Axotomy: 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.Facial Nerve Injuries: 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.Nerve Regeneration: Renewal or physiological repair of damaged nerve tissue.Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.Facial Nerve: 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.Sciatic Nerve: 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.Denervation: The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)Nerve Crush: Treatment of muscles and nerves under pressure as a result of crush injuries.Ganglia, Spinal: 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.Retrograde Degeneration: 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.Motor Neurons: Neurons which activate MUSCLE CELLS.Wallerian Degeneration: 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.GAP-43 Protein: 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.Optic Nerve: 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.Red Nucleus: 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, Afferent: Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.Optic Nerve Injuries: 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.Stilbamidines: STILBENES with AMIDINES attached.Retinal Ganglion Cells: 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.Axonal Transport: 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)Autonomic Fibers, Postganglionic: Nerve fibers which project from cell bodies of AUTONOMIC GANGLIA to SYNAPSES on target organs.Peripheral Nerves: 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, Sympathetic: 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.Self Mutilation: 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.Neurofilament Proteins: 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)Hypoglossal Nerve: 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.Nerve Degeneration: 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.Rats, Sprague-Dawley: 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.Superior Cervical Ganglion: The largest and uppermost of the paravertebral sympathetic ganglia.Neurons: 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.Spinal Nerves: 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.Peripheral Nerve Injuries: Injuries to the PERIPHERAL NERVES.Nissl Bodies: Subcellular structures found in nerve cell bodies and DENDRITES. They consist of granular endoplasmic reticulum (ENDOPLASMIC RETICULUM, ROUGH) and RIBOSOMES.Hypoglossal Nerve Injuries: Traumatic injuries to the HYPOGLOSSAL NERVE.Schwann Cells: Neuroglial cells of the peripheral nervous system which form the insulating myelin sheaths of peripheral axons.Glossopharyngeal Nerve: 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.Nerve Growth Factors: Factors which enhance the growth potentialities of sensory and sympathetic nerve cells.Spinal Cord: A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.Sciatic Neuropathy: 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)Lampreys: 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.Neurites: 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.Muscle Denervation: The resection or removal of the innervation of a muscle or muscle tissue.Femoral Neuropathy: 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.Neural Conduction: The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.Sensory Receptor Cells: 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.Intermediate Filaments: 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.Cell Survival: 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.Activating Transcription Factor 3: An activating transcription factor that plays a key role in cellular responses to GENOTOXIC STRESS and OXIDATIVE STRESS.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Trauma, Nervous System: Traumatic injuries to the brain, cranial nerves, spinal cord, autonomic nervous system, or neuromuscular system, including iatrogenic injuries induced by surgical procedures.Aplysia: 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.Medial Forebrain Bundle: 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.Neurotrophin 3: 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.Nerve Tissue ProteinsTubulin: 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.Rhizotomy: Surgical interruption of a spinal or cranial nerve root. (From Dorland, 28th ed)Galanin: 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.Autonomic Denervation: 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)

ABSTRACT: The purpose of this study was to determine the effect of retinal ganglion cell (RGC) axotomy and death on the thickness of the inner plexiform (IPL), inner nuclear (INL), and outer plexiform layers (OPL), as well as the densities of short- (S) and middle-to-long-wavelength (M/L) cones in the porcine retina. Unilateral, peripapillary RGC axotomy was performed in six domestic pigs using an argon laser. In eight additional pigs the optic nerve was surgically transected. With the exception of two eyes that underwent sham surgeries, the contralateral eyes were not treated and served as controls. Damage to the retinal vasculature was ruled out with fluorescein angiography. Nine months later the retinas were flat mounted, and biopsies were taken at four retinal locations. Cone densities were determined with anti-visual pigment antibodies, COS-1 for M/L and OS-2 for S pigment. Semithin cross sections were made through all biopsies to measure the thickness of the retinal layers. The effect of ...
... 3 times by MTT assay. Activation of TrkB and signaling substances was confirmed by European blot evaluation SU-5402 downstream. Intravitreal shots of 29D7 had been performed after optic nerve axotomy and following RGC success was quantified using β-III tubulin immunostaining. Regeneration was evaluated using retrograde fluorogold tracing within an optic nerve-peripheral nerve graft model. Outcomes. Just like brain-derived neurotrophic element (BDNF) the 29D7 antibody highly promoted RGC success and neurite development in vitro weighed against medium only or control IgG. Forskolin which weakly backed RGC success alone potentiated the result of 29D7. Intravitreal shot of 29D7 improved RGC success however not regeneration in vivo 14 days after optic nerve damage. Conclusions. Collectively these results demonstrate the prospect of antibody-mediated TrkB agonism like a potential restorative method of enhance RGC success after optic ...
Understanding the basic mechanisms of neural regeneration after injury is a pre-requisite for developing appropriate treatments. Traditional approaches to model axonal lesions, such as high intensity power laser ablation or sharp metal scratching, are complex to implement, have low throughputs, and generate cuts that are difficult to modulate. We present here a novel reproducible microfluidic approach to model in vitro mechanical lesion of tens to hundreds of axons simultaneously in a controlled manner. The dimensions of the induced axonal injury and its distance from the neuronal cell body are precisely controlled while preserving both the proximal and distal portions of axons. We have observed that distal axons undergo Wallerianlike anterograde degeneration after axotomy; in contrast, proximal portions of the axons remain un-degenerated, possessing the potential to re-grow. More importantly, surpassing the previous axotomy methods performed in petridish in which local microenvironments cannot ...
De Felipe, C. and Belmonte, C. (1999), c-Jun expression after axotomy of corneal trigeminal ganglion neurons is dependent on the site of injury. European Journal of Neuroscience, 11: 899-906. doi: 10.1046/j.1460-9568.1999.00498.x ...
The present study shows that peripheral nerve injury induces PAP-II expression in peripherin-containing small DRG neurons which mostly expressed neither CGRP nor IB4, followed by a shift to NPY-containing large DRG neurons 14 days after peripheral axotomy ...
The T-type Ca2+ channel Cav3.2 is expressed in nociceptive and mechanosensitive sensory neurons. The mechanosensitive D-hair (down-hair) neurons, which innervate hair follicles, are characterized by a large-amplitude Cav3.2 T-current involved in the amplification of slow-moving stimuli. The molecules and signalling pathways that regulate T-current expression in mechanoreceptors are unknown. In the present study, we investigated the effects of NT-4 (neurotrophin-4) on Cav3.2 T-current expression in D-hair neurons in vitro. Interruption of the supply of NT-4 with peripheral nerve axotomy induced a non-transcriptional decrease in the T-current amplitude of fluorogold-labelled axotomized sensory neurons. The T-current amplitude was restored by incubation with NT-4. Deletion of NT-4 through genetic ablation resulted in a similar selective loss of the large-amplitude T-current in NT-4−/− sensory neurons, which was rescued by the addition of NT-4. NT-4 had no effect on the T-current in ...
Retinas were isolated from Brown Norwegian male rats 9-12 weeks of age and cultured on 0.4 µm Millicell culture plate inserts in Neurobasal-A medium at 37ºC in 5% CO2. A Helios gene gun system was used for particle-mediated transfer of a YFP-expressing plasmid to RGCs. Retinal explants were treated with a broad-spectrum, irreversible caspase inhibitor (Boc-D-FMK) to prevent apoptosis. The morphology of RGCs was observed by confocal microscopy. ...
The authors examined the mechanisms of KCC2 down-regulation in axotomized spinal motor neurons with and without reinnervation of muscle. They first established a system to measure KCC2 expression throughout somatodendritic membranes. Next, they used genetic approaches to demonstrate that microglia, BDNF, and TrKB are not responsible for the KCC2 down-regulation caused by sciatic transection; instead, KCC2 is dependent on neuromuscular innervation. Overall, the reviewers felt that the study is well done and includes a comprehensive set of experiments addressing fundamental questions related to factors contributing to the downregulation of KCC2 expression in motor neurons. However, reviewers and the reviewing editor agreed that there are a few issues to be addressed before further considering this work for publication. Major considerations are on the interpretation of the results for KCC2 regulation mechanism, neuron types expressing KCC2 (and not expressing), and KCC2 internalization vs. protein ...
Nerve transection is a condition in which nerve fibers that run throughout the body are cut. There are several common causes of...
Autophagy is an essential recycling pathway implicated in neurodegeneration either as a pro-survival or a pro-death mechanism. Its role after axonal injury is still uncertain. Axotomy of the optic nerve is a classical model of neurodegeneration. It induces retinal ganglion cell death, a process also occurring in glaucoma and other optic neuropathies. We analyzed autophagy induction and cell survival following optic nerve transection (ONT) in mice. Our results demonstrate activation of autophagy shortly after axotomy with autophagosome formation, upregulation of the autophagy regulator Atg5 and apoptotic death of 50% of the retinal ganglion cells (RGCs) after 5 days. Genetic downregulation of autophagy using knockout mice for Atg4B (another regulator of autophagy) or with specific deletion of Atg5 in retinal ganglion cells, using the Atg5flox/flox mice reduces cell survival after ONT, whereas pharmacological induction of autophagy in vivo increases the number of surviving cells. In conclusion, ...
Purpose: Anterograde trans-synaptic degeneration along the visual pathway has been observed in glaucomatous patients and experimental glaucoma models. The aim of this study is to investigate the mechanisms and extent of trans-synaptic changes in the visual system as well as in the distant somatosensory cortex using a rodent model of optic nerve axotomy. It is known that the rat primary somatosensory centre has structural and functional inter-linkages with the visual cortex.. Methods: Optic nerve injury in the form of axotomy was performed in adult Sprague-Dawley rats. Animals were sacrificed at regular time points and tissues harvested. Immunoblotting followed by densitometric analysis was used to determine the phosphorylation profile of Akt in the dorsal lateral geniculate nucleus (dLGN), the visual cortex and the primary somatosensory cortex (S1). The neuronal cell size and cell density were measured using Nissl staining. The prevalence of apoptosis was characterized by terminal ...
The effect of a change in neurofilament (NF) and tubulin gene expression on the elongation of axonal sprouts by adult rat sensory neurons was examined. Distal sciatic nerve crush axotomy was used to initiate changes in cytoskeletal gene expression in lumbar dorsal root ganglion (DRG) neurons. In situ hybridization of DRG neurons with 35S- labeled cDNA probes revealed a significant reduction in the level of mRNAs for the low-molecular weight-NF protein and a significant increase in the level of beta tubulin mRNAs by 2 weeks after axotomy. A novel modification of the axonal transport paradigm was used to examine the biochemical composition of the regenerating axons formed by primed and unprimed DRG neurons. Primed neurons (which had sustained a crush axotomy of the distal sciatic nerve 2 weeks earlier) and unprimed (normal) neurons were labeled by microinjection of 35S-methionine and then stimulated to regenerate axons by a crush located very close to the DRG. In this paradigm, axonal sprouts that ...
Evidence that activation of P2X7R does not exacerbate neuronal death after optic nerve transection and focal cerebral ischemia in mice. Exp Neurol. 2017 Jun 29;: Authors: Caglayan B, Caglayan AB, Beker MC, Yalcin E, Beker M, Kelestemur T, Sertel E, Ozturk G, Kilic U, Sahin F, Kilic E Abstract Conflicting data in the literature about the function of P2X7R in survival following...
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TY - JOUR. T1 - Cell type-specific changes of the membrane properties of peripherally- axotomized dorsal root ganglion neurons in a rat model of neuropathic pain. AU - Kim, Y. I.. AU - Na, H. S.. AU - Kim, S. H.. AU - Han, H. C.. AU - Yoon, Y. W.. AU - Sung, B.. AU - Nam, H. J.. AU - Shin, S. L.. AU - Hong, S. K.. PY - 1998/5/21. Y1 - 1998/5/21. N2 - Recent evidence indicates that neuropathic pain from partial peripheral nerve injury is maintained by electrophysiologically abnormal signals from injured sensory neurons. To gain an insight into the mechanisms underlying this electrophysiological abnormality, we examined the effects of S1 spinal nerve transection on the membrane properties of S1 dorsal root ganglion neurons one to two weeks after injury. This injury produced significant action potential broadening [40% (1 ms) in C-, 149% (1.5 ms) in Aδ- and 84% (0.5 ms) in Aα/β-cells], which was primarily due to the enhancement of the shoulder appearing on the falling phase of the action ...
Trigeminal ganglia neurons significantly affect the amplitude and type of 5-HT receptor gene expression following activation of their axon terminals and sensitisation by painful stimuli. Moreover, these neurons significantly alter gene expression in cytoskeletal proteins following injury. The aim of the present study was to determine whether peripheral and/or central deafferenting lesions affect gene expression in serotonergic receptors that are involved in pain transmission. Adult rats were subjected to unilateral ablation of the facial sensory and motor cortices. Fifteen days after the surgery, degeneration of the cortico-trigeminal pathway was observed. Presynaptic deafferentation of the primary trigeminal neurons and central afferents of the contralateral ganglia was conducted. As a consequence of the excision of the meninges covering the ablated cortices, the peripheral axotomy of the trigeminal-vascular primary neurons of the ipsi-lateral side was induced. Serotonergic receptor (5-HT5A/5B/1B/1D/1F
Axonal degeneration is an early feature of several neurodegenerative conditions, but the sequence of events leading to this axonal loss is still unknown. The role of calcium in this degenerative process has long been accepted, but there is no detailed understanding of the calcium source(s) and dynamics. Chelation of extracellular calcium protects against axonal degeneration triggered by axotomy (George et al., 1995), and depletion of intracellular calcium stores protects against axonal degeneration under ischemic conditions (Stys, 2005). We showed previously that a crucial event during axonal degeneration is the opening of the mPTP (Barrientos et al., 2011), which is highly dependent on calcium levels (Halestrap et al., 1986). The data that we present here establishes that the release of ER-derived calcium store is a critical step in Wallerian degeneration by activating the mPTP that leads to axonal loss.. Our results show that chelation of external calcium can protect from neurofilament ...
Researchers at Max Planck Florida Institute for Neuroscience develop a technique to visualize and control the neural activities that underlie behavior Since
A large thoracic spinal cord injury disconnects the hindlimb (HL) sensory-motor cortex from its target, the lumbar spinal cord. The fate of the synaptic structures of the axotomized cortical neurons is not well studied. We evaluated the density of spines on axotomized corticospinal neurons at 3, 7, and 21 days after the injury in adult mice expressing yellow fluorescence protein in a subset of layer 5 neurons. Spine density of the dendritic segment proximal to the soma (in layer 5) declined as early as 3 days after injury, far preceding the onset of somatic atrophy. In the distal segment (in layer 2/3), spine loss was slower and less severe than in the proximal segment. Axotomy of corticospinal axons in the brainstem (pyramidotomy) induced a comparable reduction of spine density, demonstrating that the loss is not restricted to the neurons axotomized in the thoracic spinal cord. Surprisingly, in both forms of injury, the spine density of putative non-axotomized layer 5 neurons was reduced as ...
Traumatic brain injury (TBI) is a leading cause of disability worldwide. Annually, 150 to 200/1,000,000 people become disabled as a result of brain trauma. Axonal degeneration is a critical, early event following TBI of all severities but whether axon degeneration is a driver of TBI remains unclear. Molecular pathways underlying the pathology of TBI have not been defined and there is no efficacious treatment for TBI. Despite this significant societal impact, surprisingly little is known about the molecular mechanisms that actively drive axon degeneration in any context and particularly following TBI. Although severe brain injury may cause immediate disruption of axons (primary axotomy), it is now recognized that the most frequent form of traumatic axonal injury (TAI) is mediated by a cascade of events that ultimately result in secondary axonal disconnection (secondary axotomy) within hours to days. Proposed mechanisms include immediate post-traumatic cytoskeletal destabilization as a direct result of
Wld(S) (slow Wallerian degeneration) is a remarkable protein that can suppress Wallerian degeneration of axons and synapses, but how it exerts this effect remains unclear. Here, using Drosophila and mouse models, we identify mitochondria as a key site of action for Wld(S) neuroprotective function. Targeting the NAD(+) biosynthetic enzyme Nmnat to mitochondria was sufficient to fully phenocopy Wld(S), and Wld(S) was specifically localized to mitochondria in synaptic preparations from mouse brain. Axotomy of live wild-type axons induced a dramatic spike in axoplasmic Ca(2+) and termination of mitochondrial movement-Wld(S) potently suppressed both of these events. Surprisingly, Wld(S) also promoted increased basal mitochondrial motility in axons before injury, and genetically suppressing mitochondrial motility in vivo dramatically reduced the protective effect of Wld(S). Intriguingly, purified mitochondria from Wld(S) mice exhibited enhanced Ca(2+) buffering capacity. We propose that the enhanced ...
Axons damaged by acute injury, toxic insults, or neurodegenerative diseases execute a poorly defined autodestruction signaling pathway leading to widespread fragmentation and functional loss. Here, we describe an approach to study Wallerian degeneration in the Drosophila L1 wing vein that allows for analysis of axon degenerative phenotypes with single-axon resolution in vivo. This method allows for the axotomy of specific subsets of axons followed by examination of progressive axonal degeneration and debris clearance alongside uninjured control axons. We developed new Flippase (FLP) reagents using proneural gene promoters to drive FLP expression very early in neural lineages. These tools allow for the production of mosaic clone populations with high efficiency in sensory neurons in the wing. We describe a collection of lines optimized for forward genetic mosaic screens using MARCM (mosaic analysis with a repressible cell marker; i.e., GFP-labeled, homozygous mutant) on all major autosomal arms (
Wallerian degenaration is a pattern of damage in nerve fibers in which the axon of a nerve breaks down because of a lesion on the...
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Motor and sensory proprioceptive axons reinnervate muscles after peripheral nerve transections followed by microsurgical reattachment; nevertheless, motor coordination remains abnormal and stretch reflexes absent. We analyzed the possibility that permanent losses of central IA afferent synapses, as a consequence of peripheral nerve injury, are responsible for this deficit. VGLUT1 was used as a marker of proprioceptive synapses on rat motoneurons. After nerve injuries synapses are stripped from motoneurons, but while other excitatory and inhibitory inputs eventually recover, VGLUT1 synapses are permanently lost on the cell body (75-95% synaptic losses) and on the proximal 100 μm of dendrite (50% loss). Lost VGLUT1 synapses did not recover, even many months after muscle reinnervation. Interestingly, VGLUT1 density in more distal dendrites did not change. To investigate whether losses are due to VGLUT1 downregulation in injured IA afferents or to complete synaptic disassembly and regression of IA ventral
For more than a century, scientists believed that injured axons severed from the neuron cell body passively wasted away due to a lack of nutrients. However, a mouse mutation identified in the early 1990s - called slow Wallerian degeneration (Wlds) - was able to suppress axon degeneration for weeks. This finding forced scientists to reassess Wallerian degeneration, the process through which an injured axon degenerates, as a passive process and consider the possibility that an active program of axon auto-destruction, akin to apoptotic death, was at work instead. If Wallerian degeneration was an active process, hypothesized Dr. Freeman, a Howard Hughes Medical Institute Early Career Scientist, then it should be possible through forward genetic screens in Drosophila to identify mutants exhibiting Wlds-like axon protection. Freeman and colleagues screened more than 2,000 Drosophila mutants for ones that exhibited long-term survival of severed axons. Freeman says this was a heroic effort on the part ...
Abstract: Axotomy-induced degradation of retinal ganglion cells (RGC) can be delayed if the destructive features of activated Microglial cells are pharmacologically neutralized, and prevented if the axons are permitted to regrow into transplanted autologous peripheral nerve (PN) pieces. Axotomized central nervous system neurons, whose regenerating axons are guided to their natural target areas in the brain with the aid of PN grafts, are capable of establishing synaptic contacts with normal morphological and electrophysiological properties. This study was undertaken to 1) morphometrically characterize and classify the regenerating rat RGC, 2) examine target-dependent effects on survival of subsets of neurons, and 3) investigate whether reconnected neurons are capable of restoring visual functions. In analogy to the normal rat retina, as a first step, the retrogradely labeled, regenerating RGC were categorized into five classes which are morphologically distinct and reminiscent of normal RGC ...
TY - JOUR. T1 - Testosterone treatment attenuates the effects of facial nerve transection on glial fibrillary acidic protein (GFAP) levels in the hamster facial motor nucleus. AU - Coers, Susanna. AU - Tanzer, Lisa. AU - Jones, Kathryn. PY - 2002. Y1 - 2002. N2 - Testosterone propionate (TP) administration coincident with facial nerve injury accelerates the recovery rate from facial muscle paralysis in the hamster. One mechanism by which TP could augment peripheral nerve regeneration is through glial fibrillary acidic protein (GFAP) regulation in the facial motor nucleus. In a previous study, axotomy alone induces increases in GFAP mRNA, with TP significantly attenuating the axotomy-induced increases in GFAP mRNA. In the present study, immunoblotting techniques were used to extend our previous GFAP mRNA studies to the protein level. Castrated male hamsters were subjected to a right facial nerve transection, with half of the animals receiving subcutaneous implants of 100% crystalline TP. The left ...
Maintenance of ocular viability is one of the major impediments to successful whole eye transplantation. We provide a comprehensive understanding of the current literature to help guide future studies in order to overcome this hurdle. A systematic multistage review of published literature was performed. Three specific questions were addressed: (1) Is recovery of visual function following eye transplantation greater in cold-blooded vertebrates when compared with mammals? (2) Is outer retina function following enucleation and reperfusion improved compared with enucleation alone? (3) Following optic nerve transection, is there a correlation between RGC survival and either time after transection or proximity of the transection to the globe? In a majority of the studies performed in the literature, recovery of visual function can occur after whole eye transplantation in cold-blooded vertebrates. Following enucleation (and reperfusion), outer retinal function is maintained from four to nine hours. ...
Brachial plexus lesion results in loss of motor and sensory function, being more harmful in the neonate. Therefore, this study evaluated neuroprotection and regeneration after neonatal peripheral nerve coaptation with fibrin sealant. Thus, P2 neonatal Lewis rats were divided into three groups: AX: sciatic nerve axotomy (SNA) without treatment; AX+FS: SNA followed by end-to-end coaptation with fibrin sealant derived from snake venom; AX+CFS: SNA followed by end-to-end coaptation with commercial fibrin sealant. Results were analyzed 4, 8, and 12 weeks after lesion. Astrogliosis, microglial reaction, and synapse preservation were evaluated by immunohistochemistry. Neuronal survival, axonal regeneration, and ultrastructural changes at ventral spinal cord were also investigated. Sensory-motor recovery was behaviorally studied. Coaptation preserved synaptic covering on lesioned motoneurons and led to neuronal survival. Reactive gliosis and microglial reaction decreased in the same groups (AX+FS, AX+CFS) at 4
A DAP12-Dependent Signal Promotes Pro-Inflammatory Polarization in Microglia Following Nerve Injury and Exacerbates Degeneration of Injured NeuronsA DAP12-Dependent Signal Promotes Pro-Inflammatory Polarization in Microglia Following Nerve Injury and Exacerbates Degeneration of Injured Neurons ...
The predominant therapy for peripheral nerve transection is anastomosis by suture. However, sutures have been known to lead to tissue inflammation, granulomas, and poor functional outcomes. While adhesives offer a promising alternative, fibrin-the predominant bio-glue-can transmit disease. Here we examine a photocrosslinkable chitosan hydrogel for use in surgical therapies for peripheral nerve injury. Prepared by conjugating 4-azidobenzoic acid to amino groups of chitosan using carbodiimide chemistry, this formulation demonstrates a high potential of in-situ photocrosslinking. A 40 mg/mL solution gels under 40 s of UV illumination. This gel is demonstrated to be cytocompatible with neural cell populations and is not acutely toxic to nerve conduction ex vivo. Mechanical testing of nerves anastomosed by this hydrogel had tensile strengths comparable to conventional fibrin glues. These results show chitosan hydrogel to be biocompatible and mechanically suitable for use in nerve repair. Keywords-chitosan;
TY - GEN. T1 - Cycloheximide reduces retinal ganglion cell death induced by tectal ablation in neonatal rats. AU - Harvey, Alan. AU - Cui, Q.. AU - Robertson, Donald. PY - 1993. Y1 - 1993. M3 - Conference paper. VL - 4. SP - 36. EP - 36. BT - Australian Neuroscience Society Meeting. A2 - Powis, D.. PB - Australian Neuroscience Society. CY - Melbourne. ER - ...
Nerve injury triggers numerous changes in the injured neurons and surrounding nonneuronal cells that ultimately result in successful target reinnervation or cell death. c-Jun is a component of the heterodimeric AP-1 transcription factor, and c-Jun is highly expressed in response to neuronal trauma. Here we have investigated the role of c-jun during axonal regeneration using mice lacking c-jun in the central nervous system. After transection of the facial nerve, the absence of c-Jun caused severe defects in several aspects of the axonal response, including perineuronal sprouting, lymphocyte recruitment, and microglial activation. c-Jun-deficient motorneurons were atrophic, resistant to axotomy-induced cell death, and showed reduced target muscle reinnervation. Expression of CD44, galanin, and alpha7beta1 integrin, molecules known to be involved in regeneration, was greatly impaired, suggesting a mechanism for c-Jun-mediated axonal growth. Taken together, our results identify c-Jun as an important ...
Sigma-Aldrich offers abstracts and full-text articles by [Adrianna Kalous, Matthew R Nangle, Agustin Anastasia, Barbara L Hempstead, Janet R Keast].
... Nous avons organisé un déjeuner pour Mme Joy Smith, et nous avons été invités dans la tribune de la
Purpose: Phosphorylation is a major type of protein post-translational modification. In this study, we evaluated the phosphoproteomic changes in the retina induced by optic nerve crush (ONC) in the mouse, an acute model of central nervous system (CNS) axonal injury. The functional role of an identified major phosphoprotein was further studied. Methods: Intraorbital ONC was performed in adult C57BL/6J mice. Retinas were collected at 0, 6, and 12 h following optic nerve injury. Retinal proteins labeled with CyDye-C2 were subjected to 2D-PAGE. 2D gel phosphoprotein staining was performed, followed by in-gel and cross-gel image analysis. The ratio change of protein differential phosphorylation following ONC was obtained. Proteins with significant changes in phosphorylation (ratios ≥ 1.5) in retinas of the injured eyes compared to the control eyes were spot-picked, tryptic digested, and peptide fragments were analyzed by MALDI-TOF (MS) and TOF/TOF (tandem MS/MS). Proteins identity was based on 10 or more
Wallerian degeneration (Fig. 2 A, left) is undoubtedly the most thoroughly investigated form of axon loss-and indeed, ongoing research is revealing the molecular pathways that result in the removal of severed axon segments. The starting point for this mechanistic deconstruction of Wallerian axon dismantling has been the serendipitous identification of a spontaneous mouse mutant with profoundly delayed Wallerian degeneration (WLDS [Wallerian degeneration slow]; Lunn et al., 1989). Molecular genetic analysis of this mutant has resulted in the surprising identification of enzymes of the NAD biosynthetic pathway as central players in axon degeneration (Coleman et al., 1998; Conforti et al., 2000), even though the details of the underlying molecular mechanisms that actually result in axon fragmentation remain to be elucidated. Importantly, the phylogenetic conservation of WLDS sensitivity has allowed identification of Wallerian-like degeneration events in "screenable" organisms, such as Drosophila ...
Hi, Im Laura, a student at Columbia Graduate School of Journalism. This fall I began work on my Masters with a concentration in magazine writing. Growing up in New Jersey afforded me the chance to see many-a-show, and this passion for the theater resulted in my transfer to Barnard College in 2006. While at school, I balanced a major in neuroscience with my duties as theater editor of Columbia Daily Spectator. As editor, I was responsible for managing all theatrical content. As a writer, I reported at the Tony Awards and broke news of the Local One stagehand strike. I also interviewed notable entertainment personalities, including Duncan Sheik, Lauren Graham, Bob Saget, Cynthia Nixon and Mike Birbiglia. This summer I have had the privilege of honing my critical skills at the National Critics Institute, hosted at the Eugene ONeill Theater Center. As I attend J-School, I continue to explore my interest in sleep disorders at Weill Cornell Medical College. I recognize that my background in ...
Despite surgical innovation, the sensory and motor outcome after peripheral nerve injury is incomplete. In this thesis, the biological pathways potentially responsible for the poor functional recoveries were investigated in both the distal nerve stump/target organ, spinal motoneurons and dorsal root ganglia (DRG). The effect of delayed nerve repair was determined in a rat sciatic nerve transection model. There was a dramatic decline in the number of regenerating motoneurons and myelinated axons found in the distal nerve stumps of animals undergoing nerve repair after a delay of 3 and 6 months. RT-PCR of the distal nerve stumps showed a decline in expression of Schwann cells (SC) markers, with a progressive increase in fibrotic and proteoglycan scar markers, with increased delayed repair time. Furthermore, the yield of SC which could be isolated from the distal nerve segments progressively fell with increased delay in repair time. Consistent with the impaired distal nerve stumps the target medial ...
A reduction in mechanical hyperalgesia, which is connected to the treatment with both paclitaxel and vincristine in TRPV4 knockout M Nozzles associated observed, suggesting that TRPV4 a therapeutic target for the treatment of chemotherapy-induced neuropathy may represent toxic. Further work is required to suppress the site of action for CB2 agonists identify paclitaxelevoked neuropathy. Upregulation of CB2 receptors in the dorsal horn of the spinal cord has been following nerve injury or severed cord ligation of the sciatic nerve in rats reported. In addition, the expression in DRG culture CB2 is up-regulated by prior axotomy. CB2 receptors have been localized recently in the central nervous system, and in particular of microglia, which are associated with macrophages. Thus, it is noteworthy that paclitaxel the number of macrophages into the spinal cord and both the DRG obtained Ht. Further work is needed to determine whether there are CB2 receptors in the CNS or DRG of paclitaxel-treatment ...
120 hours revision of 500 Video Lectures Crash Course on Anatomy, Physiology, Biochemistry based on University Previous Exam Question Papers..
Using KENACOMB ONT during pregnancy may raise the risk of children developing some disorder (commpon for some such kind of drugs), however it depends upon how KENACOMB ONT ingredients pass through placenta and may have effect on baby - Strength of KENACOMB ONT is major factor in determination of such side effects, The possible danger in pregnancy are under research. FERRER FARMA S.A. Canada publish leaflet about KENACOMB ONT every update to describe possible risks of using KENACOMB ONT side effect in pregnancy and pregnant women. You may download FERRER FARMA S.A. issued leaflet regarding side effects of KENACOMB ONT - NYSTATIN. Pregnancy Side Effects can be easily know by Atc code of KENACOMB ONT ATC CODE.. ...
Using CORTIZONE-5 ONT 0.5% during pregnancy may raise the risk of children developing some disorder (commpon for some such kind of drugs), however it depends upon how CORTIZONE-5 ONT 0.5% ingredients pass through placenta and may have effect on baby - Strength of CORTIZONE-5 ONT 0.5% is major factor in determination of such side effects, The possible danger in pregnancy are under research. DOCTOR ESTEVE S.A. Canada publish leaflet about CORTIZONE-5 ONT 0.5% every update to describe possible risks of using CORTIZONE-5 ONT 0.5% side effect in pregnancy and pregnant women. You may download DOCTOR ESTEVE S.A. issued leaflet regarding side effects of CORTIZONE-5 ONT 0.5% - HYDROCORTISONE. Pregnancy Side Effects can be easily know by Atc code of CORTIZONE-5 ONT 0.5% ATC CODE.. ...
pass the suture then transversely across the epineurium 3 mm from the edge of the nerve stump and then back through the tube in an inside to outside direction ...
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". ...
... deposition/tangle formation induces microglial activation and synaptic pruning/axotomy beginning with astrocytic release of ...
"In vivo single branch axotomy induces GAP-43-dependent sprouting and synaptic remodeling in cerebellar cortex". Proceedings of ...
"Regulation of ciliary neurotrophic factor receptor alpha in sciatic motor neurons following axotomy". Neuroscience. 91 (4): ...
... and was able to prevent apoptosis of motor neurons induced by axotomy. The encoded protein is processed to a mature secreted ... "Developing motor neurons rescued from programmed and axotomy-induced cell death by GDNF". Nature. 373 (6512): 344-6. doi: ...
1999). "Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy". Nature Medicine. ...
doi:10.1016/s0092-8674(00)81733-x. Bonfanti, L (1996). "Protection of retinal ganglion cells from natural and axotomy-induced ...
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 ...
2007). Cyclosporin-A treatment attenuates delayed cytoskeletal alterations and secondary axotomy following mild axonal stretch ...
It has also been detected in motor neurons of embryonic rats and is suggested to aid development and to reduce axotomy.[5] ...
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 ...
Weishaupt JH, Klöcker N, Bähr M (2005). "Axotomy-induced early down-regulation of POU-IV class transcription factors Brn-3a and ...
1995). "A novel RING-H2 motif protein downregulated by axotomy: its characteristic localization at the postsynaptic density of ...
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 ...
Craniotomy Pallidotomy Thalamotomy Lobotomy Bilateral cingulotomy Cordotomy Rhizotomy Laminotomy Foraminotomy Axotomy Vagotomy ...
Using the experimental model provided by the facial motor nucleus following axotomy Kreutzberg and his fellow workers ...
Schwann cells in particular show a significant upregulation of a number of trophic factors after undergoing axotomy. One major ...
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 ... Surgical axotomy[edit]. This section possibly contains original research. Please improve it by verifying the claims made and ... The Axotomy Response[edit]. Peripheral (extrinsic)[edit]. This drawing compares a normal neuron to one undergoing chromatolysis ...
The new cone growth occurs in the beginning of regeneration of axon, which may be the result of an axotomy, and she is credited ...
Exogenous administration of NAD+ prior to axotomy also delayed axonal degeneration, but to a lesser extent in NMNAT1 expressed ...
... appears to have neuroprotective activity as its biosynthesis is increased 2-10 fold upon axotomy in the peripheral ...
For example, in the rat, retinal ganglion cell soma sizes will increase following axotomy before returning to near normal cell ...
The semi-eyeblink returned significantly earlier (3.71 + 0.97 vs 9.57 + 1.86 days post axotomy) in stimulated rats (P = 0.008 ... The semi-eyeblink returned significantly earlier (3.71 + 0.97 vs 9.57 + 1.86 days post axotomy) in stimulated rats (P = 0.008 ... The semi-eyeblink returned significantly earlier (3.71 + 0.97 vs 9.57 + 1.86 days post axotomy) in stimulated rats (P = 0.008 ... The semi-eyeblink returned significantly earlier (3.71 + 0.97 vs 9.57 + 1.86 days post axotomy) in stimulated rats (P = 0.008 ...
The slow Wallerian degeneration gene in vivo protects motor axons but not their cell bodies after avulsion and neonatal axotomy ... Persistence of neuromuscular junctions after axotomy in mice with slow Wallerian degeneration (C57Bl/Wlds). Eur J Neurosci. ... Stimulation of nicotinamide adenine dinucleotide biosynthetic pathways delays axonal degeneration after axotomy. J Neurosci. ...
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 ... Surgical axotomy[edit]. This section possibly contains original research. Please improve it by verifying the claims made and ... The Axotomy Response[edit]. Peripheral (extrinsic)[edit]. This drawing compares a normal neuron to one undergoing chromatolysis ...
... axotomy). Here we use femtosecond laser surgery for axotomy in the roundworm Caenorhabditis elegans and show that these axons ... Neurosurgery: functional regeneration after laser axotomy.. Yanik MF1, Cinar H, Cinar HN, Chisholm AD, Jin Y, Ben-Yakar A. ...
The results demonstrate that central chemo-axotomy of the TRPV1+ afferents underlies RTX analgesia and refine the neurobiology ... Pain control through selective chemo-axotomy of centrally projecting TRPV1+ sensory neurons. ... Pain control through selective chemo-axotomy of centrally projecting TRPV1+ sensory neurons. ...
Psychology definition for Axotomy in normal everyday language, edited by psychologists, professors and leading students. Help ... Axotomy. Axotomy is a neurological procedure by which an axon is being trimmed or incised. This type of surgery is being done ...
Role of GAP-43 in mediating the responsiveness of cerebellar and precerebellar neurons to axotomy.. Wehrlé R1, Caroni P, Sotelo ... Adult Purkinje cells, which in control adult rats do not express GAP-43, are extremely resistant to the effects of axotomy but ... do not sprout but retract their axons and die after axotomy. Furthermore, mature Purkinje cells in cerebellar explants of ... transgenic mice that overexpress GAP-43 do not regenerate after axotomy, even in the presence of a permissive substrate ( ...
The greater vulnerability of the VP MCNs versus the OT MCNs to the axotomy-induced cell death in our experiments (Table 1) is ... The effects of TTX and KCl on MCN survival after axotomy. We used the organotypic culture model system to further examine the ... It is well known that axotomy leads to neuronal degeneration in the CNS (Ramon y Cajal, 1928), and the vasopressin (VP) and ... Axotomy typically leads to retrograde neuronal degeneration in the CNS. Studies in the hypothalamo-neurohypophysial system (HNS ...
Long-Term Effects of Axotomy on β. -Tubulin and NF Gene Expression in Rat DRG Neurons. Yuan Qing Jiang, Judith Pickett, and ... in situ hybridization studies indicated that both crush and cut/ligation axotomy resulted in significantly lower NF-. L. mRNA ... DRG neurons at 12 weeks post-axotomy. Discrepancies in the conclusions from Northern blotting and in situ hybridization ... mRNA levels had largely returned to control levels at 12 weeks following crush axotomy but were still substantially depressed ...
Axotomy-Induced Ganglioside Processing: A Mediator of Axon Regeneration Restricted to the PNS. Andrew Kaplan and Ricardo L. ... Because axon regeneration was assessed only 1 h after axotomy, however, it is possible that axons may still be regeneration- ... Interestingly, GM1 enrichment was not observed after axotomy (Kappagantula et al., 2014, their Fig. 5B), despite the presence ... 2014) determined that in the absence of calcium, axotomy failed to induce p38MAPK activity and that forced activation of ...
De Felipe, C. and Belmonte, C. (1999), c-Jun expression after axotomy of corneal trigeminal ganglion neurons is dependent on ... c-Jun expression after axotomy of corneal trigeminal ganglion neurons is dependent on the site of injury. ...
We present a surgical protocol detailing how to perform a cut or crush axotomy on the facial nerve in the mouse. The facial ... There are many advantages to studying nerve injury using the facial nerve axotomy model. First, the facial nerve axotomy ... Facial Nerve Axotomy in Mice: A Model to Study Motoneuron Response to Injury. Deborah N. Olmstead1,2, Nichole A. Mesnard- ... The facial nerve axotomy can also be used to study the accompanying central and peripheral glial cells22, target musculature21 ...
After axotomy a subpopulation of RGCs was labeled with the GAP-43 antibody and mRNA levels of GAP-43 increased significantly. ... Ultrastructural analysis of the optic nerves was also performed at different times after axotomy with and without treatment. ... FGF-2 Enhances Adult Retinal Ganglion Cell Regeneration After Axotomy You will receive an email whenever this article is ... I Soto, C del Cueto, RE Blanco; FGF-2 Enhances Adult Retinal Ganglion Cell Regeneration After Axotomy . Invest. Ophthalmol. Vis ...
Laser axotomy followed by time-lapse imaging is a sensitive way to assay the effects of mutations in C. elegans on axon... ... B shows laser axotomy of one axon without damaging a nearby axon about 1 um away. Laser was set to about 10% power (0.3 mW ... Laser axotomy followed by time-lapse imaging is a sensitive way to assay the effects of mutations in C. elegans on axon ... Laser axotomy followed by time-lapse microscopy is a sensitive assay for axon regeneration phenotypes in C. elegans1. The main ...
It is not clear whether neuronal death begins within I week of axotomy or continues beyond 2 months after axotomy. Similarly, ... A similar conclusion can be drawn from the result found using both rhGGF-2 and SCs in PHB conduits 4 months after axotomy. ... Primary sensory neurons and satellite cells after peripheral axotomy in the adult rat: timecourse of cell death & elimination. ... Neuronal death begins within I day of peripheral axotomy, the majority occurs within the first 2 months, and limited death is ...
Effect of Erythropoietin Axotomy-Induced Apoptosis in Rat Retinal Ganglion Cells. Long-Term Effect of Optic Nerve Axotomy on ... Cells with a positive reaction for DNA fragmentation were observed in eyes subjected to axotomy and experimental glaucoma but ... PURPOSE: To investigate whether retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis. ... CONCLUSION: Some retinal ganglion cells injured by glaucoma and by axotomy die by apoptosis. ...
6A,E). SNL reduced SLI area in peripheral nerves proximal to axotomy, ganglia, and dorsal roots (Fig. 7D, F; Table 1).. Open ... After painful axotomy KATP channels are downregulated in large, myelinated somata and also in SLI, which are also of smaller ... Sampling sites were the dorsal root proximal to DRG, the DRG, and the peripheral nerve distal to DRG but proximal to axotomy ... We were able to identify the distribution of functional KATP channels and their alterations by axotomy by staining for SUR1 ...
The mechanisms of primary sensory neuron degeneration were also investigated in the DRG following peripheral nerve axotomy, ... and distal peripheral nerve axotomy (PNA) 7 and 14 days postoperatively, we aimed to gain more insight about the mechanism ... and distal peripheral nerve axotomy (PNA). Neuronal degeneration was indicated by decreased immunostaining for microtubule- ... Morphological and Molecular Characterization of the Spinal Cord after Ventral Root Avulsion or Distal Peripheral Nerve Axotomy ...
... MULDOON, J.L. ; WALKER, C.L. ; BEST, A.R. ... Keywords: Facial Nerve Axotomy Recovery ; peripheral nerves ; methylene blue (MB) ; polyethylene glycol (PEG) ... 2016, April 8. Effects of Methylene Blue and Polyethelene Glycol on Facial Nerve Axotomy Recovery. Poster session presented at ... Effects of Methylene Blue and Polyethelene Glycol on Facial Nerve Axotomy Recovery. Login ...
The effect of axotomy was quantified by optic nerve axon density measurements and RGC counts. The parametric t-test and the ... Unilateral, peripapillary RGC axotomy was performed in six domestic pigs using an argon laser. In eight additional pigs the ... The effect of ganglion cell axotomy on other cells in the porcine retina [electronic resource] /. by Koma?romy, Andra?s M. ... ABSTRACT: The purpose of this study was to determine the effect of retinal ganglion cell (RGC) axotomy and death on the ...
Axotomy of the optic nerve is a classical model of neurodegeneration. It induces retinal ganglion cell death, a process also ... Autophagy promotes survival of retinal ganglion cells after optic nerve axotomy in mice. Natalia Rodríguez-Muela, Francisco ... Autophagy promotes survival of retinal ganglion cells after optic nerve axotomy in mice ... Our results demonstrate activation of autophagy shortly after axotomy with autophagosome formation, upregulation of the ...
Amino acid levels in the guinea pig spinal gray matter after axotomy of primary sensory and descending tracts.. @article{ ... Potashner1986AminoAL, title={Amino acid levels in the guinea pig spinal gray matter after axotomy of primary sensory and ...
Involvement of MAPK, Akt/GSK-3β and AMPK/mTOR signaling pathways in protection of remote glial cells from axotomy-induced ... We showed that axotomy not only mechanically injures glial cells at the cutting location, but also induces necrosis or ... Inhibition of MEK1/2, p38, Akt, GSK-3β and mTOR increased axotomy-induced apoptosis of remote glial cells, whereas inhibition ... Severe mechanical nerve injury such as axotomy can lead to neuron degeneration and death of surrounding glial cells. ...
... of the NADPH-d-positive IML neurons were found to send their axons to the pelvic nerve 1 week after axotomy, whereas nearly 25 ... of the FG-labeled neurons were found to be negative for NADPH-d. Thus, these results indicate that pelvic axotomy in the rat ... and the staining intensity of NADPH-d-positive neurons in the IML region increased remarkably 1 week after pelvic axotomy; the ... region may include different neurons showing different responses in nitric oxide synthase expression after peripheral axotomy. ...
  • Results: An electrical stimulation model of the rat facial nerve following axotomy was established. (elsevier.com)
  • Results of Northern blotting of total RNA obtained from the DRG indicated that NF- L and NF- Μ mRNA levels had largely returned to control levels at 12 weeks following crush axotomy but were still substantially depressed following cut/ligation injury of the sciatic nerve at that time. (hindawi.com)
  • Treatment methods involving methylene blue (MB) and polyethylene glycol (PEG) have shown combinational effects in sciatic nerve axotomies. (iupui.edu)
  • In this study, the authors could propose more reliable peripheral nerve axotomy model than the conventional sciatic nerve axotomy model by specifically transecting L5 spinal nerve and confining the investigating area within the L5 spinal segment. (bvsalud.org)
  • Taken together, these findings suggest that death of nigral dopaminergic neurons following axotomy can be attenuated by targeting cell signaling events upstream of c-Jun N-terminal mitogen-activated protein kinase/c-Jun. (carleton.ca)
  • Adult Purkinje cells, which in control adult rats do not express GAP-43, are extremely resistant to the effects of axotomy but cannot regenerate axons. (nih.gov)
  • A combination of approaches performed using the region that directly encompasses an adenylate and uridylate (AU)-rich element within the AChE 3'-untranslated region demonstrated a decrease in RNA-protein complexes in response to axotomy of the SCG and, specifically, a decrease in HuD binding. (unm.edu)
  • The marked upregulation of ApoJ in both instances suggests a general role of this protein in the neuronal response to axotomy. (diva-portal.org)
  • Furthermore, mature Purkinje cells in cerebellar explants of transgenic mice that overexpress GAP-43 do not regenerate after axotomy, even in the presence of a permissive substrate (cerebellar embryonic tissue) and, contrary to the case in wild-type mice, they do not survive in the in vitro conditions and undergo massive cell death. (nih.gov)
  • In mature animals, where survival factors are derived locally or via autocrine loops, axotomy of peripheral neurons and motoneurons can lead to a robust regenerative response without any neuronal death. (wikipedia.org)
  • Taken collectively these data demonstrate that thoracic propriospinal (TPS) neurons mount a very dynamic response following low thoracic axotomy that includes a strong regenerative response, but also results in the cell death of many axotomized TPS neurons in the first week after spinal cord injury. (beds.ac.uk)
  • Other changes are regenerative in nature and because most of these occur in the superficial dorsal horn, which is where fine primary afferents end, we wished to ask whether peripheral axotomy results in a change in the distribution in these fine afferents. (utmb.edu)
  • Axotomy typically leads to retrograde neuronal degeneration in the CNS. (jneurosci.org)
  • It is well known that axotomy leads to neuronal degeneration in the CNS ( Ramon y Cajal, 1928 ), and the vasopressin (VP) and oxytocin (OT) magnocellular neurons (MCNs) of the hypothalamo-neurohypophysal system (HNS) have served as classical in vivo models for the study of this phenomenon. (jneurosci.org)
  • Pharmacological inhibition of MLKs, MKK4-activating kinases, significantly reduced the phosphorylation of c-Jun and abrogated dopaminergic neuronal degeneration following MFB axotomy. (carleton.ca)
  • ABSTRACT: The purpose of this study was to determine the effect of retinal ganglion cell (RGC) axotomy and death on the thickness of the inner plexiform (IPL), inner nuclear (INL), and outer plexiform layers (OPL), as well as the densities of short- (S) and middle-to-long-wavelength (M/L) cones in the porcine retina. (openthesis.org)
  • abstract = "Peripheral axotomy of the cranial nerves has been reported to induce expression of nitric oxide synthase (NOS) in the relative motor neurons. (elsevier.com)
  • Axotomy may cause neuronal cell death, especially in embryonic or neonatal animals, as this is the period in which neurons are dependent on their targets for the supply of survival factors. (wikipedia.org)
  • Experimentally, a well-accepted model to mimic axotomy injury retrograde repercussion to spinal neurons is the neonatal peripheral nerve axotomy [ 13 - 18 ]. (hindawi.com)
  • Previous results and additional data from this study indicated that NF- and BS-I-positive ganglion cells are proportionally more likely to be lost after neonatal axotomy and that SP-positive cells are more likely to remain. (elsevier.com)
  • Facial nerve axotomy was unilaterally performed in Cx3cr1-Mfp2 −/− and control mice, and microglial functioning in response to neuronal injury was subsequently analyzed by histology and real-time PCR. (springer.com)
  • Studies in the hypothalamo-neurohypophysial system (HNS) have suggested that neural activity is supportive of magnocellular neuronal (MCN) survival after axotomy. (jneurosci.org)
  • In addition, we found that potassium depolarization rescues OT and VP MCNs from axotomy-induced neurodegeneration in vitro and also reverses the deleterious effect of TTX on the survival of both OT and VP MCNs in the SON. (jneurosci.org)
  • We present a surgical protocol detailing how to perform a cut or crush axotomy on the facial nerve in the mouse. (jove.com)
  • Effect of crush and axotomy of phrenic n. (bezmialem.edu.tr)
  • Introduction: In this study we investigated the effect of crush and axotomy of phrenic nerves on oxidative stress and antioxidant enzyme activities in rat diaphragm muscle. (bezmialem.edu.tr)
  • Results: The malondialdehyde level increased in diaphragm muscles after both crush and axotomy. (bezmialem.edu.tr)
  • The antioxidant enzymes, such as superoxide dismutase, glutathione peroxidase, carbonic anhydrase, and catalase, decreased in diaphragm muscles after both crush and axotomy. (bezmialem.edu.tr)
  • The facial nerve axotomy can be employed to study the physiological response to nerve injury and test therapeutic techniques. (jove.com)
  • Concerning Wt animals, we found a reduction in synaptophysin immunoreactivity and an increase of MHC class I molecules in facial motoneurons after axotomy. (ejh.it)
  • Although many times axotomy occurs due to intended surgical treatment, it is also often directly related to one of many pathologies/injuries. (wikipedia.org)
  • Primary axotomy occurs immediately and is characterized as complete mechanical transaction of axons. (wikipedia.org)
  • More often, secondary axotomy occurs, evolving over time and ultimately leading to disconnection. (wikipedia.org)
  • Independently of the axotomy model, RGC death occurs in two phases, one quick and one protracted, and there is a lineal and topographical correlation between the appearance of PMCs and the loss of traced RGCs. (biomedcentral.com)
  • Axotomy-induced RGC death occurs earlier than RGC clearance and there is an inverse correlation between RGC loss and PMC appearance, both numerically and topographically, suggesting that phagocytosis occurs as a direct response to RGC death rather than to axonal damage. (biomedcentral.com)
  • By comparing morphological and molecular changes in spinal motoneurons after L4-L5 ventral root avulsion (VRA) and distal peripheral nerve axotomy (PNA) 7 and 14 days postoperatively, we aimed to gain more insight about the mechanism behind injury-induced motoneuron degeneration. (diva-portal.org)
  • These findings suggest that axotomy increases the type II PKC of the severed neurons, and type II PKC seems to phosphorylate some protein, such as GAP-43, and plays some role in the retrograde neuronal reaction. (mysciencework.com)
  • When developing experimental strategies, other factors have to be considered, such as axotomy-induced cell death and secondary degeneration (Schwartz, 2004a), scar formation (Rhodes and Fawcett, 2004), and factors intrinsic to neurons themselves. (utah.edu)
  • Unilateral, peripapillary RGC axotomy was performed in six domestic pigs using an argon laser. (openthesis.org)
  • Agrin gene expression in ciliary ganglion neurons following preganglionic denervation and postganglionic axotomy. (escholarship.org)
  • Major changes in agrin gene expression following axotomy but not denervation are consistant with the notion that agrin synthesized by ganglionic neurons exerts its effects in the periphery rather than at synapses formed between ciliary ganglion neurons and their preganglionic input. (escholarship.org)
  • Specific expression of type II protein kinase c after axotomy. (mysciencework.com)
  • Specific expression of type II protein kinase c after axotomy in the dorsal motor nucleus of the vagus nerve and the hypoglossal nucleus. (mysciencework.com)
  • Protein kinase C (PKC) and growth-associated protein-43 (GAP-43) were investigated immunohistochemically in the dorsal motor nucleus of the vagus nerve and the hypoglossal nucleus after axotomy using monoclonal antibodies against type I, II and III PKC and GAP-43. (mysciencework.com)
  • After axotomy, HuD transcript and protein levels also decreased. (unm.edu)
  • en] Peripherin is an intermediate filament protein that is expressed in peripheral and enteric neurons. (ac.be)
  • Discrepancies in the conclusions from Northern blotting and in situ hybridization experiments were also noted in the case of tubulin mRNA changes at long intervals after axotomy. (hindawi.com)
  • Severe mechanical nerve injury such as axotomy can lead to neuron degeneration and death of surrounding glial cells. (ovid.com)
  • We used the crayfish stretch receptor that consists of a single mechanoreceptor neuron enveloped by satellite glial cells as a simple, but informative model object in the study of the role of various signaling proteins in axotomy-induced death of remote glial cells. (ovid.com)
  • In DRG and dorsal roots proximal to axotomy SLI were smaller and showed decreased SUR1 immunofluorescence. (springer.com)
  • Axotomy of the lingual nerve was done proximal to its communication with the hypoglossal nerve. (indmedica.com)
  • The results demonstrate that central chemo-axotomy of the TRPV1+ afferents underlies RTX analgesia and refine the neurobiology underlying effective clinical use of TRPV1 agonists for pain control. (jci.org)
  • After axotomy of the adult rat SCG neurons, AChE transcript levels decreased by 50 and 85% by the first and fourth day, respectively. (unm.edu)
  • The aim of this study was to propose new more reliable peripheral nerve transection model to overcome the defect of the traditional sciatic axotomy model by specifically transecting L5 spinal nerve just after emerging from the intervertebral foramen and confining analysis area to the L5 spinal segment. (bvsalud.org)
  • Stimulation of the hypoglossal nerve, even afterlingual nerve axotomy, showed secretion from the lingual glands on the same side as stimulation. (indmedica.com)
  • Similar, but less dramatic changes in agrin expression following axotomy were also observed in unoperated neurons on the contralateral side. (escholarship.org)
  • Because loss of DRG neuronal K ATP currents is involved in the pathophysiology of pain after peripheral nerve injury, we characterized the distribution of the K ATP channel subunits in rat DRG, and determined their alterations by painful axotomy using RT-PCR, immunohistochemistry and electron microscopy. (springer.com)
  • We found both in the in vivo and in vitro studies that inhibition of neural activity in the supraoptic nucleus (SON) by tetrodotoxin (TTX) significantly increased the extent of MCN degeneration after axotomy. (jneurosci.org)
  • En el presente trabajo hemos demostrado que la autofagia juega un papel citoprotector para estas neuronas ya que su activación farmacológica rescata de la muerte, tanto in vitro como in vivo, mientras que su bloqueo genético exacerba la degeneración. (sebbm.es)
  • La mutación no impide la integración de Vps54 en el complejo GARP, sin embargo su vida media se ve drásticamente reducida in vivo. (sebbm.es)
  • In contrast to the peripheral response, the axotomy response in central neurons (neurons in the Central Nervous System ) almost always leads to cell death. (wikipedia.org)
  • Raising the extracellular KCl in the culture medium to 25 mM rescued the MCNs from the axotomy- and TTX-induced cell death. (jneurosci.org)