Transection or severing of an axon. This type of denervation is used often in experimental studies on neuronal physiology and neuronal death or survival, toward an understanding of nervous system disease.
Traumatic injuries to the facial nerve. This may result in FACIAL PARALYSIS, decreased lacrimation and salivation, and loss of taste sensation in the anterior tongue. The nerve may regenerate and reform its original pattern of innervation, or regenerate aberrantly, resulting in inappropriate lacrimation in response to gustatory stimuli (e.g., "crocodile tears") and other syndromes.
Renewal or physiological repair of damaged nerve tissue.
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and SALIVARY GLANDS, and convey afferent information for TASTE from the anterior two-thirds of the TONGUE and for TOUCH from the EXTERNAL EAR.
A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. The sciatic nerve, which is the main continuation of the sacral plexus, is the largest nerve in the body. It has two major branches, the TIBIAL NERVE and the PERONEAL NERVE.
The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)
Treatment of muscles and nerves under pressure as a result of crush injuries.
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.
Pathologic changes that occur in the axon and cell body of a neuron proximal to an axonal lesion. The process is characterized by central chromatolysis which features flattening and displacement of the nucleus, loss of Nissl bodies, and cellular edema. Central chromatolysis primarily occurs in lower motor neurons.
Neurons which activate MUSCLE CELLS.
Degeneration of distal aspects of a nerve axon following injury to the cell body or proximal portion of the axon. The process is characterized by fragmentation of the axon and its MYELIN SHEATH.
A nervous tissue specific protein which is highly expressed in NEURONS during development and NERVE REGENERATION. It has been implicated in neurite outgrowth, long-term potentiation, SIGNAL TRANSDUCTION, and NEUROTRANSMITTER release. (From Neurotoxicology 1994;15(1):41-7) It is also a substrate of PROTEIN KINASE C.
The 2nd cranial nerve which conveys visual information from the RETINA to the brain. The nerve carries the axons of the RETINAL GANGLION CELLS which sort at the OPTIC CHIASM and continue via the OPTIC TRACTS to the brain. The largest projection is to the lateral geniculate nuclei; other targets include the SUPERIOR COLLICULI and the SUPRACHIASMATIC NUCLEI. Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM.
A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the CEREBELLUM via the superior cerebellar peduncle and a projection from the ipsilateral MOTOR CORTEX.
Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.
Injuries to the optic nerve induced by a trauma to the face or head. These may occur with closed or penetrating injuries. Relatively minor compression of the superior aspect of orbit may also result in trauma to the optic nerve. Clinical manifestations may include visual loss, PAPILLEDEMA, and an afferent pupillary defect.
STILBENES with AMIDINES attached.
Neurons of the innermost layer of the retina, the internal plexiform layer. They are of variable sizes and shapes, and their axons project via the OPTIC NERVE to the brain. A small subset of these cells act as photoreceptors with projections to the SUPRACHIASMATIC NUCLEUS, the center for regulating CIRCADIAN RHYTHM.
The directed transport of ORGANELLES and molecules along nerve cell AXONS. Transport can be anterograde (from the cell body) or retrograde (toward the cell body). (Alberts et al., Molecular Biology of the Cell, 3d ed, pG3)
Nerve fibers which project from cell bodies of AUTONOMIC GANGLIA to SYNAPSES on target organs.
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.
Ganglia of the sympathetic nervous system including the paravertebral and the prevertebral ganglia. Among these are the sympathetic chain ganglia, the superior, middle, and inferior cervical ganglia, and the aorticorenal, celiac, and stellate ganglia.
The act of injuring one's own body to the extent of cutting off or permanently destroying a limb or other essential part of a body.
Type III intermediate filament proteins that assemble into neurofilaments, the major cytoskeletal element in nerve axons and dendrites. They consist of three distinct polypeptides, the neurofilament triplet. Types I, II, and IV intermediate filament proteins form other cytoskeletal elements such as keratins and lamins. It appears that the metabolism of neurofilaments is disturbed in Alzheimer's disease, as indicated by the presence of neurofilament epitopes in the neurofibrillary tangles, as well as by the severe reduction of the expression of the gene for the light neurofilament subunit of the neurofilament triplet in brains of Alzheimer's patients. (Can J Neurol Sci 1990 Aug;17(3):302)
The 12th cranial nerve. The hypoglossal nerve originates in the hypoglossal nucleus of the medulla and supplies motor innervation to all of the muscles of the tongue except the palatoglossus (which is supplied by the vagus). This nerve also contains proprioceptive afferents from the tongue muscles.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
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 largest and uppermost of the paravertebral sympathetic ganglia.
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.
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.
Injuries to the PERIPHERAL NERVES.
Subcellular structures found in nerve cell bodies and DENDRITES. They consist of granular endoplasmic reticulum (ENDOPLASMIC RETICULUM, ROUGH) and RIBOSOMES.
Traumatic injuries to the HYPOGLOSSAL NERVE.
Neuroglial cells of the peripheral nervous system which form the insulating myelin sheaths of peripheral axons.
The 9th cranial nerve. The glossopharyngeal nerve is a mixed motor and sensory nerve; it conveys somatic and autonomic efferents as well as general, special, and visceral afferents. Among the connections are motor fibers to the stylopharyngeus muscle, parasympathetic fibers to the parotid glands, general and taste afferents from the posterior third of the tongue, the nasopharynx, and the palate, and afferents from baroreceptors and CHEMORECEPTOR CELLS of the carotid sinus.
Factors which enhance the growth potentialities of sensory and sympathetic nerve cells.
A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.
Disease or damage involving the SCIATIC NERVE, which divides into the PERONEAL NERVE and TIBIAL NERVE (see also PERONEAL NEUROPATHIES and TIBIAL NEUROPATHY). Clinical manifestations may include SCIATICA or pain localized to the hip, PARESIS or PARALYSIS of posterior thigh muscles and muscles innervated by the peroneal and tibial nerves, and sensory loss involving the lateral and posterior thigh, posterior and lateral leg, and sole of the foot. The sciatic nerve may be affected by trauma; ISCHEMIA; COLLAGEN DISEASES; and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1363)
Common name for the only family (Petromyzontidae) of eellike fish in the order Petromyzontiformes. They are jawless but have a sucking mouth with horny teeth.
In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell.
The resection or removal of the innervation of a muscle or muscle tissue.
Disease involving the femoral nerve. The femoral nerve may be injured by ISCHEMIA (e.g., in association with DIABETIC NEUROPATHIES), nerve compression, trauma, COLLAGEN DISEASES, and other disease processes. Clinical features include MUSCLE WEAKNESS or PARALYSIS of hip flexion and knee extension, ATROPHY of the QUADRICEPS MUSCLE, reduced or absent patellar reflex, and impaired sensation over the anterior and medial thigh.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.
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.
Cytoplasmic filaments intermediate in diameter (about 10 nanometers) between the microfilaments and the microtubules. They may be composed of any of a number of different proteins and form a ring around the cell nucleus.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
An activating transcription factor that plays a key role in cellular responses to GENOTOXIC STRESS and OXIDATIVE STRESS.
Elements of limited time intervals, contributing to particular results or situations.
Traumatic injuries to the brain, cranial nerves, spinal cord, autonomic nervous system, or neuromuscular system, including iatrogenic injuries induced by surgical procedures.
An opisthobranch mollusk of the order Anaspidea. It is used frequently in studies of nervous system development because of its large identifiable neurons. Aplysiatoxin and its derivatives are not biosynthesized by Aplysia, but acquired by ingestion of Lyngbya (seaweed) species.
A complex group of fibers arising from the basal olfactory regions, the periamygdaloid region, and the septal nuclei, and passing to the lateral hypothalamus. Some fibers continue into the tegmentum.
A neurotrophic factor involved in regulating the survival of visceral and proprioceptive sensory neurons. It is closely homologous to nerve growth factor beta and BRAIN-DERIVED NEUROTROPHIC FACTOR.
A microtubule subunit protein found in large quantities in mammalian brain. It has also been isolated from SPERM FLAGELLUM; CILIA; and other sources. Structurally, the protein is a dimer with a molecular weight of approximately 120,000 and a sedimentation coefficient of 5.8S. It binds to COLCHICINE; VINCRISTINE; and VINBLASTINE.
Surgical interruption of a spinal or cranial nerve root. (From Dorland, 28th ed)
A neuropeptide of 29-30 amino acids depending on the species. Galanin is widely distributed throughout the BRAIN; SPINAL CORD; and INTESTINES. There are various subtypes of GALANIN RECEPTORS implicating roles of galanin in regulating FOOD INTAKE; pain perception; memory; and other neuroendocrine functions.
The removal or interruption of some part of the autonomic nervous system for therapeutic or research purposes.

The optically determined size of exo/endo cycling vesicle pool correlates with the quantal content at the neuromuscular junction of Drosophila larvae. (1/532)

According to the current theory of synaptic transmission, the amplitude of evoked synaptic potentials correlates with the number of synaptic vesicles released at the presynaptic terminals. Synaptic vesicles in presynaptic boutons constitute two distinct pools, namely, exo/endo cycling and reserve pools (). We defined the vesicles that were endocytosed and exocytosed during high K+ stimulation as the exo/endo cycling vesicle pool. To determine the role of exo/endo cycling vesicle pool in synaptic transmission, we estimated the quantal content electrophysiologically, whereas the pool size was determined optically using fluorescent dye FM1-43. We then manipulated the size of the pool with following treatments. First, to change the state of boutons of nerve terminals, motoneuronal axons were severed. With this treatment, the size of exo/endo cycling vesicle pool decreased together with the quantal content. Second, we promoted the FM1-43 uptake using cyclosporin A, which inhibits calcineurin activities and enhances endocytosis. Cyclosporin A increased the total uptake of FM1-43, but neither the size of exo/endo cycling vesicle pool nor the quantal content changed. Third, we increased the size of exo/endo cycling vesicle pool by forskolin, which enhances synaptic transmission. The forskolin treatment increased both the size of exo/endo cycling vesicle pool and the quantal content. Thus, we found that the quantal content was closely correlated with the size of exo/endo cycling vesicle pool but not necessarily with the total uptake of FM1-43 fluorescence by boutons. The results suggest that vesicles in the exo/endo cycling pool primarily participate in evoked exocytosis of vesicles.  (+info)

Central peptidergic neurons are hyperactive during collateral sprouting and inhibition of activity suppresses sprouting. (2/532)

Little is known regarding the effect of chronic changes in neuronal activity on the extent of collateral sprouting by identified CNS neurons. We have investigated the relationship between activity and sprouting in oxytocin (OT) and vasopressin (VP) neurons of the hypothalamic magnocellular neurosecretory system (MNS). Uninjured MNS neurons undergo a robust collateral-sprouting response that restores the axon population of the neural lobe (NL) after a lesion of the contralateral MNS (). Simultaneously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory activity. We therefore tested the hypothesis that sprouting MNS neurons are hyperactive by measuring changes in cell and nuclear diameters, OT and VP mRNA pools, and axonal cytochrome oxidase activity (COX). Each of these measures was significantly elevated during the period of most rapid axonal growth between 1 and 4 weeks after the lesion, confirming that both OT and VP neurons are hyperactive while undergoing collateral sprouting. In a second study the hypothesis that chronic inhibition of neuronal activity would interfere with the sprouting response was tested. Chronic hyponatremia (CH) was induced 3 d before the hypothalamic lesion and sustained for 4 weeks to suppress neurosecretory activity. CH abolished the lesion-induced increases in OT and VP mRNA pools and virtually eliminated measurable COX activity in MNS terminals. Counts of the total number of axon profiles in the NL revealed that CH also prevented axonal sprouting from occurring. These results are consistent with the hypothesis that increased neuronal activity is required for denervation-induced collateral sprouting to occur in the MNS.  (+info)

Differential expression of the mRNA for the vanilloid receptor subtype 1 in cells of the adult rat dorsal root and nodose ganglia and its downregulation by axotomy. (3/532)

Sensitivity to the pungent vanilloid, capsaicin, defines a subpopulation of primary sensory neurons that are mainly polymodal nociceptors. The recently cloned vanilloid receptor subtype 1 (VR1) is activated by capsaicin and noxious heat. Using combined in situ hybridization and histochemical methods, we have characterized in sensory ganglia the expression of VR1 mRNA. We show that this receptor is almost exclusively expressed by neurofilament-negative small- and medium-sized dorsal root ganglion cells. Within this population, VR1 mRNA is detected at widely varying levels in both the NGF receptor (trkA)-positive, peptide-producing cells that elicit neurogenic inflammation and the functionally less characterized glial cell line-derived neurotrophic factor-responsive cells that bind lectin Griffonia simplicifolia isolectin B4 (IB4). Cells without detectable levels of VR1 mRNA are found in both classes. A subpopulation of the IB4-binding cells that produce somatostatin has relatively low levels of VR1 mRNA. A previously uncharacterized population of very small cells that express the receptor tyrosine kinase (RET) and that do not label for trkA or IB4-binding has the highest relative levels of VR1 mRNA. The majority of small visceral sensory neurons of the nodose ganglion also express VR1 mRNA, in conjunction with the BDNF receptor trkB but not trkA. Axotomy results in the downregulation of VR1 mRNA in dorsal root ganglion cells. Our data emphasize the heterogeneity of VR1 mRNA expression by subclasses of small sensory neurons, and this may result in their differential sensitivity to chemical and noxious heat stimuli. Our results also indicate that peripherally derived trophic factors may regulate levels of VR1 mRNA.  (+info)

Cannabinoid suppression of noxious heat-evoked activity in wide dynamic range neurons in the lumbar dorsal horn of the rat. (4/532)

The effects of cannabinoid agonists on noxious heat-evoked firing of 62 spinal wide dynamic range (WDR) neurons were examined in urethan-anesthetized rats (1 cell/animal). Noxious thermal stimulation was applied with a Peltier device to the receptive fields in the ipsilateral hindpaw of isolated WDR neurons. To assess the site of action, cannabinoids were administered systemically in intact and spinally transected rats and intraventricularly. Both the aminoalkylindole cannabinoid WIN55,212-2 (125 microg/kg iv) and the bicyclic cannabinoid CP55,940 (125 microg/kg iv) suppressed noxious heat-evoked activity. Responses evoked by mild pressure in nonnociceptive neurons were not altered by CP55,940 (125 microg/kg iv), consistent with previous observations with another cannabinoid agonist, WIN55,212-2. The cannabinoid induced-suppression of noxious heat-evoked activity was blocked by pretreatment with SR141716A (1 mg/kg iv), a competitive antagonist for central cannabinoid CB1 receptors. By contrast, intravenous administration of either vehicle or the receptor-inactive enantiomer WIN55,212-3 (125 microg/kg) failed to alter noxious heat-evoked activity. The suppression of noxious heat-evoked activity induced by WIN55,212-2 in the lumbar dorsal horn of intact animals was markedly attenuated in spinal rats. Moreover, intraventricular administration of WIN55,212-2 suppressed noxious heat-evoked activity in spinal WDR neurons. By contrast, both vehicle and enantiomer were inactive. These findings suggest that cannabinoids selectively modulate the activity of nociceptive neurons in the spinal dorsal horn by actions at CB1 receptors. This modulation represents a suppression of pain neurotransmission because the inhibitory effects are selective for pain-sensitive neurons and are observed with different modalities of noxious stimulation. The data also provide converging lines of evidence for a role for descending antinociceptive mechanisms in cannabinoid modulation of spinal nociceptive processing.  (+info)

CNTF, not other trophic factors, promotes axonal regeneration of axotomized retinal ganglion cells in adult hamsters. (5/532)

PURPOSE: To investigate the in vivo effects of trophic factors on the axonal regeneration of axotomized retinal ganglion cells in adult hamsters. METHODS: The left optic nerve was transected intracranially or intraorbitally, and a peripheral nerve graft was apposed or sutured to the axotomized optic nerve to enhance regeneration. Trophic factors were applied intravitreally every 5 days. Animals were allowed to survive for 3 or 4 weeks. Regenerating retinal ganglion cells (RGCs) were labeled by applying the dye Fluoro-Gold to the distal end of the peripheral nerve graft 3 days before the animals were killed. RESULTS: Intravitreal application of ciliary neurotrophic factor substantially enhanced the regeneration of damaged axons into a sciatic nerve graft in both experimental conditions (intracranial and intraorbital optic nerve transections) but did not increase the survival of distally axotomized RGCs. Basic fibroblast growth factor and neurotrophins such as nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 failed to enhance axonal regeneration of distally axotomized RGCs. CONCLUSIONS: Neurons of the adult central nervous system can regenerate in response to trophic supply after injury, and ciliary neurotrophic factor is at least one of the trophic factors that can promote axonal regeneration of axotomized RGCs.  (+info)

Neurotrophin modulation of the monosynaptic reflex after peripheral nerve transection. (6/532)

The effects of neurotrophin-3 (NT-3) and NT-4/5 on the function of axotomized group Ia afferents and motoneurons comprising the monosynaptic reflex pathway were investigated. The axotomized medial gastrocnemius (MG) nerve was provided with NT-3 or NT-4/5 for 8-35 d via an osmotic minipump attached to its central end at the time of axotomy. After this treatment, monosynaptic EPSPs were recorded intracellularly from MG or lateral gastrocnemius soleus (LGS) motoneurons in response to stimulation of the heteronymous nerve under pentobarbital anesthesia. Controls were preparations with axotomized nerves treated directly with vehicle; other axotomized controls were administered subcutaneous NT-3. Direct NT-3 administration (60 microgram/d) not only prevented the decline in EPSP amplitude from axotomized afferents (stimulate MG, record LGS) observed in axotomy controls but, after 5 weeks, led to EPSPs larger than those from intact afferents. These central changes were paralleled by recovery of group I afferent conduction velocity. Removal of NT-3 4-5 weeks after beginning treatment resulted in a decline of conduction velocity and EPSP amplitude within 1 week to values characteristic of axotomy. The increased synaptic efficacy after NT-3 treatment was associated with enhanced connectivity of single afferents to motoneurons. NT-4/5 induced modest recovery in group I afferent conduction velocity but not of the EPSPs they elicited. NT-3 or NT-4/5 had no effect on the properties of treated motoneurons or their monosynaptic EPSPs. We conclude that NT-3, and to a limited extent NT-4/5, promotes recovery of axotomized group Ia afferents but not axotomized motoneurons or the synapses on them.  (+info)

Ultrastructural analysis of ectopic synaptic boutons arising from peripherally regenerated primary afferent fibers. (7/532)

The central axons of peripherally regenerated Abeta primary sensory neurons were impaled in the dorsal columns of alpha-chloralose-anesthetized cats 9-12 mo after axotomy. The adequate peripheral stimulus was determined, and the afferent fibers intracellularly stimulated while simultaneously recording the resulting cord dorsum potentials (CDPs). Fibers that successfully had reinnervated the skin responded to light tactile stimulation, and evoked CDPs that suggested dorsally located boutons were stained intracellularly with horseradish peroxidase (HRP). Two HRP-stained regenerated Abeta afferent fibers were recovered that supported large numbers of axon collaterals and swellings in laminae I, IIo, and IIi. Sections containing the ectopic collateral fibers and terminals in the superficial dorsal horn were embedded in plastic. Analyses of serial ultrathin sections revealed that ectopic projections from both regenerated fibers supported numerous synaptic boutons filled with clear round vesicles, a few large dense core vesicles (LDCVs) and several mitochondria (>3). All profiles examined in serial sections (19) formed one to three asymmetric axo-dendritic contacts. Unmyelinated portions of ectopic fibers giving rise to en passant and terminal boutons often contained numerous clear round vesicles. Several boutons (47%) received asymmetric contacts from axon terminals containing pleomorphic vesicles. These results strongly suggest that regenerated Abeta fibers activated by light tactile stimuli support functional connections in the superficial dorsal horn that have distinct ultrastructural features. In addition, the appearance of LDCVs suggests that primary sensory neurons are capable of changing their neurochemical phenotype.  (+info)

Nature of the retrograde signal from injured nerves that induces interleukin-6 mRNA in neurons. (8/532)

In previous studies, interleukin-6 was shown to be synthesized in approximately one-third of lumbar dorsal root ganglion neurons during the first week after nerve transection. In present studies, interleukin-6 mRNA was found to be induced also in axotomized facial motor neurons and sympathetic neurons. The nature of the signal that induces interleukin-6 mRNA in neurons after nerve injury was analyzed. Blocking of retrograde axonal transport by injection of colchicine into an otherwise normal nerve did not induce interleukin-6 mRNA in primary sensory neurons, but injection of colchicine into the nerve stump prevented induction of interleukin-6 mRNA by nerve transection. Therefore, it was concluded that interleukin-6 is induced by an injury factor arising from the nerve stump rather than by interruption of normal retrograde trophic support from target tissues or distal nerve segments. Next, injection into the nerve of a mast cell degranulating agent was shown to stimulate interleukin-6 mRNA in sensory neurons and systemic administration of mast cell stabilizing agents to mitigate the induction of interleukin-6 mRNA in sensory neurons after nerve injury. These data implicate mast cells as one possible source of the factors that lead to induction of interleukin-6 mRNA after nerve injury. In search of a possible function of inducible interelukin-6, neuronal death after nerve transection was assessed in mice with null deletion of the interleukin-6 gene. Retrograde death of neurons in the fifth lumbar dorsal root ganglion was 45% greater in knockout than in wild-type mice. Thus, endogenous interleukin-6 contributes to the survival of axotomized neurons.  (+info)

There are several types of facial nerve injuries, including:

1. Bell's palsy: This is a condition that affects the facial nerve and causes weakness or paralysis of the muscles on one side of the face. It is often temporary and resolves on its own within a few weeks.
2. Facial paralysis: This is a condition in which the facial nerve is damaged, leading to weakness or paralysis of the muscles of facial expression. It can be caused by trauma, tumors, or viral infections.
3. Ramsay Hunt syndrome: This is a rare condition that occurs when the facial nerve is affected by a virus, leading to symptoms such as facial paralysis and pain in the ear.
4. Traumatic facial nerve injury: This can occur as a result of trauma to the head or face, such as a car accident or a fall.
5. Tumor-related facial nerve injury: In some cases, tumors can grow on the facial nerve and cause damage.
6. Ischemic facial nerve injury: This occurs when there is a reduction in blood flow to the facial nerve, leading to damage to the nerve fibers.
7. Neurofibromatosis type 2: This is a rare genetic disorder that can cause tumors to grow on the facial nerve, leading to damage and weakness of the facial muscles.

Treatment for facial nerve injuries depends on the underlying cause and severity of the injury. In some cases, physical therapy may be recommended to help regain strength and control of the facial muscles. Surgery may also be necessary in some cases to repair damaged nerve fibers or remove tumors.

1. Neurodegenerative diseases: In conditions such as Alzheimer's disease and Parkinson's disease, there is evidence of retrograde degeneration of neurons, whereby affected neurons lose their mature characteristics and adopt more primitive features.
2. Retinal degeneration: In certain eye disorders, such as retinitis pigmentosa, there is retrograde degeneration of the retina, leading to loss of vision.
3. Cardiac disease: In some cases of heart failure, there is evidence of retrograde degeneration of the heart muscle, whereby the heart becomes less efficient and cannot pump blood effectively.
4. Cancer: Retrograde degeneration can occur in cancer, whereby tumor cells undergo a process of de-differentiation, losing their mature characteristics and adopting more primitive features.

In each of these cases, retrograde degeneration is often associated with a loss of function and can lead to severe clinical consequences. Understanding the mechanisms of retrograde degeneration is important for developing effective treatments and improving outcomes for patients with these conditions.

The process of Wallerian degeneration begins with the loss of myelin sheaths that surround the axons and are essential for their proper functioning. As a result of this degeneration, the axoplasm (the cytoplasmic contents of an axon) is exposed to the extracellular space, leading to a series of degradative changes within the axon. These changes include:

1. Breakdown of organelles and their membranes
2. Release of cellular contents into the extracellular space
3. Activation of proteolytic enzymes that degrade axonal structures
4. Influx of ionic fluids and water into the axon, leading to swelling and eventually rupture of the axon.

The onset and progression of Wallerian degeneration depend on various factors, including the severity of the initial injury, the age of the individual, and the presence of any underlying medical conditions. The degenerative process can be slowed down or even halted by various interventions, such as local application of neurotrophic factors or axonal regeneration promoters.

Wallerian degeneration is a common phenomenon in many neurodegenerative diseases and injuries, including traumatic brain injury, multiple sclerosis, and peripheral nerve damage. Understanding the mechanisms of Wallerian degeneration can provide valuable insights into the pathogenesis of these conditions and may lead to the development of novel therapeutic strategies for their management.

Types of Optic Nerve Injuries:

1. Traumatic optic neuropathy: This type of injury is caused by direct damage to the optic nerve as a result of trauma, such as a car accident or sports injury.
2. Ischemic optic neuropathy: This type of injury is caused by a lack of blood flow to the optic nerve, which can lead to cell death and vision loss.
3. Inflammatory optic neuropathy: This type of injury is caused by inflammation of the optic nerve, which can be caused by conditions such as multiple sclerosis or sarcoidosis.
4. Tumor-induced optic neuropathy: This type of injury is caused by a tumor that compresses or damages the optic nerve.
5. Congenital optic nerve disorders: These are present at birth and can cause vision loss or blindness. Examples include optic nerve hypoplasia and coloboma.

Symptoms of Optic Nerve Injuries:

* Blurred vision or double vision
* Loss of peripheral vision
* Difficulty seeing in dim lighting
* Pain or discomfort in the eye or head
* Redness or swelling of the eye

Diagnosis and Treatment of Optic Nerve Injuries:

Diagnosis is typically made through a combination of physical examination, imaging tests such as MRI or CT scans, and visual field testing. Treatment depends on the underlying cause of the injury, but may include medication, surgery, or vision rehabilitation. In some cases, vision loss may be permanent, but early diagnosis and treatment can help to minimize the extent of the damage.

Prognosis for Optic Nerve Injuries:

The prognosis for optic nerve injuries varies depending on the underlying cause and severity of the injury. In some cases, vision may be partially or fully restored with treatment. However, in other cases, vision loss may be permanent. It is important to seek medical attention immediately if any symptoms of an optic nerve injury are present, as early diagnosis and treatment can improve outcomes.

Self-mutilation is not the same as suicide, although it can be a risk factor for suicidal behavior. People who engage in self-mutilation may do so as a way to try to regulate their emotions, express feelings that they cannot put into words, or cope with traumatic events. It is important to note that self-mutilation is not a healthy or effective way to manage emotions or cope with stress, and it can lead to physical and emotional scars, infections, and worsening mental health.

Self-mutilation can be difficult to recognize, as it often occurs in secret and can be hidden by clothing or makeup. However, some common signs that someone may be engaging in self-mutilation include:

* Unexplained cuts, scars, or bruises
* Frequent injuries or wounds that do not heal properly
* Difficulty concentrating or memory problems
* Mood swings or emotional instability
* Withdrawal from social activities or relationships
* Substance abuse or addiction

If you suspect that someone you know is engaging in self-mutilation, it is important to approach the situation with sensitivity and compassion. Encourage them to seek professional help from a mental health provider, such as a therapist or counselor. A mental health professional can work with the individual to identify the underlying causes of their behavior and develop healthy coping strategies.

Treatment for self-mutilation typically involves a combination of psychotherapy and medication. Therapy can help individuals understand the underlying causes of their behavior, develop healthy coping strategies, and learn how to manage negative emotions in a more productive way. Medications such as antidepressants or mood stabilizers may be prescribed to help regulate mood and reduce impulsivity.

In summary, self-mutilation is a behavior where an individual intentionally causes harm to their own body, often as a coping mechanism for emotional pain or distress. It can take many forms, including cutting, burning, or hitting oneself. Treatment typically involves a combination of psychotherapy and medication, and it is important to approach the situation with sensitivity and compassion. If you suspect that someone you know is engaging in self-mutilation, encourage them to seek professional help from a mental health provider.

There are many different types of nerve degeneration that can occur in various parts of the body, including:

1. Alzheimer's disease: A progressive neurological disorder that affects memory and cognitive function, leading to degeneration of brain cells.
2. Parkinson's disease: A neurodegenerative disorder that affects movement and balance, caused by the loss of dopamine-producing neurons in the brain.
3. Amyotrophic lateral sclerosis (ALS): A progressive neurological disease that affects nerve cells in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death.
4. Multiple sclerosis: An autoimmune disease that affects the central nervous system, causing inflammation and damage to nerve fibers.
5. Diabetic neuropathy: A complication of diabetes that can cause damage to nerves in the hands and feet, leading to pain, numbness, and weakness.
6. Guillain-Barré syndrome: An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and paralysis.
7. Chronic inflammatory demyelinating polyneuropathy (CIDP): An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and numbness.

The causes of nerve degeneration are not always known or fully understood, but some possible causes include:

1. Genetics: Some types of nerve degeneration may be inherited from one's parents.
2. Aging: As we age, our nerve cells can become damaged or degenerate, leading to a decline in cognitive and physical function.
3. Injury or trauma: Physical injury or trauma to the nervous system can cause nerve damage and degeneration.
4. Infections: Certain infections, such as viral or bacterial infections, can cause nerve damage and degeneration.
5. Autoimmune disorders: Conditions such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) are caused by the immune system attacking and damaging nerve cells.
6. Toxins: Exposure to certain toxins, such as heavy metals or pesticides, can damage and degenerate nerve cells.
7. Poor nutrition: A diet that is deficient in essential nutrients, such as vitamin B12 or other B vitamins, can lead to nerve damage and degeneration.
8. Alcoholism: Long-term alcohol abuse can cause nerve damage and degeneration due to the toxic effects of alcohol on nerve cells.
9. Drug use: Certain drugs, such as chemotherapy drugs and antiviral medications, can damage and degenerate nerve cells.
10. Aging: As we age, our nerve cells can deteriorate and become less functional, leading to a range of cognitive and motor symptoms.

It's important to note that in some cases, nerve damage and degeneration may be irreversible, but there are often strategies that can help manage symptoms and improve quality of life. If you suspect you have nerve damage or degeneration, it's important to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.

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.

The hypoglossal nerve is a cranial nerve that controls the movement of the tongue and is responsible for its protrusion, withdrawal, and lateral movement. Hypoglossal nerve injuries can occur due to various reasons such as trauma, surgery, or tumors. These injuries can result in symptoms such as tongue weakness or paralysis, difficulty speaking or swallowing, and loss of taste sensation on the tip of the tongue.

The severity of hypoglossal nerve injuries can vary from mild to severe, and the treatment options depend on the cause and extent of the injury. Mild cases may resolve on their own with time, while more severe cases may require surgical intervention or other treatments such as physical therapy or medications. In this article, we will discuss the causes, symptoms, diagnosis, and treatment options for hypoglossal nerve injuries in detail.

Causes of Hypoglossal Nerve Injuries:

Hypoglossal nerve injuries can occur due to various reasons such as:

Trauma: Traumatic injuries to the face or neck can cause damage to the hypoglossal nerve, resulting in tongue weakness or paralysis.

Surgery: Surgical procedures in the head and neck region can sometimes result in injury to the hypoglossal nerve.

Tumors: Tumors in the head and neck region can compress or injure the hypoglossal nerve, leading to tongue weakness or paralysis.

Infections: Infections such as meningitis or abscesses in the head and neck region can damage the hypoglossal nerve.

Neurodegenerative diseases: Certain neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) can affect the hypoglossal nerve, leading to tongue weakness or paralysis.

Symptoms of Hypoglossal Nerve Injuries:

The symptoms of hypoglossal nerve injuries can vary depending on the severity and location of the injury. Common symptoms include:

Tongue weakness or paralysis: Weakness or paralysis of the tongue can make it difficult to speak, eat, or swallow.

Drooling: Inability to control salivation due to tongue weakness or paralysis can lead to drooling.

Difficulty articulating words: Slurred speech or difficulty articulating words due to tongue weakness or paralysis.

Facial weakness or paralysis: Weakness or paralysis of the facial muscles can cause drooping or weakness in the face.

Difficulty swallowing: Difficulty swallowing due to tongue weakness or paralysis can lead to dysphagia.

Causes of Hypoglossal Nerve Injuries:

Hypoglossal nerve injuries can occur due to various reasons, including:

Trauma: Traumatic injuries to the face or neck can cause damage to the hypoglossal nerve, resulting in tongue weakness or paralysis.

Surgery: Surgical procedures in the head and neck region can sometimes cause nerve damage, leading to hypoglossal nerve injuries.

Neurological conditions: Certain neurological conditions such as stroke, multiple sclerosis, or tumors can cause hypoglossal nerve injuries.

Viral infections: Viral infections such as HIV or Lyme disease can cause inflammation of the nerves, including the hypoglossal nerve.

Treatment options for Hypoglossal Nerve Injuries:

Treatment options for hypoglossal nerve injuries depend on the underlying cause and severity of the injury. Some possible treatment options include:

Physical therapy: Physical therapy exercises can help improve tongue strength and mobility.

Medications: Medications such as antiviral drugs or steroids may be prescribed to manage symptoms.

Surgery: In some cases, surgery may be necessary to relieve compression or repair damaged nerve tissue.

Speech therapy: Speech therapy can help improve communication skills and address swallowing difficulties.

It's important to seek medical attention if you experience any symptoms of hypoglossal nerve injuries, as prompt treatment can help prevent long-term complications and improve outcomes.

Femoral neuropathy is a type of peripheral neuropathy that affects the femoral nerve, which runs from the lower back down to the thigh and leg. This condition can cause a range of symptoms, including pain, numbness, and weakness in the affected limb.

Causes of Femoral Neuropathy
-------------------------

There are several potential causes of femoral neuropathy, including:

1. Trauma or injury to the nerve
2. Compression or entrapment of the nerve due to a herniated disc or other soft tissue abnormality
3. Inflammation or infection of the nerve
4. Vitamin deficiencies, such as vitamin B12 deficiency
5. Chronic conditions such as diabetes or rheumatoid arthritis

Symptoms of Femoral Neuropathy
----------------------------

The symptoms of femoral neuropathy can vary depending on the severity and location of the nerve damage. Common symptoms include:

1. Pain, numbness, or tingling in the thigh or leg
2. Weakness or muscle wasting in the affected limb
3. Difficulty moving the affected limb or maintaining balance
4. Sensitivity to touch or temperature changes
5. Loss of reflexes in the affected limb

Diagnosis and Treatment of Femoral Neuropathy
---------------------------------------------

Femoral neuropathy can be difficult to diagnose, as it may be mistaken for other conditions such as a muscle strain or sciatica. To diagnose femoral neuropathy, a healthcare provider will typically perform a physical examination and order imaging tests such as an MRI or EMG to confirm the presence of nerve damage.

Treatment for femoral neuropathy depends on the underlying cause of the condition. Conservative treatments may include:

1. Pain management with medication or injections
2. Physical therapy to improve strength and balance
3. Lifestyle changes such as weight loss or avoiding activities that exacerbate the condition
4. Electrical stimulation or other alternative therapies

In some cases, surgery may be necessary to relieve compression on the nerve or repair any structural issues. It is important to seek medical attention if symptoms persist or worsen over time, as early treatment can improve outcomes and reduce the risk of long-term complications.

Living with Femoral Neuropathy
------------------------------

Living with femoral neuropathy can be challenging, but there are several strategies that can help manage symptoms and improve quality of life. These may include:

1. Pain management: Maintaining a consistent pain management plan can help reduce discomfort and improve mobility.
2. Assistive devices: Using canes, walkers, or other assistive devices can help improve balance and stability.
3. Physical therapy: Regular physical therapy sessions can help maintain strength and flexibility in the affected limb.
4. Lifestyle changes: Making lifestyle changes such as losing weight, avoiding activities that exacerbate the condition, and taking regular breaks to rest the affected limb can help manage symptoms.
5. Alternative therapies: Electrical stimulation or other alternative therapies may be helpful in managing symptoms.
6. Support groups: Joining a support group can provide emotional support and connect individuals with others who are experiencing similar challenges.

It is important to remember that each person's experience with femoral neuropathy is unique, and what works for one person may not work for another. It is essential to work closely with a healthcare provider to develop a personalized treatment plan that addresses individual needs and goals. With the right treatment and support, it is possible to manage symptoms of femoral neuropathy and improve quality of life.

Trauma to the nervous system can have a profound impact on an individual's quality of life, and can lead to a range of symptoms including:

* Headaches
* Dizziness and vertigo
* Memory loss and difficulty concentrating
* Mood changes such as anxiety, depression, or irritability
* Sleep disturbances
* Changes in sensation, such as numbness or tingling
* Weakness or paralysis of certain muscle groups

Trauma to the nervous system can also have long-lasting effects, and may lead to chronic conditions such as post-traumatic stress disorder (PTSD), chronic pain, and fibromyalgia.

Treatment for trauma to the nervous system will depend on the specific nature of the injury and the severity of the symptoms. Some common treatments include:

* Medication to manage symptoms such as pain, anxiety, or depression
* Physical therapy to help regain strength and mobility
* Occupational therapy to help with daily activities and improve function
* Cognitive-behavioral therapy (CBT) to address any emotional or psychological issues
* Alternative therapies such as acupuncture, massage, or meditation to help manage symptoms and promote relaxation.

It's important to seek medical attention if you experience any symptoms of trauma to the nervous system, as prompt treatment can help reduce the risk of long-term complications and improve outcomes.

Laser axotomy is a technique is under development that allows for precise axon severing. Laser axotomy could enable doctors to ... There are two modes of axotomy that can occur as a result of a TBI. Primary axotomy occurs immediately and is characterized as ... An axotomy is the cutting or otherwise severing of an axon. Derived from axo- (=axon) and -tomy (=surgery). This type of ... Axotomy may cause neuronal cell death, especially in embryonic or neonatal animals, as this is the period in which neurons are ...
"Functional regeneration after laser axotomy". Nature. 432 (7019): 822. doi:10.1038/432822a. ISSN 1476-4687. PMID 15602545. ...
Axotomy also induces the loss of basophilic staining in the event of central chromatolysis of the neuronal cell. The loss of ... It is clear that axotomy is one of the most direct inducers of chromatolysis and if further research were put into elucidating ... It is an induced response of the cell usually triggered by axotomy, ischemia, toxicity to the cell, cell exhaustion, virus ... The enlargement of nuclear components due to axotomy can be explained by the alteration of the cell's cytoskeleton. The ...
Kobayashi S, Shirao T, Sasaki T (2001). "Drebrin expression is increased in spinal motoneurons of rats after axotomy". Neurosci ...
Taniuchi, M.; Clark, H. B.; Johnson, E. M. (1986). "Induction of nerve growth factor receptor in Schwann cells after axotomy". ...
"Regulation of ciliary neurotrophic factor receptor alpha in sciatic motor neurons following axotomy". Neuroscience. 91 (4): ...
January 1995). "Developing motor neurons rescued from programmed and axotomy-induced cell death by GDNF". Nature. 373 (6512): ... rescues cells from axotomy-induced death, and prevents chronic degeneration. These neuronal populations die in the course of ... and was able to prevent apoptosis of motor neurons induced by axotomy. GDNF is synthesized as a 211 amino acid-long protein ...
"Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy." Nat Med 5, no. 1 (Jan ...
... phenotypes caused by mutations in the axotomy-induced gene, Nna1". Science. 295 (5561): 1904-6. Bibcode:2002Sci...295.1904F. ...
1999). "Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy". Nature Medicine. ...
Fuchs, P. A.; Henderson, L. P.; Nicholls, John G. (1 February 1982). "Axotomy of single fluorescent nerve fibers in developing ...
"Cyclosporin-A treatment attenuates delayed cytoskeletal alterations and secondary axotomy following mild axonal stretch injury ...
Liu XH, Collier RJ, Youle RJ (2002). "Inhibition of axotomy-induced neuronal apoptosis by extracellular delivery of a Bcl-XL ...
"Upregulation of heat shock proteins rescues motoneurones from axotomy-induced cell death in neonatal rats". Exp. Neurol. 176 (1 ...
Effects of Axotomy and Glial-Derived Neurotrophic Factor". Molecular and Cellular Neuroscience. 12 (4): 256-268. doi:10.1006/ ...
Trophic effects of androgen: receptor expression and the survival of laryngeal motor neurons after axotomy, J. Neurosci. 16: ... receptor expression and the survival of laryngeal motor neurons after axotomy". Journal of Neuroscience. 16 (21): 6625-6633. ...
"In vivo single branch axotomy induces GAP-43-dependent sprouting and synaptic remodeling in cerebellar cortex". Proceedings of ...
"Neuronal preservation and reactive gliosis attenuation following neonatal sciatic nerve axotomy by a fluorinated cannabidiol ...
1994). "Axotomy induces intranuclear immunolocalization of neuron-specific enolase in facial and hypoglossal neurons of the rat ...
Expression is also increased after axonal injury, such as peripheral axotomy in motor neurons and dorsal root ganglia. This ...
Bonfanti, L (1996). "Protection of retinal ganglion cells from natural and axotomy-induced cell death in neonatal transgenic ...
Nakayama M, Miyake T, Gahara Y, Ohara O, Kitamura T (July 1995). "A novel RING-H2 motif protein downregulated by axotomy: its ...
Following axotomy of cultured neurons, significant upregulation in Aurora B kinase gene expression was observed coinciding with ...
"The slow Wallerian degeneration gene in vivo protects motor axons but not their cell bodies after avulsion and neonatal axotomy ...
Weishaupt JH, Klöcker N, Bähr M (2005). "Axotomy-induced early down-regulation of POU-IV class transcription factors Brn-3a and ...
It has also been detected in motor neurons of embryonic rats and is suggested to aid development and to reduce axotomy. The ...
Studies have shown that in cases of reversible neuronal injury, such as axotomy, neuron signals cause microglia to produce ... also called secondary axotomy, and the upregulation of fibrous extracellular matrix components which eventually form the scar ...
... axotomy, or the optical tweezing or isolation of intracellular material. Terms under deliberation Optoporation: Has been ...
... which inhibits NGF-p75NTR binding and prevents the death of RGCs in axotomy and glaucoma. In addition, in combination with ...
Using the experimental model provided by the facial motor nucleus following axotomy Kreutzberg and his fellow workers ...
Pain control through selective chemo-axotomy of centrally projecting TRPV1+ sensory neurons Matthew R Sapio 1 , John K Neubert ... Pain control through selective chemo-axotomy of centrally projecting TRPV1+ sensory neurons Matthew R Sapio et al. J Clin ... The results demonstrate that central chemo-axotomy of the TRPV1+ afferents underlies RTX analgesia and refine the neurobiology ...
Hai PH, Doh-Ura K, Nakanishi H. Impairment of microglial responses to facial nerve axotomy in cathepsin S-deficient mice. ... Finally, we compared axotomy-induced neuronal death in the two groups and found that the percentage of motoneurons that ... Finally, we compared axotomy-induced neuronal death in the two groups and found that the percentage of motoneurons that ... Finally, we compared axotomy-induced neuronal death in the two groups and found that the percentage of motoneurons that ...
... or axotomy (Hefti, 1986). It is interesting to note that apoptosis also occurs during hair cell degeneration attributable to ...
Effect of Lisuride and LSD on Monoamine Synthesis after Axotomy or Res... Arch.Pharmacol.. 1978. ...
MeSH Terms: Animals; Axotomy; Biomarkers/analysis; Brain/drug effects; Brain/metabolism; Dopamine/analysis; Dopamine/metabolism ... Title: Methamphetamine-induced deficits of brain monoaminergic neuronal markers: distal axotomy or neuronal plasticity. ...
It has been found that treatment with proteasome inhibitors such as MG132 or lactacystin induces secondary axotomy of stretch- ... Experimental sciatic nerve axotomy showed an axonal accumulation of Aβ and promotion of the pathological formation of Aβ ... Expansion of the dendritic tree of motoneurons innervating neck muscles of the adult cat after permanent axotomy. J. Comp. ... Cyclosporin-A treatment attenuates delayed cytoskeletal alterations and secondary axotomy following mild axonal stretch injury ...
... axotomy,128,1,R,1, axotomisation,post-axotomy,3,1,R,1, axotomisation,postaxotomy,3,1,R,1, ballistocardiography, ...
focus on paracrine actions of activated satellite cells after axotomy.. Levy Bde F; Cunha Jdo C; Chadi G. Int J Neurosci; 2007 ...
Thus, axotomy causes its release at the injury site. However, most osteopontin-positive α-RGCs, the main neuronal population ... Regenerative failure in the mammalian optic nerve is generally attributed to axotomy-induced retinal ganglion cell (RGC) death ...
A regenerative effect of BoNT/A was demonstrated in the rat femoral nerve axotomy model by Irintchev et al. [30]. Nerve injury ... 30] by examining the ability of the neurotoxin to antagonize axotomy-induced alterations in the density of excitatory and ... Trauma to peripheral nerves such as crush or axotomy leads to marked alterations in the axon proximal and distal to the site of ... nerve crush and axotomy. These actions have been attributed primarily to increased proliferation of Schwann cells and ...
Following axotomy, the nerve cell body immediately undergoes changes in morphology and protein synthesis to support axonal ...
Diffusion tensor magnetic resonance imaging of Wallerian degeneration in rat spinal cord after dorsal root axotomy. J Neurosci ...
Autoimmune T cells protect neurons from non-essential degeneration after essential nervous methodology axotomy. The youngster ...
F, The results of laser axotomy of the halo of axons. After axotomy, the axons retracted (black arrows) followed by various ... with and without axotomy of the central branch. Expression of α9k1 without the central axotomy led to upregulation of a known ... C, Adult rat DRG explant neurites immediately and 2 h after axotomy by a glass-pulled pipette where the demarcation line is ... In vitro sensory axon regeneration of adult rat DRG explants and human iPSC-derived sensory neurons after axotomy in the ...
... enhancer region of the galanin gene that directs expression to the dorsal root ganglion and confers responsiveness to axotomy ...
Axotomy of roundworm neurons was performed by femtosecond laser surgery, after which the axons functionally regenerated. ...
Systems view of axotomy with RNA-Seq analysis of Dorsal Root Ganglion, Dorsal Horn and Ventral Horn. Neuroscience. Washington ... Pain control through selective chemo-axotomy of centrally projecting TRPV1+ sensory neurons. J Clin Invest. Apr 2;128(4):1657- ...
Pain control through selective chemo-axotomy of centrally projecting TRPV1+ sensory neurons. J Clin Invest 128, 1657-1670. ...
Microglia showed a strong increase in many different integrin subunits following facial nerve axotomy. These intrinsic, ...
Axotomy Preferred Term Term UI T058768. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1998). ... Axotomy Preferred Concept UI. M0029338. Scope Note. Transection or severing of an axon. This type of denervation is used often ... Axotomy. Tree Number(s). E04.525.210.158. Unique ID. D019771. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/D019771 ...
However, 24 hr after axotomy, there was a 13-fold increase in the percentage of apoptotic nuclei in the distal nerve stumps of ... The expression of both the p75 and nerve growth factor (NGF) genes was upregulated after axotomy in neonatal wild-type nerves. ... Induction of postnatal schwann cell death by the low-affinity neurotrophin receptor in vitro and after axotomy. (2000) Journal ...
PlexinA2 limits recovery from corticospinal axotomy by mediating oligodendrocyte-derived Sema6A growth inhibitionShim SO, ... PlexinA2 limits recovery from corticospinal axotomy by mediating oligodendrocyte-derived Sema6A growth inhibition Molecular And ...
Prominent expression of bFGF in dorsal root ganglia after axotomy.. 7:2458-2468. 1995 ... Y and galanin binding sites in rat and monkey lumbar dorsal root ganglia and spinal cord and effect of peripheral axotomy.. 7: ...
Axon growth after axotomy was also promoted by synaptamide addition to either side of the chamber. Using bodipy-synaptamide and ... For in vitro studies, mouse P0 primary cortical neurons were plated on an axon chamber and axotomy was performed on 7DIV when ...
Axotomy Preferred Term Term UI T058768. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1998). ... Axotomy Preferred Concept UI. M0029338. Scope Note. Transection or severing of an axon. This type of denervation is used often ... Axotomy. Tree Number(s). E04.525.210.158. Unique ID. D019771. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/D019771 ...
Axotomy MeSH DeCS ID:. 1381 Unique ID:. D001369 NLM Classification:. WL 102.5 ...
1264 value of [symbol] in hypoglossal axotomy, undated File - Box: 55, Folder: 23 ...
Ventral root axotomy regeneration after mesenchymal stem cell transplantation. Kerstetter-Fogle, Amber E. ...
  • Finally, we compared axotomy-induced neuronal death in the two groups and found that the percentage of motoneurons that survived in CS-/- mice was significantly smaller than that in wildtype mice. (elsevierpure.com)
  • Methamphetamine-induced deficits of brain monoaminergic neuronal markers: distal axotomy or neuronal plasticity. (nih.gov)
  • Axotomy of roundworm neurons was performed by femtosecond laser surgery, after which the axons functionally regenerated. (nanowerk.com)
  • For in vitro studies, mouse P0 primary cortical neurons were plated on an axon chamber and axotomy was performed on 7DIV when axons were sufficiently grown into the other side of the axon chamber. (nih.gov)
  • During her PhD (advised by Dr. Martin Schwab) she investigated the reorganization of corticospinal neurons after axotomy and their role in the recovery of forelimb motor function in rats. (nih.gov)
  • 2006. Examination of cellular and molecular events associated with optic nerve axotomy. (nih.gov)
  • Regenerative failure in the mammalian optic nerve is generally attributed to axotomy-induced retinal ganglion cell (RGC) death, an insufficient intrinsic regenerative capacity, and an extrinsic inhibitory environment. (neurosciencenews.com)
  • This thesis focuses on the effects of CDNF and MANF treatment in vivo on optic nerve axotomy. (medipol.edu.tr)
  • In order to study these mechanisms, optic nerve axotomy was performed. (medipol.edu.tr)
  • Neuropeptide Y and galanin binding sites in rat and monkey lumbar dorsal root ganglia and spinal cord and effect of peripheral axotomy. (duke.edu)
  • In rats with a spinal dorsal column crush injury, a preconditioning peripheral sciatic nerve axotomy, or NgR1(310)ecto-Fc decoy protein treatment or ChondroitinaseABC (ChABC) treatment independently support similar degrees of regeneration by ascending primary afferent fibers into the vicinity of the injury site. (listlabs.com)
  • Prominent expression of bFGF in dorsal root ganglia after axotomy. (duke.edu)
  • To understand the underlying mechanisms, we established in vivo laser axotomy assay in C. elegans . (nih.gov)
  • Seems to prevent the degeneration of motor axons after axotomy. (nih.gov)
  • To better understand the role of CS in microglia, we investigated microglial responses after a facial nerve axotomy in CS-deficient (CS-/-) and wild-type mice. (elsevierpure.com)
  • Hai, PH , Doh-Ura, K & Nakanishi, H 2007, ' Impairment of microglial responses to facial nerve axotomy in cathepsin S-deficient mice ', Journal of Neuroscience Research , vol. 85, no. 10, pp. 2196-2206. (elsevierpure.com)
  • Ventral root axotomy regeneration after mesenchymal stem cell transplantation. (bvsalud.org)
  • The present study strongly suggests that CS plays a role in the migration and activation of microglia to protect facial motoneurons against axotomy-induced injury. (elsevierpure.com)
  • Microglia in both groups accumulated in the facial motor nucleus following axotomy. (elsevierpure.com)
  • Neurotrophins, such as NGF and BDNF, have been tested in animal models of glaucoma and while some studies have shown them to reduce RGC death, [ 46 ] exogenous BDNF may not provide long-lasting neuroprotection to RGC in optic nerve axotomy or glaucoma models. (medscape.com)
  • 2006. Examination of cellular and molecular events associated with optic nerve axotomy. (nih.gov)
  • Traumatic injury to the peripheral and central nervous systems very often causes axotomy, where an axon loses connections with its target resulting in loss of function. (nih.gov)
  • For in vitro studies, mouse P0 primary cortical neurons were plated on an axon chamber and axotomy was performed on 7DIV when axons were sufficiently grown into the other side of the axon chamber. (nih.gov)
  • Axon growth after axotomy was also promoted by synaptamide addition to either side of the chamber. (nih.gov)
  • In contrast, spontaneous regeneration rarely occurs after axotomy in the spinal cord and brain. (nih.gov)
  • Reduction of either protein increases axonal regrowth following axotomy. (bvsalud.org)
  • Methamphetamine-induced deficits of brain monoaminergic neuronal markers: distal axotomy or neuronal plasticity. (nih.gov)