, and it can also be a side effect of certain medications or medical procedures. Treatment options for hyperalgesia depend on the underlying cause of the condition, but may include pain management techniques, physical therapy, and medication adjustments.

In clinical settings, hyperalgesia is often assessed using a pinprick test or other pain tolerance tests to determine the patient's sensitivity to different types of stimuli. The goal of treatment is to reduce the patient's pain and improve their quality of life.

There are several different types of pain, including:

1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.

The medical field uses a range of methods to assess and manage pain, including:

1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.

It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.

Neuralgia is often difficult to diagnose and treat, as the underlying cause can be challenging to identify. However, various medications and therapies can help manage the pain and other symptoms associated with this condition. These may include pain relievers, anticonvulsants, antidepressants, and muscle relaxants, as well as alternative therapies such as acupuncture or physical therapy.

Some common forms of neuralgia include:

1. Trigeminal neuralgia: This is a condition that affects the trigeminal nerve, which carries sensation from the face to the brain. It is characterized by sudden, intense pain in the face, typically on one side.
2. Postherpetic neuralgia (PHN): This is a condition that occurs after a shingles infection, and is characterized by persistent pain in the affected area.
3. Occipital neuralgia: This is a condition that affects the nerves in the back of the head and neck, and can cause pain in the back of the head, neck, and face.
4. Geniculate neuralgia: This is a rare condition that affects the nerves in the jaw and ear, and can cause pain in the jaw, face, and ear.

Overall, neuralgia is a complex and debilitating condition that can significantly impact an individual's quality of life. It is important for individuals experiencing symptoms of neuralgia to seek medical attention to determine the underlying cause and develop an appropriate treatment plan.

The symptoms of neuritis can vary depending on the specific nerve affected and the severity of the inflammation. Some common symptoms include:

* Pain along the course of the affected nerve
* Numbness or tingling in the affected area
* Weakness or muscle wasting in the affected muscles
* Difficulty moving or controlling the affected limbs
* Sensory loss or altered sensation in the affected area

Neuritis can affect any nerve in the body, but it is most common in the:

* Peripheral nerves (nerves that connect the brain and spinal cord to the rest of the body)
* Optic nerve (which carries visual information from the eye to the brain)
* Auditory nerve (which carries sound information from the inner ear to the brain)
* Spinal nerves (which run down the spine and carry sensory information to and from the brain)

Treatment of neuritis depends on the underlying cause and the severity of the condition. It may involve medications such as pain relievers, anti-inflammatory drugs, or corticosteroids, as well as physical therapy and lifestyle modifications to manage symptoms and promote healing. In some cases, surgery may be necessary to relieve compression or damage to the affected nerve.

Preventive measures for neuritis include:

* Maintaining a healthy lifestyle, including regular exercise, a balanced diet, and adequate sleep
* Avoiding exposure to toxins or other harmful substances that can damage nerves
* Managing chronic conditions such as diabetes, autoimmune disorders, or infections that can increase the risk of neuritis.

Neurogenic inflammation is often characterized by a heightened immune response, increased production of cytokines, and activation of immune cells such as macrophages and microglia. This condition can lead to a range of symptoms including pain, swelling, redness, and loss of function in the affected area.

Neurogenic inflammation can be difficult to diagnose as it can mimic other conditions such as infection or autoimmune disorders. Treatment options for neurogenic inflammation vary depending on the underlying cause but may include immunosuppressive medications, anti-inflammatory drugs, and therapies aimed at reducing nerve damage and promoting healing.

In summary, neurogenic inflammation is a complex condition that can result from various forms of nervous system damage or injury. It is characterized by an exaggerated immune response, increased production of pro-inflammatory cytokines, and activation of immune cells. Accurate diagnosis and appropriate treatment are essential to prevent further nerve damage and promote healing.

There are two main types of pulpitis:

1. Reversible pulpitis: This type of pulpitis is reversible and can be treated with conservative measures such as a filling or a root canal. The inflammation and infection in the pulp tissue can resolve with proper treatment, and the tooth can survive.
2. Irreversible pulpitis: This type of pulpitis is irreversible and cannot be treated with conservative measures. The inflammation and infection in the pulp tissue are severe and have damaged the pulp beyond repair. In this case, the only option is to extract the tooth.

Symptoms of pulpitis may include:

* Sensitivity to hot or cold foods and drinks
* Pain when biting or chewing
* Swelling and tenderness in the affected gum tissue
* Discoloration of the tooth

If left untreated, pulpitis can lead to more severe conditions such as an abscess or bacterial endocarditis, which can have serious consequences. Therefore, it is essential to seek professional dental care if symptoms of pulpitis are present. A dentist will perform a thorough examination and may take X-rays to determine the extent of the damage and recommend appropriate treatment.

Treatment options for pulpitis depend on the severity of the condition and may include:

* Conservative measures such as fillings or crowns to address any underlying decay or structural issues
* Root canal therapy to remove the infected pulp tissue and preserve the tooth
* Extraction of the affected tooth if the damage is too severe or if the tooth cannot be saved.

The exact mechanisms by which alcohol causes nerve damage are not fully understood, but it is thought that long-term alcohol consumption can lead to oxidative stress, inflammation, and damage to the protective covering of nerve fibers. This can disrupt the normal functioning of the nerves, leading to the symptoms of alcoholic neuropathy.

The risk of developing alcoholic neuropathy increases with the amount and duration of alcohol consumption. Other factors that may contribute to the development of this condition include poor nutrition, certain medications, and underlying medical conditions such as diabetes or liver disease.

There is no cure for alcoholic neuropathy, but abstaining from alcohol can help slow the progression of the condition. Treatment may also involve managing underlying medical conditions, taking pain relievers to manage symptoms, and physical therapy to improve mobility and coordination.

In summary, alcoholic neuropathy is a type of nerve damage that occurs as a result of excessive alcohol consumption over an extended period of time. It can cause a range of symptoms and can be managed with abstinence, treatment of underlying medical conditions, and pain relief medication.

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

Pruritus can be acute or chronic, depending on its duration and severity. Acute pruritus is usually caused by a specific trigger, such as an allergic reaction or insect bite, and resolves once the underlying cause is treated or subsides. Chronic pruritus, on the other hand, can persist for months or even years and may be more challenging to diagnose and treat.

Some common causes of pruritus include:

1. Skin disorders such as atopic dermatitis, psoriasis, eczema, and contact dermatitis.
2. Allergic reactions to medications, insect bites, or food.
3. Certain systemic diseases such as kidney disease, liver disease, and thyroid disorders.
4. Pregnancy-related itching (obstetric pruritus).
5. Cancer and its treatment, particularly chemotherapy-induced itching.
6. Nerve disorders such as peripheral neuropathy and multiple sclerosis.
7. Infections such as fungal, bacterial, or viral infections.
8. Parasitic infestations such as scabies and lice.

Managing pruritus can be challenging, as it often leads to a vicious cycle of scratching and skin damage, which can exacerbate the itching sensation. Treatment options for pruritus depend on the underlying cause, but may include topical corticosteroids, oral antihistamines, immunomodulatory drugs, and other medications. In severe cases, hospitalization may be necessary to address the underlying condition and provide symptomatic relief.

In conclusion, pruritus is a common symptom with many possible causes, ranging from skin disorders to systemic diseases and infections. Diagnosis and management of pruritus require a comprehensive approach, involving both physical examination and laboratory tests to identify the underlying cause, as well as appropriate treatment options to provide relief and prevent complications.

Peripheral Nervous System Diseases can result from a variety of causes, including:

1. Trauma or injury
2. Infections such as Lyme disease or HIV
3. Autoimmune disorders such as Guillain-Barré syndrome
4. Genetic mutations
5. Tumors or cysts
6. Toxins or poisoning
7. Vitamin deficiencies
8. Chronic diseases such as diabetes or alcoholism

Some common Peripheral Nervous System Diseases include:

1. Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
2. Multiple Sclerosis (MS) - an autoimmune disease that affects the CNS and PNS, causing a range of symptoms including numbness, weakness, and vision problems.
3. Peripheral Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
4. Guillain-Barré syndrome - an autoimmune disorder that causes muscle weakness and paralysis.
5. Charcot-Marie-Tooth disease - a group of inherited disorders that affect the nerves in the feet and legs, leading to muscle weakness and wasting.
6. Friedreich's ataxia - an inherited disorder that affects the nerves in the spine and limbs, leading to coordination problems and muscle weakness.
7. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) - an autoimmune disorder that causes inflammation of the nerves, leading to pain, numbness, and weakness in the affected areas.
8. Amyotrophic Lateral Sclerosis (ALS) - a progressive neurological disease that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness, atrophy, and paralysis.
9. Spinal Muscular Atrophy - an inherited disorder that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.
10. Muscular Dystrophy - a group of inherited disorders that affect the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.

It's important to note that this is not an exhaustive list and there may be other causes of muscle weakness. If you are experiencing persistent or severe muscle weakness, it is important to see a healthcare professional for proper evaluation and diagnosis.

There are several types of migraine disorders, including:

1. Migraine without aura: This is the most common type of migraine, characterized by a throbbing headache on one side of the head, often accompanied by sensitivity to light and sound, nausea, and vomiting.
2. Migraine with aura: This type of migraine is characterized by aura symptoms, such as visual disturbances, speech difficulties, and other neurological symptoms, which occur before the headache.
3. Chronic migraine: This type of migraine is characterized by headaches that occur 15 days or more per month, and can be accompanied by other symptoms such as fatigue, depression, and anxiety.
4. Hemiplegic migraine: This is a rare type of migraine that is characterized by a temporary weakness or paralysis on one side of the body, often accompanied by a severe headache.
5. Familial hemiplegic migraine: This is a rare inherited condition that is characterized by recurrent episodes of temporary weakness or paralysis on one side of the body, often accompanied by headaches.
6. Sporadic hemiplegic migraine: This is a rare condition that is characterized by recurrent episodes of temporary weakness or paralysis on one side of the body, often accompanied by headaches, but without a clear family history.
7. Migraine-related disorders: These are conditions that are associated with migraine, such as stroke, seizures, and autonomic dysfunction.

Migraine disorders can be difficult to diagnose, as the symptoms can vary in severity and frequency, and may overlap with other conditions. However, there are several diagnostic criteria that healthcare providers use to identify migraine disorders, including:

1. Headache frequency: Migraine headaches typically occur more frequently than headaches caused by other conditions, such as tension headaches or sinus headaches.
2. Headache severity: Migraine headaches can be severe and debilitating, often requiring bed rest or medication to relieve the pain.
3. Associated symptoms: Migraine headaches are often accompanied by other symptoms, such as sensitivity to light and sound, nausea, vomiting, and visual disturbances.
4. Family history: A family history of migraine can increase the likelihood of a diagnosis.
5. Physical examination: A healthcare provider may perform a physical examination to look for signs of migraine, such as tenderness in the head and neck muscles or changes in the sensation and strength of the limbs.
6. Imaging tests: Imaging tests, such as CT or MRI scans, may be ordered to rule out other conditions that can cause similar symptoms.
7. Medication trials: Healthcare providers may prescribe medications to treat migraine headaches and observe the patient's response to determine if the condition is migraine-related.

There are several types of headaches, including:

1. Tension headaches: These headaches are caused by muscle tension in the neck and scalp and can be treated with over-the-counter pain relievers.
2. Sinus headaches: These headaches are caused by inflammation or infection in the sinuses and can be treated with antibiotics or decongestants.
3. Cluster headaches: These headaches occur in clusters or cycles and can be very severe, often waking the patient up during the night.
4. Rebound headaches: These headaches are caused by overuse of pain medications and can be treated by stopping the medication and using alternative therapies.
5. Hormonal headaches: These headaches are related to changes in hormone levels, such as those experienced during menstruation or menopause.
6. Caffeine headaches: These headaches are caused by excessive caffeine consumption and can be treated by reducing or avoiding caffeine intake.
7. Dehydration headaches: These headaches are caused by dehydration and can be treated by drinking plenty of water.
8. Medication overuse headaches: These headaches are caused by taking too much pain medication and can be treated by stopping the medication and using alternative therapies.
9. Chronic daily headaches: These headaches are defined as headaches that occur 15 days or more per month and can be caused by a variety of factors, including muscle tension, sinus problems, and other underlying conditions.
10. Migraine headaches: These headaches are characterized by severe pain, often on one side of the head, along with other symptoms such as nausea, vomiting, and sensitivity to light and sound. They can be treated with over-the-counter or prescription medications, as well as alternative therapies such as acupuncture and relaxation techniques.

Headaches can be caused by a variety of factors, including:

1. Muscle tension: Tight muscles in the neck and scalp can lead to headaches.
2. Sinus problems: Inflammation or infection in the sinuses can cause headaches.
3. Allergies: Seasonal allergies or allergies to certain foods or substances can cause headaches.
4. Eye strain: Prolonged use of computers, smartphones, or other digital devices can cause eye strain and lead to headaches.
5. Sleep disorders: Poor sleep quality or insomnia can contribute to headaches.
6. Hormonal changes: Changes in estrogen levels, such as those experienced during menstruation or menopause, can cause headaches.
7. Dehydration: Not drinking enough water can lead to dehydration and contribute to headaches.
8. Poor posture: Slouching or hunching over can lead to muscle tension and contribute to headaches.
9. Stress: High levels of stress can cause muscle tension and contribute to headaches.
10. Diet: Certain foods, such as alcohol, caffeine, chocolate, and MSG, can trigger headaches in some people.

It is important to seek medical attention if you experience any of the following symptoms along with your headache:

1. Fever
2. Confusion or disorientation
3. Severe neck stiffness
4. Pain that worsens with movement or coughing
5. Headaches that occur more frequently or are more severe than usual
6. Headaches that interfere with daily activities or sleep
7. Sudden, severe headaches in someone who has never experienced them before
8. Headaches in someone who is taking certain medications or has a history of medical conditions such as migraines or stroke.

A healthcare professional can help determine the underlying cause of your headaches and recommend appropriate treatment options.

Types of Peripheral Nerve Injuries:

1. Traumatic Nerve Injury: This type of injury occurs due to direct trauma to the nerve, such as a blow or a crush injury.
2. Compression Neuropathy: This type of injury occurs when a nerve is compressed or pinched, leading to damage or disruption of the nerve signal.
3. Stretch Injury: This type of injury occurs when a nerve is stretched or overstretched, leading to damage or disruption of the nerve signal.
4. Entrapment Neuropathy: This type of injury occurs when a nerve is compressed or trapped between two structures, leading to damage or disruption of the nerve signal.

Symptoms of Peripheral Nerve Injuries:

1. Weakness or paralysis of specific muscle groups
2. Numbness or tingling in the affected area
3. Pain or burning sensation in the affected area
4. Difficulty with balance and coordination
5. Abnormal reflexes
6. Incontinence or other bladder or bowel problems

Causes of Peripheral Nerve Injuries:

1. Trauma, such as a car accident or fall
2. Sports injuries
3. Repetitive strain injuries, such as those caused by repetitive motions in the workplace or during sports activities
4. Compression or entrapment of nerves, such as carpal tunnel syndrome or tarsal tunnel syndrome
5. Infections, such as Lyme disease or diphtheria
6. Tumors or cysts that compress or damage nerves
7. Vitamin deficiencies, such as vitamin B12 deficiency
8. Autoimmune disorders, such as rheumatoid arthritis or lupus
9. Toxins, such as heavy metals or certain chemicals

Treatment of Peripheral Nerve Injuries:

1. Physical therapy to improve strength and range of motion
2. Medications to manage pain and inflammation
3. Surgery to release compressed nerves or repair damaged nerves
4. Electrical stimulation therapy to promote nerve regeneration
5. Platelet-rich plasma (PRP) therapy to stimulate healing
6. Stem cell therapy to promote nerve regeneration
7. Injection of botulinum toxin to relieve pain and reduce muscle spasticity
8. Orthotics or assistive devices to improve mobility and function

It is important to seek medical attention if you experience any symptoms of a peripheral nerve injury, as early diagnosis and treatment can help prevent long-term damage and improve outcomes.

Some common types of somatosensory disorders include:

1. Peripheral neuropathy: This is a condition that affects the peripheral nerves outside of the central nervous system. It can be caused by a variety of factors, including diabetes, infections, and certain medications.
2. Neuralgia: This is a chronic pain disorder that is characterized by episodes of intense pain, often accompanied by numbness or tingling.
3. Sensory ataxia: This is a condition that affects the sensory nerves and can cause difficulties with balance, coordination, and spatial awareness.
4. Dystonia: This is a movement disorder that can cause involuntary contractions of muscles, leading to abnormal postures or movements.
5. Restless leg syndrome: This is a condition characterized by an uncomfortable sensation in the legs, often described as a creeping or crawling feeling. It can be accompanied by an urge to move the legs to relieve the discomfort.
6. Paresthesia: This is a condition that causes numbness, tingling, or burning sensations in the skin, often in the hands and feet.
7. Hyperesthesia: This is a condition characterized by an increased sensitivity to touch, temperature, or other sensory stimuli.
8. Hypersensitivity to sound or light: This is a condition where individuals may experience discomfort or pain from ordinary sounds or lights that would not normally cause discomfort.
9. Tactile defensiveness: This is a condition where individuals may have an abnormal aversion to certain textures or sensations, such as the feel of clothing or the taste of certain foods.
10. Sensory processing disorder: This is a condition where the brain has difficulty processing and integrating sensory information from the environment, leading to difficulties with sensory integration and motor planning.

It's important to note that these conditions are not mutually exclusive, and individuals may experience overlapping symptoms or multiple conditions at once. It's also worth noting that these conditions can be present in individuals of all ages, genders, and backgrounds.

In mammals, nociceptors are found in any area of the body that can sense noxious stimuli. External nociceptors are found in ... The majority of nociceptors are classified by which of the environmental modalities they respond to. Some nociceptors respond ... Thermal nociceptors are activated by noxious heat or cold at various temperatures. There are specific nociceptor transducers ... Peripheral sensitization represents a form of functional plasticity of the nociceptor. The nociceptor can change from being ...
Some nociceptors are unspecialized free nerve endings that have their cell bodies outside the spinal column in the dorsal root ... Nociceptors are categorized according to the axons which travel from the receptors to the spinal cord or brain. After nerve ... Nociceptors have a certain threshold; that is, they require a minimum intensity of stimulation before they trigger a signal. ... Other nociceptors rely on specialised structures in the skin to transduce noxious information such as nociceptive schwann cells ...
Dozens of different types of nociceptor ion channels have so far been identified, and their exact functions are still being ... Superficial somatic pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well- ... At the peripheral end of the nociceptor, noxious stimuli generate currents that, above a given threshold, send signals along ... Lynn B (1984). "Cutaneous nociceptors". In Winlow W, Holden AV (eds.). The neurobiology of pain: Symposium of the Northern ...
Lynn B (1984). "Cutaneous nociceptors". In Winlow W; Holden AV (eds.). The neurobiology of pain: Symposium of the Northern ...
Lynn B (1984). "Cutaneous nociceptors". In Winlow W, Holden AV (ed.). The neurobiology of pain: Symposium of the Northern ...
ISBN 978-1-4377-1604-7. Belmonte, Carlos; Gallar Juana (1996). "6: Corneal Nociceptors". Neurobiology of Nociceptors. Oxford ...
Learning and memory using nociceptors in the sea hare, Aplysia has been described. Mollusk neurons are able to detect ... Nociceptors: a phylogenetic view. Journal of Comparative Physiology A, 195: 1089-1106 Wasserthal, Lutz T. (1998). Chapter 25: ...
Her publications include: Braithwaite, Victoria (2003). "Do fishes have nociceptors? Evidence for the evolution of a vertebrate ... nociceptors). She showed that fish produce pain-killing opioids in the same way that mammals do. She then investigated whether ...
Nerve impulses from nociceptors may reach the brain, where information about the stimulus (e.g. quality, location, and ... Most insects do not possess nociceptors, one known exception being the fruit fly. In vertebrates, endogenous opioids are ... St John Smith, E.; Lewin, G.R. (2009). "Nociceptors: a phylogenetic view". Journal of Comparative Physiology A. 195 (12): 1089- ... 2003). "Do fishes have nociceptors? Evidence for the evolution of a vertebrate sensory system". Proc Biol Sci. 270 (1520): 1115 ...
Nociceptors in fish were first identified in 2002. The study was designed to determine whether nociceptors were present in the ... Rainbow trout also have corneal nociceptors. Out of 27 receptors investigated in one study, seven were polymodal nociceptors ... Further studies found nociceptors to be more widely distributed over the bodies of rainbow trout, as well as those of cod and ... Bony fish possess nociceptors that are similar in function to those in mammals. There are two types of nerve fibre relevant to ...
Therefore, they satisfy accepted definitions of nociceptors. They also show similarities to vertebrate Aδ nociceptors, ... Nociceptors are sensory receptors that respond to potentially damaging stimuli by sending nerve signals to the brain. Although ... Similarly, capsaicin triggers nociceptors in some invertebrates, but this substance is not noxious to Drosophila melanogaster ( ... Nociceptors have been identified in a wide range of invertebrate species, including annelids, molluscs, nematodes and ...
Following beak trimming of older or adult hens, the nociceptors in the beak stump show abnormal patterns of neural discharge, ... The beak is a complex, functional organ with an extensive nervous supply including nociceptors that sense pain and noxious ... "Guidance on keeping of Chickens" (PDF). Breward, J., (1984). Cutaneous nociceptors in the chicken beak. Proceedings of the ...
Following beak trimming of older or adult hens, the nociceptors in the beak stump show abnormal patterns of neural discharge, ... Breward, J., (1984). Cutaneous nociceptors in the chicken beak. Proceedings of the Journal of Physiology, London 346: 56 Gentle ...
Pain receptors are known as nociceptors. Two main types of nociceptors exist, A-fiber nociceptors and C-fiber nociceptors. A- ...
Brain Brain tissue itself contains no nociceptors; brain tumors cause pain by pressing on blood vessels or the membrane that ... Invasion of soft tissue by a tumor can cause pain by inflammatory or mechanical stimulation of nociceptors, or destruction of ... Tumors can cause pain by crushing or infiltrating tissue, or by releasing chemicals that make nociceptors responsive to stimuli ... and they release chemicals that stimulate nociceptors. As they grow, tumors compress, consume, infiltrate or cut off blood ...
Once stimulated, a nociceptor sends a message up the length of the nerve fiber to the nerve cells in the brain, signalling that ... Dubin AE, Patapoutian A (November 2010). "Nociceptors: the sensors of the pain pathway". The Journal of Clinical Investigation ...
Mechano-sensitive C nociceptors, also known as polymodal C nociceptors are activated by several kinds of stimuli, i.e. ... The mechano-insensitive C nociceptors, also known as silent nociceptors, differ from polymodal afferents in other respects as ... The mechano-insensitive nociceptors may be sensitized particularly by inflammatory mediators to render them mechano-responsive ... Most studies are focused on C nociceptors. The nociceptive C-fibers constitute a very large proportion of somatic afferent ...
Fitzgerald, Maria (1978). The sensitization of cutaneous nociceptors (PhD thesis). University College London. OCLC 926251169. " ...
Fitzgerald studies the developmental physiology and neurobiology of nociceptor circuits in the brain and spinal cord. Her work ... Fitzgerald, Maria (1978). The sensitization of cutaneous nociceptors (PhD thesis). University College London. OCLC 926251169. ...
Once a danger receptor (called "nociceptor") has been stimulated, the signal travels via the sensory nerve to the dorsal ( ... Interneuron Nociceptor Reflex Solomon; Schmidt (1990). "13". In Carol, Field (ed.). Human Anatomy & physiology (2 ed.). ...
"Bradykinin Induces TRPV1 Exocytotic Recruitment in Peptidergic Nociceptors". Frontiers in Pharmacology. 7: 178. doi:10.3389/ ...
Two major classes of human C-fibre nociceptors exist: mechano-responsive nociceptors and mechano-insensitive nociceptors. ... Mechano-responsive nociceptors have been shown in studies to respond to mostly pain, and mechano-insensitive receptors respond ... Overall, itch sensation is mediated by A-delta and C nociceptors located in the uppermost layer of the skin. Using single-cell ... In addition, expression of neuro growth factors (NGF) can cause structural changes in nociceptors, such as sprouting. NGF is ...
Puri, S. & Faulkes, Z. (2010). "Do decapod crustaceans have nociceptors for extreme pH?". PLOS ONE. 5 (4): e10244. Bibcode: ... which may be specialized nociceptors. The common brown shrimp Crangon crangon and the prawns Palaemon serratus and Palaemon ...
Mechanical nociceptors respond to excess pressure or mechanical deformation, such as a pinch. Chemical nociceptors respond to a ... Nociceptors respond to potentially damaging stimuli by sending signals to the spinal cord and brain. This process, called ... They are found in internal organs as well as on the surface of the body to "detect and protect". Nociceptors detect different ... Nociceptors are responsible for processing pain and temperature changes. The burning pain and irritation experienced after ...
Therefore, not all noxious stimuli are adequate stimuli of nociceptors. The adequate stimuli of nociceptors are termed ...
... people with the condition also have hyper-excitable nociceptors. When people with fibromyalgia are subjected to intense stimuli ...
Thermal nociceptors are activated by noxious heat or cold at various temperatures. Mechanical nociceptors respond to excess ... Chemical nociceptors respond to a wide variety of chemicals, some of which are signs of tissue damage. They are involved in the ... Nociceptors detect different kinds of damaging stimuli or actual damage. Those that only respond when tissues are damaged are ... Nociceptors respond to potentially damaging stimuli by sending signals to the spinal cord and brain. This process, called ...
Snider, W. D.; McMahon, S. B. (Apr 1998). "Tackling pain at the source: new ideas about nociceptors". Neuron. 20 (4): 629-32. ... as the neck of the posterior column and receives information from mechanoreceptors and danger information from nociceptors. It ...
Formaldehyde Nociceptor Withdrawal reflex Carter, Matt; Shieh, Jennifer C. (2010). "Nociception". Guide to Research Techniques ... reflecting direct activation of nociceptors and the late or tonic phase (15 to 20 minutes after the injection) reflecting ... caused by stimulation of nociceptors. These assays measure the existence of pain through behaviors such as withdrawal, licking ...
However a small fraction of these fast fibres, termed "ultrafast nociceptors", also transmit pain. Type Aδ fibers are the ... and nociceptors and thermoreceptors by type III and IV sensory fibers. Type Aα fibers include the type Ia and type Ib sensory ... afferent fibers of nociceptors. Aδ fibers carry information from peripheral mechanoreceptors and thermoreceptors to the dorsal ...
Nociceptors located in the TG and DRG are the primary sensors of damaging or potentially damaging stimuli for the head and body ... Nociceptors in these tissues are critical first neurons in the pain pathway. Injury to peripheral neurons in these tissues can ... While nociceptors in these two tissues show a high degree of functional similarity, there are important differences in their ... These findings have implications for the relative capacity of these nociceptors to be sensitized upon injury. Altogether, our ...
Developing nociceptor-selective treatments for acute and chronic pain Selwyn Jayakar 1 , Jaehoon Shim 1 , Sooyeon Jo 2 , Bruce ... Developing nociceptor-selective treatments for acute and chronic pain Selwyn Jayakar et al. Sci Transl Med. 2021. . ... 2a: Two complementary approaches to identify novel analgesic targets. Human iPSC-derived nociceptors can be used to identify ... Studying human nociceptors: from fundamentals to clinic. Middleton SJ, Barry AM, Comini M, Li Y, Ray PR, Shiers S, ...
nociceptors. Gain Without Pain: New Clues for Analgesic Design Posted on November 7th, 2013. by Dr. Francis Collins ... nociceptors, pain, pain medication, protein, scorpion toxin, venom ...
How nociceptors shape dendritic cell responses *Yvonne Bordon. In Brief. 10 May 2023. ...
Cellular models of human nociceptors have enabled the screening of small molecule and gene therapy approaches on nociceptor ... Studying human nociceptors: from fundamentals to clinic.. Middleton, Steven J; Barry, Allison M; Comini, Maddalena; Li, Yan; ... We hope our ability to directly investigate human nociceptors will not only aid our understanding of the fundamental ... Nociceptors remain an attractive therapeutic target their sensitization makes an important contribution to many chronic pain ...
The protocol included in this technology is the most efficient and reproducible nociceptor differentiation protocol for human ... exclusively into nociceptors (also called sensory neurons) under chemically defined conditions. The use of hPSCs, including ... simultaneous manipulation of specific cell signaling pathways allows the scalable production of large numbers of nociceptors, ...
nociceptors. the relatively unspecialized nerve cell endings that initiate the sensation of pain ... fibers innervating outer hair cells respond to cellular damage resulting from loud sound and thus may serve as the nociceptors ...
Gut-innervating nociceptors found to regulate the intestinal microbiota and promote tissue protection According to a recent ... study, substance P produced by the nociceptors present in the gut lining confers protection against inflammation and tissue ...
Nociceptors depend on cap-dependent translation to rapidly induce proteins synthesis in. * Post author By careersfromscience ... Nociceptors depend on cap-dependent translation to rapidly induce proteins synthesis in response to pro-inflammatory indicators ... NGF and IL-6 quickly stimulate Rabbit Polyclonal to OR2Z1 cap-dependent translation in nociceptors, leading to long-term ... are particular towards the initiation stage of translation which axonal proteins synthesis can be impaired in nociceptor ...
Nociceptors are primarily involved in transmitting pain signals. The cell bodies of nociceptors are located in the spinal cord ... NaV1.7 sodium channels are found in nerve cells called nociceptors. Nociceptors are part of the peripheral nervous system, ... This lack of sodium ions blocks nociceptors from transmitting pain signals from the site of an injury to the brain. ... In people with this condition, the axons that extend from the nociceptors and transmit pain signals degenerate over time. The ...
RNA was extracted from GFP+ and GFP- neurons, and quantitative PCR (qPCR) was run for specific markers of TRPV1 nociceptors (34 ... We used probes for mRNAs encoding Nav1.8 to identify nociceptors (Figure 4A) and found a high degree of colocalization between ... Here, we identified ALKAL2, the ligand for the RTK ALK, as a biomarker of inflammation-induced nociceptor sensitization. We ... Overall, our work uncovers the ALKAL2/ALK signaling axis as a central regulator of nociceptor-induced sensitization. We propose ...
Specialized Mechanosensory Nociceptors Mediating Rapid Responses to Hair Pull.. Ghitani N, Barik A, Szczot M, Thompson JH, Li C ...
Molecular profiling and spatial distribution of visceral nociceptors. *Anatomical or functional localization of nociceptive or ...
Sneddon, LU, Braithwaite, VA and Gentle, MJ 2003 Do fish-es have nociceptors? Evidence for the evolution of a vertebrate ...
Nociceptors / physiology* Actions. * Search in PubMed * Search in MeSH * Add to Search ...
Noxious stimuli usually cause pain and pain usually arises from noxious stimuli, but exceptions to these apparent truisms are the basis for clinically important problems and provide valuable insight into the neural code for pain. In this Review, we discuss how painful sensations arise. We argue that …
Nociceptors are primarily involved in transmitting pain signals. The cell bodies of nociceptors are located in the spinal cord ... NaV1.7 sodium channels are found in nerve cells called nociceptors. Nociceptors are part of the peripheral nervous system, ... This lack of sodium ions blocks nociceptors from transmitting pain signals from the site of an injury to the brain. ... In people with this condition, the axons that extend from the nociceptors and transmit pain signals degenerate over time. The ...
Are the neurons nociceptors, non- nociceptors? Do the neurons respond exclusively to [one type of sensory input, such as touch ... They still have all those nociceptors innervating that tissue. And so its an important area that Dr. Bonica [identified].And ... and those are the ones that are classically the nociceptors that are found there. In addition, if you apply substance P to the ...
Nociceptors: thermal allodynia and thermal pain.. Viana F. Handb Clin Neurol; 2018; 156():103-119. PubMed ID: 30454584. [TBL] ... Sensitization of colonic nociceptors by TNFα is dependent on TNFR1 expression and p38 MAPK activity.. Barker KH; Higham JP; ...
The UB researchers had been investigating sensory neurons called nociceptors, which activate in response to pain caused by ... "Therefore, it is reasonable to consider CGRP+ nociceptors as potential analgesic targets," they wrote. Bhattacharjee and first ... Calcitonin gene-related peptide (CGRP)-containing nociceptors had also previously been identified as the principal coordinators ... The team investigated the effects of pharmacologically inhibiting endocytosis in peripheral nociceptor neurons during ...
Due to direct stimulation of intact nociceptors. *. D. Rarely responsive to opioid analgesics ...
Squid Have Nociceptors That Display Widespread Long-Term Sensitization and Spontaneous Activity after Bodily Injury Robyn J. ...
Sensory neuronsSpinal cordNociceptorsPhysiologyCytology About , FAQ , Policies , Developer Resources, Credits ...
... "irritable nociceptor" subgroup described by others.13,14,20,45 Sensitized nociceptors are associated with overexpression of ... According to the concept that damaged and surviving nociceptors are the key players in the pathophysiology of neuropathic pain, ... Ongoing hyperactivity in surviving nociceptors may be responsible for ongoing pain10 and may lead to some central sensitization ... Capsaicin-sensitive C- and A-fibre nociceptors control long-term potentiation-like pain amplification in humans. Brain 2015;138 ...
Nociceptors-To sense pain, thousands of specialized sensory nerve cells or neurons (nociceptors) throughout the body trigger a ... Nociceptors in the head and face relay pain signals directly to the brain stem, where pain pathways converge. ... have a mutation in part of a gene that plays a role in electrical activity of nociceptors and other types of neurons. A ...
  • Nociceptors in these tissues are critical first neurons in the pain pathway. (iasp-pain.org)
  • This technology includes a robust and highly efficient protocol that differentiates human pluripotent stem cells (hPSCs) exclusively into nociceptors (also called sensory neurons) under chemically defined conditions. (nih.gov)
  • We demonstrate that the consequences from the RNA decoy on translation are particular towards the initiation stage of translation which axonal proteins synthesis can be impaired in nociceptor neurons. (careersfromscience.org)
  • The UB researchers had been investigating sensory neurons called nociceptors, which activate in response to pain caused by injury. (genengnews.com)
  • The team investigated the effects of pharmacologically inhibiting endocytosis in peripheral nociceptor neurons during inflammation, using a small lipidated inhibitor peptide. (genengnews.com)
  • Nociceptors- To sense pain, thousands of specialized sensory nerve cells or neurons (nociceptors) throughout the body trigger a series of responses to a noxious (painful) stimulus. (nih.gov)
  • Nociceptors are part of the peripheral nervous system, which connects the brain and spinal cord to cells that detect sensations such as touch, smell, and pain. (medlineplus.gov)
  • The authors further explained, "Peripheral sensitization of dorsal root ganglion (DRG) nociceptors initiates inflammatory pain and is driven by inflammatory mediators released from immune cells and damaged tissue. (genengnews.com)
  • Nociceptors remain an attractive therapeutic target their sensitization makes an important contribution to many chronic pain states, they are located outside the blood-brain barrier , and they are relatively specific. (bvsalud.org)
  • 13. Sensitization of colonic nociceptors by TNFα is dependent on TNFR1 expression and p38 MAPK activity. (nih.gov)
  • We hope our ability to directly investigate human nociceptors will not only aid our understanding of the fundamental neurobiology underlying acute and chronic pain but also help bridge the translational gap. (bvsalud.org)
  • The preclinical research, conducted by neuroscientists and pharmacologists at the University at Buffalo (UB) Jacobs School of Medicine and Biomedical Sciences, showed that administration of specific lipidated peptide molecules-peptides modified with lipid molecules-to the site of pain, blocked nociceptor endocytosis, and significantly reduced acute and chronic pain-like behaviors and provided prolonged analgesia. (genengnews.com)
  • Added the authors, "We utilized genetic and pharmacological approaches to inhibit nociceptor endocytosis demonstrating its role in the development and maintenance of acute and chronic inflammatory pain. (genengnews.com)
  • According to a recent study, substance P produced by the nociceptors present in the gut lining confers protection against inflammation and tissue damage by increasing the number of beneficial microbes. (news-medical.net)
  • Differences between dorsal root and trigeminal ganglion nociceptors in mice revealed by translational profiling. (iasp-pain.org)
  • The cell bodies of nociceptors are located in the spinal cord. (medlineplus.gov)
  • NaV1.7 sodium channels are found in nerve cells called nociceptors. (medlineplus.gov)
  • Our small peptides are able to penetrate nerve endings and provide long-lasting pain relief after a single administration," said Arin Bhattacharjee, PhD, who is associate professor of pharmacology and toxicology in the Jacobs School, and senior author of the team's published paper in Nature Communications , which is titled, "Inhibiting endocytosis in CGRP + nociceptors attenuates inflammatory pain-like behavior. (genengnews.com)
  • Both are also packed with nerves, specifically nerve ending receptors called nociceptors that are good at detecting actual or potential tissue damage. (wired.com)
  • Nociceptors located in the TG and DRG are the primary sensors of damaging or potentially damaging stimuli for the head and body, respectively, and are key drivers of chronic pain states. (iasp-pain.org)
  • These technological advances have emphasized the maladaptive plastic changes occurring in human nociceptors following injury that contribute to chronic pain . (bvsalud.org)
  • Studying human nociceptors has revealed new therapeutic targets for the suppression of chronic pain and enhanced repair. (bvsalud.org)
  • Nociceptors are primarily involved in transmitting pain signals. (medlineplus.gov)
  • This lack of sodium ions blocks nociceptors from transmitting pain signals from the site of an injury to the brain. (medlineplus.gov)
  • In people with this condition, the axons that extend from the nociceptors and transmit pain signals degenerate over time. (medlineplus.gov)
  • Nociceptors in the head and face relay pain signals directly to the brain stem, where pain pathways converge. (nih.gov)
  • Cellular models of human nociceptors have enabled the screening of small molecule and gene therapy approaches on nociceptor function, and in some cases have enabled correlation with clinical outcomes. (bvsalud.org)
  • Nociceptors depend on cap-dependent translation to rapidly induce proteins synthesis in response to pro-inflammatory indicators. (careersfromscience.org)
  • Contribution of TRPC3 to store-operated calcium entry and inflammatory transductions in primary nociceptors. (rndsystems.com)
  • Genome editing in human induced pluripotent stem cell -derived nociceptors enables the interrogation of the causal role of genes in the regulation of nociceptor function. (bvsalud.org)
  • Many of these techniques are difficult to implement at scale, current induced pluripotent stem cell differentiation protocols do not generate the full diversity of nociceptor populations , and we still have a relatively poor understanding of inter-individual variation in nociceptors due to factors such as age, sex , or ethnicity . (bvsalud.org)
  • Therefore, it is reasonable to consider CGRP+ nociceptors as potential analgesic targets," they wrote. (genengnews.com)
  • While nociceptors in these two tissues show a high degree of functional similarity, there are important differences in their development lineages, their functional connections to the central nervous system, and recent genome-wide analyses of gene expression suggest that they possess some unique genomic signatures. (iasp-pain.org)
  • This unbiased method independently confirms several findings of differences between TG and DRG nociceptors described in the literature but also suggests preferential utilization of key signaling pathways. (iasp-pain.org)
  • Our findings demonstrate previously unrecognized differences between TG and DRG nociceptors that provide new insight into how injury may differentially drive plasticity states in nociceptors in these two tissues. (iasp-pain.org)
  • Both human and rodent nociceptors are more heterogeneous at a molecular level than previously appreciated, and while we find that there are broad similarities between human and rodent nociceptors there are also important differences involving ion channel function, expression, and cellular excitability. (bvsalud.org)
  • These findings have implications for the relative capacity of these nociceptors to be sensitized upon injury. (iasp-pain.org)
  • They lack nociceptors , also known as pain receptors, which eliminates one of the common ethical issues relating to eating animals. (treehugger.com)
  • Altogether, our data provide a comprehensive, comparative view of transcriptome and translatome activity in TG and DRG nociceptors that enhances our understanding of nociceptor biology.The DRG and TG provide sensory information from the body and head, respectively. (iasp-pain.org)
  • Calcitonin gene-related peptide (CGRP)-containing nociceptors had also previously been identified as the principal coordinators of thermal and mechanical sensitivity in various pain models, the team continued. (genengnews.com)
  • For example, we have shown that NGF plays a critical role in the acquisition of transduction competence by nociceptors. (mdc-berlin.de)
  • Studying human nociceptors: from fundamentals to clinic. (bvsalud.org)
  • The protocol included in this technology is the most efficient and reproducible nociceptor differentiation protocol for human pluripotent stem cells. (nih.gov)
  • In addition to nociceptors, NaV1.8 sodium channels have also been found in heart muscle cells where, by controlling the flow of sodium ions, they likely play a role in maintaining a normal heart rhythm. (medlineplus.gov)
  • Many of the mutations result in NaV1.8 sodium channels that open more easily than usual, increasing the flow of sodium ions that produce nerve impulses within nociceptors. (medlineplus.gov)
  • These nonfunctional subunits do not allow NaV1.7 sodium channels to open, preventing the flow of sodium ions into nociceptors. (nih.gov)
  • This technology includes a robust and highly efficient protocol that differentiates human pluripotent stem cells (hPSCs) exclusively into nociceptors (also called sensory neurons) under chemically defined conditions. (nih.gov)
  • Nociceptors- To sense pain, thousands of specialized sensory nerve cells or neurons (nociceptors) throughout the body trigger a series of responses to a noxious (painful) stimulus. (nih.gov)
  • It is known that interactions between nociceptors and dendritic cells (DCs) can modulate immune responses in barrier tissues . (bvsalud.org)
  • Finally, nociceptor -derived chemokine CCL2 contributes to the orchestration of DC-dependent local inflammation and the induction of adaptive responses against skin -acquired antigens . (bvsalud.org)
  • Thus, the combined actions of nociceptor -derived chemokines , neuropeptides , and electrical activity fine-tune DC responses in barrier tissues . (bvsalud.org)
  • Specialized Mechanosensory Nociceptors Mediating Rapid Responses to Hair Pull. (nih.gov)
  • NaV1.8 sodium channels are found in nerve cells called nociceptors that transmit pain signals. (medlineplus.gov)
  • Nociceptors are primarily involved in transmitting pain signals. (medlineplus.gov)
  • In this condition, the small fibers that extend from the nociceptors and transmit pain signals (axons) degenerate over time. (medlineplus.gov)
  • This lack of sodium ions blocks nociceptors from transmitting pain signals from the site of an injury to the brain. (nih.gov)
  • Nociceptors in the head and face relay pain signals directly to the brain stem, where pain pathways converge. (nih.gov)
  • Second, nociceptor activation induces contact-dependent calcium fluxes and membrane depolarization in DCs and enhances their production of proinflammatory cytokines when stimulated. (bvsalud.org)
  • Multimodal control of dendritic cell functions by nociceptors. (bvsalud.org)
  • Systematic testing of various cell culture conditions and simultaneous manipulation of specific cell signaling pathways allows the scalable production of large numbers of nociceptors, including the use of automated cell culture systems. (nih.gov)