Autonomic Fibers, Postganglionic
Autonomic Fibers, Preganglionic
NERVE FIBERS which project from the central nervous system to AUTONOMIC GANGLIA. In the sympathetic division most preganglionic fibers originate with neurons in the intermediolateral column of the SPINAL CORD, exit via ventral roots from upper thoracic through lower lumbar segments, and project to the paravertebral ganglia; there they either terminate in SYNAPSES or continue through the SPLANCHNIC NERVES to the prevertebral ganglia. In the parasympathetic division the fibers originate in neurons of the BRAIN STEM and sacral spinal cord. In both divisions the principal transmitter is ACETYLCHOLINE but peptide cotransmitters may also be released.
Sympathetic Fibers, Postganglionic
Nerve fibers which project from sympathetic ganglia to synapses on target organs. Sympathetic postganglionic fibers use norepinephrine as transmitter, except for those innervating eccrine sweat glands (and possibly some blood vessels) which use acetylcholine. They may also release peptide cotransmitters.
Parasympathetic Fibers, Postganglionic
Ganglia, Parasympathetic
Nerve Fibers
Ganglia, Sympathetic
Parasympathetic Nervous System
The craniosacral division of the autonomic nervous system. The cell bodies of the parasympathetic preganglionic fibers are in brain stem nuclei and in the sacral spinal cord. They synapse in cranial autonomic ganglia or in terminal ganglia near target organs. The parasympathetic nervous system generally acts to conserve resources and restore homeostasis, often with effects reciprocal to the sympathetic nervous system.
Sympathetic Nervous System
The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.
Hexamethonium Compounds
Ganglionic Blockers
Agents having as their major action the interruption of neural transmission at nicotinic receptors on postganglionic autonomic neurons. Because their actions are so broad, including blocking of sympathetic and parasympathetic systems, their therapeutic use has been largely supplanted by more specific drugs. They may still be used in the control of blood pressure in patients with acute dissecting aortic aneurysm and for the induction of hypotension in surgery.
Ganglia, Autonomic
Clusters of neurons and their processes in the autonomic nervous system. In the autonomic ganglia, the preganglionic fibers from the central nervous system synapse onto the neurons whose axons are the postganglionic fibers innervating target organs. The ganglia also contain intrinsic neurons and supporting cells and preganglionic fibers passing through to other ganglia.
Dietary Fiber
Horner Syndrome
A syndrome associated with defective sympathetic innervation to one side of the face, including the eye. Clinical features include MIOSIS; mild BLEPHAROPTOSIS; and hemifacial ANHIDROSIS (decreased sweating)(see HYPOHIDROSIS). Lesions of the BRAIN STEM; cervical SPINAL CORD; first thoracic nerve root; apex of the LUNG; CAROTID ARTERY; CAVERNOUS SINUS; and apex of the ORBIT may cause this condition. (From Miller et al., Clinical Neuro-Ophthalmology, 4th ed, pp500-11)
Muscle Fibers, Skeletal
Large, multinucleate single cells, either cylindrical or prismatic in shape, that form the basic unit of SKELETAL MUSCLE. They consist of MYOFIBRILS enclosed within and attached to the SARCOLEMMA. They are derived from the fusion of skeletal myoblasts (MYOBLASTS, SKELETAL) into a syncytium, followed by differentiation.
Pempidine
Guanethidine
An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.
Pentolinium Tartrate
Vagus Nerve
The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx).
Mineral Fibers
Long, pliable, cohesive natural or manufactured filaments of various lengths. They form the structure of some minerals. The medical significance lies in their potential ability to cause various types of PNEUMOCONIOSIS (e.g., ASBESTOSIS) after occupational or environmental exposure. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p708)
Hypogastric Plexus
Atropine
Muscle Fibers, Fast-Twitch
Muscle Fibers, Slow-Twitch
Pharmacology
Stellate Ganglion
Cotton Fiber
Norepinephrine
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
Sympathectomy
Cats
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
Ganglia
Hypohidrosis
Nictitating Membrane
Autonomic Nervous System Diseases
Diseases of the parasympathetic or sympathetic divisions of the AUTONOMIC NERVOUS SYSTEM; which has components located in the CENTRAL NERVOUS SYSTEM and PERIPHERAL NERVOUS SYSTEM. Autonomic dysfunction may be associated with HYPOTHALAMIC DISEASES; BRAIN STEM disorders; SPINAL CORD DISEASES; and PERIPHERAL NERVOUS SYSTEM DISEASES. Manifestations include impairments of vegetative functions including the maintenance of BLOOD PRESSURE; HEART RATE; pupil function; SWEATING; REPRODUCTIVE AND URINARY PHYSIOLOGY; and DIGESTION.
Neurons
Acetylcholine
Guinea Pigs
Muscle Contraction
Tubocurarine
Parasympathomimetics
Drugs that mimic the effects of parasympathetic nervous system activity. Included here are drugs that directly stimulate muscarinic receptors and drugs that potentiate cholinergic activity, usually by slowing the breakdown of acetylcholine (CHOLINESTERASE INHIBITORS). Drugs that stimulate both sympathetic and parasympathetic postganglionic neurons (GANGLIONIC STIMULANTS) are not included here.
Bethanidine
Vas Deferens
Stress Fibers
Reflex
Vasoactive Intestinal Peptide
Neuroeffector Junction
Abducens Nerve Diseases
Diseases of the sixth cranial (abducens) nerve or its nucleus in the pons. The nerve may be injured along its course in the pons, intracranially as it travels along the base of the brain, in the cavernous sinus, or at the level of superior orbital fissure or orbit. Dysfunction of the nerve causes lateral rectus muscle weakness, resulting in horizontal diplopia that is maximal when the affected eye is abducted and ESOTROPIA. Common conditions associated with nerve injury include INTRACRANIAL HYPERTENSION; CRANIOCEREBRAL TRAUMA; ISCHEMIA; and INFRATENTORIAL NEOPLASMS.
Action Potentials
Purkinje Fibers
Dimethylphenylpiperazinium Iodide
Tyramine
An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.
Synaptic Transmission
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
Nerve Fibers, Myelinated
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.
Chlorisondamine
Hexamethonium
A nicotinic cholinergic antagonist often referred to as the prototypical ganglionic blocker. It is poorly absorbed from the gastrointestinal tract and does not cross the blood-brain barrier. It has been used for a variety of therapeutic purposes including hypertension but, like the other ganglionic blockers, it has been replaced by more specific drugs for most purposes, although it is widely used a research tool.
Submandibular Gland
One of two salivary glands in the neck, located in the space bound by the two bellies of the digastric muscle and the angle of the mandible. It discharges through the submandibular duct. The secretory units are predominantly serous although a few mucous alveoli, some with serous demilunes, occur. (Stedman, 25th ed)
Efferent Pathways
Ergotamine
Sinoatrial Node
The small mass of modified cardiac muscle fibers located at the junction of the superior vena cava (VENA CAVA, SUPERIOR) and right atrium. Contraction impulses probably start in this node, spread over the atrium (HEART ATRIUM) and are then transmitted by the atrioventricular bundle (BUNDLE OF HIS) to the ventricle (HEART VENTRICLE).
Sweating
Tetrodotoxin
Phrenic Nerve
omega-Conotoxin GVIA
Phenoxybenzamine
Mossy Fibers, Hippocampal
Tyrosine 3-Monooxygenase
Parasympatholytics
Receptors, Muscarinic
Adrenergic alpha-2 Receptor Antagonists
Hypotension, Orthostatic
A significant drop in BLOOD PRESSURE after assuming a standing position. Orthostatic hypotension is a finding, and defined as a 20-mm Hg decrease in systolic pressure or a 10-mm Hg decrease in diastolic pressure 3 minutes after the person has risen from supine to standing. Symptoms generally include DIZZINESS, blurred vision, and SYNCOPE.
Nerve Endings
Branch-like terminations of NERVE FIBERS, sensory or motor NEURONS. Endings of sensory neurons are the beginnings of afferent pathway to the CENTRAL NERVOUS SYSTEM. Endings of motor neurons are the terminals of axons at the muscle cells. Nerve endings which release neurotransmitters are called PRESYNAPTIC TERMINALS.
Mecamylamine
Sympatholytics
Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.
Neuropeptide Y
A 36-amino acid peptide present in many organs and in many sympathetic noradrenergic neurons. It has vasoconstrictor and natriuretic activity and regulates local blood flow, glandular secretion, and smooth muscle activity. The peptide also stimulates feeding and drinking behavior and influences secretion of pituitary hormones.
Methacholine Compounds
Dogs
Rabbits
Rana catesbeiana
Physostigmine
Procaine
Autonomic Nervous System
The ENTERIC NERVOUS SYSTEM; PARASYMPATHETIC NERVOUS SYSTEM; and SYMPATHETIC NERVOUS SYSTEM taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the CENTRAL NERVOUS SYSTEM, especially the HYPOTHALAMUS and the SOLITARY NUCLEUS, which receive information relayed from VISCERAL AFFERENTS.
Muscle, Smooth
Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)
Peroneal Nerve
Pressoreceptors
Rats, Sprague-Dawley
Neurotransmitter Agents
Ileum
Membrane Potentials
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
Autonomic modification of the atrioventricular node during atrial fibrillation: role in the slowing of ventricular rate. (1/66)
BACKGROUND: Postganglionic vagal stimulation (PGVS) by short bursts of subthreshold current evokes release of acetylcholine from myocardial nerve terminals. PGVS applied to the atrioventricular node (AVN) slows nodal conduction. However, little is known about the ability of PGVS to control ventricular rate (VR) during atrial fibrillation (AF). METHODS AND RESULTS: To quantify the effects and establish the mechanism of PGVS on the AVN, AF was simulated by random high right atrial pacing in 11 atrial-AVN rabbit heart preparations. Microelectrode recordings of cellular action potentials (APs) were obtained from different AVN regions. Five intensities and 5 modes of PGVS delivery were evaluated. PGVS resulted in cellular hyperpolarization, along with depressed and highly heterogeneous intranodal conduction. Compact nodal AP exhibited decremental amplitude and dV/dt and multiple-hump components, and at high PGVS intensities, a high degree of concealed conduction resulted in a dramatic slowing of the VR. Progressive increase of PGVS intensity and/or rate of delivery showed a significant logarithmic correlation with a decrease in VR (P<0.001). Strong PGVS reduced the mean VR from 234 to 92 bpm (P<0.001). The PGVS effects on the cellular responses and VR during AF were fully reproduced in a model of direct acetylcholine injection into the compact AVN via micropipette. CONCLUSIONS: These studies confirmed that PGVS applied during AF could produce substantial VR slowing because of acetylcholine-induced depression of conduction in the AVN. (+info)Characterization of non-adrenergic, non-cholinergic inhibitory responses of the isolated guinea-pig trachea: differences between pre- and post-ganglionic nerve stimulation. (2/66)
1 Differences in the mechanism of non-adrenergic, non-cholinergic (NANC) inhibitory responses to preganglionic- and post-ganglionic nerve stimulation were investigated in the guinea-pig isolated trachea. 2 Stimulation of the vagus nerve at frequencies above 4 Hz elicited NANC relaxation of the trachealis muscle. Responses to low frequencies of stimulation (4-8 Hz) were abolished by the nitric oxide (NO) synthase inhibitor L-NOARG (10 microM), while a L-NOARG resistant component was observed at higher stimulus frequencies. The L-NOARG-resistant component of NANC inhibitory responses to higher frequencies of vagus nerve stimulation were significantly attenuated by the proteinase alpha-chymotrypsin (2 U/ml), suggesting that a neuropeptide such as VIP may contribute to NANC responses. 3 When postganglionic nerves were stimulated by electrical field stimulation (EFS), responses were readily elicited at frequencies below 4 Hz. Like responses to vagus nerve stimulation, responses to low frequency (<4 Hz) EFS were abolished by L-NOARG while a L-NOARG-resistant component was apparent at higher stimulus frequencies. 4 The L-NOARG-resistant component of NANC inhibitory responses to EFS was sensitive to alpha-chymotrypsin only if stimuli were delivered in either long trains at a low frequency (4 Hz for 10-30 s) or short trains of high frequency (16 Hz for 2.5-7.5 s). 5 Responses to preganglionic nerve stimulation were approximately 35% of the amplitude of responses to EFS in the same preparations. 6 In conclusion, responses to preganglionic and postganglionic NANC inhibitory nerve stimulation in the guinea-pig trachea differ in maximum amplitude, frequency-response characteristics and the contributions of cotransmitters. We suggest that these differences may be explained by filtering of preganglionic input to postganglionic NANC neurons. These results have implications in all studies where EFS is considered to be representative of physiological stimulation of post-ganglionic nerve stimulation. (+info)Inhibitory effects of clonidine and BS 100-141 on responses to sympathetic nerve stimulation in cats and rabbits. (3/66)
1. In pithed cats, the spinal sympathetic outflow was stimulated preganglionically at segments C7 and T1 and heart rate responses and nictitating membrane tone were measured in parallel. 2. Clonidine and a related drug, BS 100-141 (N-amidino-2(2,6-dichlorophenyl)acetamide hydrochloride), caused a dose-dependent inhibition of the stimulation-induced tachycardia but did not inhibit responses of the nictitating membrane. The inhibition of heart rate was antagonized by the alpha-adrenoceptor blocking drug, phentolamine. 3. In isolated hearts of rabbits, noradrenaline release in response to adrenergic nerve stimulation was reduced by clonidine and BS 100-141 and the effect was antagonized by phentolamine. 4. The results support the view that presynaptic alpha-adrenoceptors are involved in the regulation of transmitter release from adrenergic nerves. Cardiac adrenergic nerves appear more sensitive to alpha-adrenoceptor-mediated inhibition of inpulse transmission than the sympathetic nerves to the nictitating membrane. (+info)Innervation both of peri-orbital structures and of the heart by the cervical sympathetic nerves in mouse, rat, guinea-pig, rabbit and cat. (4/66)
1 In anaesthetized rats electrical stimulation of the intact cervical sympathetic nerve produced frequency-dependent lower eyelid contractions and tachycardia. 2 The tachycardia was caused by excitation of efferent fibres since it was equally evident in the pithed rat preparation, and the right nerve was more effective than the left. By contrast, no differences were seen between the responses to right and left vagal stimulation in either rats or rabbits. 3 Guanethidine inhibited both cardiac and eyelid responses, propranolol only the former and phentolamine only the latter, therby revealing the adrenergic nature of the nerves. Hexamethonium caused partial inhibition and the block was intensified by atropine. 4 The inferior eyelid of mice, guinea-pigs and rabbits as well as the nictitating membrane of rabbits and cats were contracted by cervical sympathetic nerve stimulation. In these species too, tachycardia occurred; this was more pronounced with the right than the left sympathetic nerve. The order of cardiac responsiveness was mouse greater than rat greater than guinea-pig greater than rabbit greater than cat. 5 In guinea-pigs histamine-induced bronchoconstriction was reduced by cervical sympathetic nerve stimulation. 6 That discrete cardiac pathways exist in the cervical sympathetic nerves is suggested by the reproducibility of the effects within any one species. The accessibility of the nerves greatly simplifies the examination of drugs in vivo on two different structures innervated by the sympathetic nervous system. (+info)Functional and structural changes in mammalian sympathetic neurones following interruption of their axons. (5/66)
The effects of interrupting the axons of principal neurones in the superior cervical ganglion of adult guinea-pigs were studied by means of intracellular recording, and light and electron microscopy. 1. Within 72 hr of axon interruption, the amplitude of exitatory postsynaptic potentials potentials (e.p.s.p.s) recorded in principal neurons in response to maximal preganglionic stimulation declined. E.p.s.p.s were maximally reduced (by more than 70% on average) 4-7 days following interruption, and failed to bring many cells to threshold. E.p.s.p.s. recorded in nearby neurones whose axons remained intact were unaffected. 2. In ganglia in which axon interruption was achieved by means of nerve crush (thus allowing prompt regeneration), mean e.p.s.p. amplitudes began to increase again after about 1-2 weeks. One month after the initial injury many neurones had e.p.s.p.s of normal amplitude, and by 2 months affected neurones were indistinguishable from control cells. Functional peripheral connexions were re-established during the period of synaptic recovery. 3. The mean number of synapses identified electron microscopically in ganglia in which all the major efferent branches had been crushed decreased by 65-70% in parallel with synaptic depression measured by intracellular recording. However synapse counts did not return to normal levels even after 3 months. 4. During the period of maximum synaptic depression, numerous abnormal profiles which contained accumulations of vesicular and tubular organelles, vesicles, and mitochondria were observed in electron microscopic sections. Injection of horseradish peroxidase into affected neurones demonstrated dendritic swelling which probably correspond to these profiles. 5. Little or no difference was found in the electrical properties of normal neurones and neurones whose axons had been interrupted 4-7 days previously. However, the mean amplitude of spontaneously occurring synaptic potentials was reduced, and the amplitude distribution was shifted. This abnormality of the synapses which remain on affected neurones also contributes to synaptic depression. 6. Counts of neurones in normal and experimental ganglia showed that approximately half the principal cells died 1-5 weeks after crushing the major efferent brances. This finding presumably explains the failure of synapse counts to return to control levels after recovery. 7. If axons were prevented from growing back to their target organ by chronic ligation, surviving neurones whose axons were enclosed by the ligature did not generally recover normal synaptic function. Following ligation, most affected cells died within a month. 8. Thus the integrity of a principal cell's axon is necessary for the maintenance of preganglionic synaptic contacts, and ultimately for neuronal survival. The basis of neuronal recovery from the effects of axon interruption appears to be some aspect of regeneration to the peripheral target. (+info)A study of peripheral input to and its control by post-ganglionic neurones of the inferior mesenteric ganglion. (6/66)
1. Intracellular recordings were made, in vitro, from neurones of guinea-pig inferior mesenteric ganglia (IMG) attached, via the lumbar colonic nerves, to segments of distal colon. 2. 'Spontaneous' synaptic input from colonic afferent fibres was observed in 79% of the neurones tested. In any given preparation, the level and pattern of this synaptic input to different neurones varied considerably. 3. Superfusion of colonic segments with drugs (papaverine, isoprenaline, and adenosine triphosphate) which reduce colonic motility decreased colonic afferent input to IMG neurones. 4. Superfusion of colonic segments with acetylcholine or stimulation of pelvic nerves, both of which increase colonic motility, increased colonic afferent input to IMG neurones. 5. Superfusion of colonic segments with either atropine or tubocurarine reduced the level of 'spontaneous', colonic afferent input. However, distension of these relaxed segments increased the colonic afferent input. 6. Repetitive stimulation of preganglionic inputs to the IMG inhibited afferent input from drug relaxed segments of colon that were moderately distended by the injection of air into the lumen. Superfusion of the colon with phentolamine blocked this inhibition. 7. The results of this study suggest that IMG neurones receive afferent input from mechanoreceptors located in the distal colon and that the mechanosensitivity of this afferent pathway is in part controlled by efferent noradrenergic neurones of the IMG. The IMG-colon neural circuitry can therefore be considered to form a feed-back control system which participates in the regulation of colonic motility. (+info)The relation between stimulus frequency and the relative size of the components of the biphasic response of the vas deferens to electrical stimulation at different temperatures. (7/66)
1. Electrical stimulation of the guinea-pig or rat vas deferens (pre- or post-ganglionically) at frequencies from 2-5 to 40 Hz with trains of stimuli of 30 sec duration induced a biphasic response. A rapid contraction (component A) was followed after a brief relaxation by a slower contraction (component B); the two phases were seen most clearly with stimulation frequencies of less than 10 Hz. 2. The responses to post-ganglionic stimulation were always larger than those to preganglionic stimulation. In general, at low frequencies component A exceeded component B whilst at high frequencies component B was the larger. Separation of the two components on the basis of their frequency response characteristics was better for rat than for guinea-pig vasa. 3. Log. frequency-response curves to transmural (post-ganglionic) electrical stimulation and log dose-response curves to noradrenaline were recorded for guinea-pig and rat vasa deferentia at 32 degrees, 22 degrees and 12 degrees C. For the guinea-pig reduction of bath temperature to 12 degrees C increased the amplitude of component A at 2-5 and 5 Hz; component B could not confidently be distinguished at this temperature. At 22 degrees C there was potentiation of B at lower frequencies and depression of B at higher frequencies. There was no response to noradrenaline at 12 degrees C. At 22 degrees C the response to noradrenaline was increased except to doses at or near the maximum to which the response was reduced. 4. For the rat was deferens component A was little changed by reduction of temperature. Component B at 12 degrees C was greatly depressed at higher frequencies. The response to noradreanaline was increased to lower doses and decreased to higher doses as the temperature was lowered. 5. The B component of the response of guinea-pig vasa at 22 degrees C and rat vasa at 32 degrees C was more sensitive than the A component to inhibition by thymoxamine. 6. Further analysis of the mechanisms underlying the A and B components of the biphasic response may be facilitated by relative isolation of each component by the appropriate selection of parameters of electrical stimulation and of temperature for the species being investigated. The contractions of the B component are similar to, if not identical with, those produced by exogenously applied noradrenaline. (+info)Synthesis of nitric oxide in postganglionic myenteric neurons during endotoxemia: implications for gastric motor function in rats. (8/66)
We have investigated the mechanisms underlying acute changes in gastric motor function triggered by endotoxemia. In fundal strips from rats pre-treated with endotoxin (40 microg/kg, i.p. 30 min), mechanical activity was analyzed and the source of nitric oxide (NO) was visualized by confocal microscopy of tissue loaded with the fluorescent dye DAF-FM. NOS expression was determined by quantitative RT-PCR and Western blot, and enzyme activity by the citrulline assay. Strips from endotoxin-treated rats were hypo-contractile. This was prevented by pre-incubation with the neurotoxin tetrodotoxin, the gangliar blocker hexamethonium, or non-selective and neuronal-specific NOS inhibitors (L-NOARG and TRIM, respectively). The soluble guanylyl cyclase (sGC) inhibitor ODQ and the inhibitor of small conductance Ca2+-activated K+ channels apamin prevented relaxation induced by endotoxin, nicotine, exogenous NO (DETA-NONOate), and the NO-independent sGC activator BAY 41-2272. NO synthesis was observed in neuronal soma, axons, and nerve endings of the myenteric plexus in the fundus of endotoxin-treated rats and was prevented by L-NAME, tetrodotoxin, and hexamethonium. nNOS and iNOS mRNA and protein contents were unchanged. Our findings demonstrate synthesis of NO in post-ganglionic myenteric neurons during early endotoxemia that mediates gastric hypo-contractility. The effect of NO is mediated via sGC and small conductance Ca2+-activated K+channels. (+info)
Morphometric characterization of individual sympathetic postganglionic by Gary C. Walter
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Mayo Clinic Day 2 - lethargicsmiles
What was being tested was my autonomic, specifically sympathetic, nerve function. The QSART can identify small fiber neuropathy ... If my thermoregulatory sweat test showed lesions, it would let us know if they are pre or postganglionic. Used alone, it will ... autonomic disorders, CFS, chronic disease, disease in nervous system, Dysautonomia, Exercise test, Mayo Clinic, Postural ... Autonomic Nervous System Test. This testing was pretty much was awful. First, they put electrodes type things all over my body ...
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The submandibular ganglion abuts the lingual nerve, where the postganglionic fibers originate and directly pierce the capsule ... Nerves: With the exception of the autonomic plexus to the submandibular gland, all the nerves were found external to the ... where the parasympathetic preganglionic fibers transverse through the chorda tympani of the seventh cranial nerve to join the ...
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... being mainly detected in autonomic fibers of PD, DLB, and PAF, but detected in somatic fibers of the upper dermis in MSA, ... 4 reflecting the early damage of postganglionic sympathetic branches, peripheral tissues with extensive autonomic innervation, ... Skin sympathetic fiber α-synuclein deposits: a potential biomarker for pure autonomic failure. Neurology 2013;80:725-732. ... pure autonomic failure; PD=. Parkinson disease; PSP=. progressive supranuclear palsy; RBD=. REM sleep behavior disorder; RT- ...