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Trigeminal Ganglion (trigeminal + ganglion)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Neuron,Glia Signaling in Trigeminal Ganglion: Implications for Migraine Pathology

HEADACHE, Issue 7 2007
Srikanth Thalakoti BS
Objective.,The goal of this study was to investigate neuronal,glial cell signaling in trigeminal ganglia under basal and inflammatory conditions using an in vivo model of trigeminal nerve activation. Background.,Activation of trigeminal ganglion nerves and release of calcitonin gene-related peptide (CGRP) are implicated in the pathology of migraine. Cell bodies of trigeminal neurons reside in the ganglion in close association with glial cells. Neuron,glia interactions are involved in all stages of inflammation and pain associated with several central nervous system (CNS) diseases. However, the role of neuron,glia interactions within the trigeminal ganglion under normal and inflammatory conditions is not known. Methods.,Sprague,Dawley rats were utilized to study neuron,glia signaling in the trigeminal ganglion. Initially, True Blue was used as a retrograde tracer to localize neuronal cell bodies in the ganglion by fluorescent microscopy and multiple image alignment. Dye-coupling studies were conducted under basal conditions and in response to capsaicin injection into the TMJ capsule. S100B and p38 expression in neurons and glia were determined by immunohistochemistry following chemical stimulation. CGRP levels in the ganglion were measured by radioimmunoassay in response to capsaicin. In addition, the effect of CGRP on the release of 19 different cytokines from cultured glial cells was investigated by protein microarray analysis. Results.,In unstimulated control animals, True Blue was detected primarily in neuronal cell bodies localized in clusters within the ganglion corresponding to the V3 region (TMJ capsule), V2 region (whisker pad), or V1 region (eyebrow and eye). However, True Blue was detected in both neuronal cell bodies and adjacent glia in the V3 region of the ganglion obtained from animals injected with capsaicin. Dye movement into the surrounding glia correlated with the time after capsaicin injection. Chemical stimulation of V3 trigeminal nerves was found to increase the expression of the inflammatory proteins S100B and p38 in both neurons and glia within the V3 region. Unexpectedly, increased levels of these proteins were also observed in the V2 and V1 regions of the ganglion. CGRP and the vesicle docking protein SNAP-25 were colocalized in many neuronal cell bodies and processes. Decreased CGRP levels in the ganglion were observed 2 hours following capsaicin stimulation. Using protein microarray analysis, CGRP was shown to differentially regulate cytokine secretion from cultured trigeminal ganglion glia. Conclusions.,We demonstrated that activation of trigeminal neurons leads to changes in adjacent glia that involve communication through gap junctions and paracrine signaling. This is the first evidence, to our knowledge, of neuron,glia signaling via gap junctions within the trigeminal ganglion. Based on our findings, it is likely that neuronal,glial communication via gap junctions and paracrine signaling are involved in the development of peripheral sensitization within the trigeminal ganglion and, thus, are likely to play an important role in the initiation of migraine. Furthermore, we propose that propagation of inflammatory signals within the ganglion may help to explain commonly reported symptoms of comorbid conditions associated with migraine. [source]

Regulation of FGF10 by POU transcription factor Brn3a in the developing trigeminal ganglion

DEVELOPMENTAL NEUROBIOLOGY, Issue 10 2006
Eric Cox
Abstract The POU-domain transcription factor Brn3a is expressed in specific neurons of the caudal CNS and peripheral sensory nervous system. The sensory neurons of mice lacking Brn3a exhibit marked defects in axon growth and extensive apoptosis in lategestation. Here we show that expression of thedevelopmental regulator FGF10 is approximately 35-fold increased in the developing trigeminal ganglia of Brn3a-null mice. In order to determine whether FGF10 regulates other changes in gene expression observed in Brn3a knock-out ganglia, we have used a sensory-specific enhancer to over-express FGF10 in transgenic mice. Microarray analysis of trigeminal ganglia from individual transgenic founders effectivelyexcludes the cell-autonomous activity of FGF10 as a mechanism for mediating the downstream effects of the loss of Brn3a, probably because developing sensory neurons lack the appropriate type of FGF receptor. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006 [source]

Lysosomal storage disease in Sida carpinifolia toxicosis: an induced mannosidosis in horses

EQUINE VETERINARY JOURNAL, Issue 5 2003
A. P. LORETTI
Summary Reasons for performing study: This study reports a neurological disease unrecognised until now in ponies in southern Brazil. Hypothesis: Epidemiological data strongly suggests that the ingestion of Sida carpinifolia is involved in the aetiology. We tested the hypothesis that it is an acquired lyosomal storage disease. Methods: Following the death of 3 ponies, all ponies from the premises were closely monitored; epidemiological data and clinical findings carefully recorded. Fragments of several organs, including CNS, were fixed in neutral formalin and embedded in paraffin-wax. Sections were stained with haematoxylin and eosin. Representative sections of the cerebellum and trigeminal ganglia were submitted to lectin histochemical procedures. Results: The neurological disorder, characterised by stiff gait, muscle tremors, abdominal pain and death, was observed on a farm with 3 hectares of pasture. Three of 11 ponies died 15,20 days after they had been introduced into a new paddock heavily infested by the plant Sida carpinifolia. No significant gross lesions were observed. The main histological findings included multiple cytoplasmatic vacuoles in swollen neurones in the brain, cerebellum, spinal cord, autonomic ganglia (trigeminal and celiac ganglia), and submucosal and myenteric plexus of the intestines. In the kidneys, there was marked vacuolation of the proximal convoluted tubular cells. Sections of cerebellum and trigeminal ganglion were submitted to lectin histochemistry. The vacuoles in different cerebellar and ganglion cells reacted strongly to the following lectins: Concanavalia ensiformis, Triticum vulgaris and succinylated- Triticum vulgaris. Conclusions: The pattern of staining coincides with that of both swainsonine toxicosis and inherited mannosidosis reports. The histopathological changes were similar to those described in S. carpinifolia spontaneous and experimental poisoning in goats. This disease seems to be similar to Swainsona, Oxytropis and Astragalus toxicosis. Potential relevance: S. carpinifolia should be evaluated as a possible cause in the diagnosis of equine neuropathies. [source]

Neuron,Glia Signaling in Trigeminal Ganglion: Implications for Migraine Pathology

Herpetic Cytopathic Features Confined to Folliculosebaceous Units: What does it Mean?

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005
N Walsh
The histopathological changes of herpes simplex, zoster and varicella are considered to be indistinguishable from one another. The clinical setting with adjunctive studies generally clarifies the diagnosis. Vesicular lesions in all 3 conditions can involve epidermal and adnexal epithelium with characteristic cytopathic features. We describe 3 patients with non-vesicular eruptions on the head and neck whose biopsies revealed exclusive folliculosebaceous involvement by herpes. All three patients developed typical herpes zoster within days of the biopsy. There is compelling scientific evidence in the literature indicating that, in herpes zoster, the virus is transported from dorsal root or trigeminal ganglia via myelinated nerves to the skin. These terminate at the isthmus of hair follicles and primary infection of follicular and sebaceous epithelium occurs. Secondary spread of infection to the epidermis follows. In contrast, data pertaining to recurrent herpes simplex indicates that axonal transport of the virus from sensory ganglia to the skin is directed primarily to the epidermis, via terminal non-myelinated nerve twigs. The clinical evolution of our 3 cases and scientific data in the literature indicate that exclusive folliculosebaceous involvement by herpes, in the setting of a non-vesicular eruption, represents early herpes zoster. [source]

Prevalence of HSV-1 LAT in Human Trigeminal, Geniculate, and Vestibular Ganglia and Its Implication for Cranial Nerve Syndromes

BRAIN PATHOLOGY, Issue 4 2001
Diethilde Theil
Herpes simplex virus type 1 (HSV-1) enters sensory neurons and can remain latent there until reactivation. During latency restricted HSV-1 gene expression takes place in the form of latency-associated transcripts (LAT). LAT has been demonstrated to be important not only for latency but also for reactivation, which may cause cranial nerve disorders. Tissue sections of the trigeminal ganglia (TG), geniculate ganglia (GG), and the vestibular ganglia (VG) from seven subjects were examined for the presence of LAT using the in situ hybridization technique. LAT was found on both sides in all TG (100%), on both sides of five subjects (70%) in the GG, and in none of the VG. Using a second more sensitive detection method (RT-PCR), we found LAT in the VG of seven of ten other persons (70%). This is the first study to demonstrate viral latency in the VG, a finding that supports the hypothesis that vestibular neuritis is caused by HSV-1 reactivation. The distribution of LAT in the cranial nerve ganglia indicates that primary infection occurs in the TG and GG and subsequently spreads along the faciovestibular anastomosis to the VG. [source]

CGRP blockers in migraine therapy: where do they act?

BRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2008
L Edvinsson
Calcitonin gene-related peptide (CGRP) is expressed throughout the CNS and peripheral nervous system, consistent with control of vasodilatation, nociception, motor function, secretion and olfaction. ,CGRP is prominently localized in primary afferent C and A, fibres of spinal and trigeminal ganglia. Activation of the trigeminal nerve results in antidromic release of CGRP, acting through a CGRP1 receptor. Antagonists of CGRP1 receptors reduce signalling in the trigeminovascular pathway at multiple sites, putatively inside the blood,brain barrier. Other ways of interacting with CGRP mechanisms have appeared limiting the availability of CGRP in the circulation with a specific CGRP antibody or with a CGRP-binding RNA-Spiegelmer. Either way reduces neurogenic inflammation and attenuates signalling within the trigeminovascular pathway. Specific CGRP receptor blockade has been shown to reduce the effect of released CGRP and to abort acute migraine attacks. The novel approach of reducing available CGRP is limited by the blood,brain barrier; its usefulness may be more as prophylaxis rather than as acute treatment of migraine. British Journal of Pharmacology (2008) 155, 967,969; doi:fn1; published online 8 September 2008 [source]

Neuropeptide Y modulates effects of bradykinin and prostaglandin E2 on trigeminal nociceptors via activation of the Y1 and Y2 receptors

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2007
J L Gibbs
Background and Purpose: Although previous studies have demonstrated that neuropeptide Y (NPY) modulates nociceptors, the relative contributions of the Y1 and Y2 receptors are unknown. Therefore, we evaluated the effect of Y1 and Y2 receptor activation on nociceptors stimulated by bradykinin (BK) and prostaglandin E2 (PGE2). Experimental approach: Combined immunohistochemistry (IHC) with in situ hybridization (ISH) demonstrated that Y1 - and Y2 -receptors are collocated with bradykinin 2 (B2)-receptors in rat trigeminal ganglia (TG). The relative functions of the Y1 and Y2 receptors in modulating BK/PGE2 -evoked CGRP release and increased intracellular calcium levels in cultured TG neurons were evaluated. Key results: The Y1 and Y2 receptors are co-expressed with B2 in TG neurons, suggesting the potential for direct NPY modulation of BK responses. Pretreatment with the Y1 agonist [Leu31,Pro34]-NPY, inhibited BK/PGE2 -evoked CGRP release. Conversely, pretreatment with PYY(3-36), a Y2 agonist, increased BK/PGE2 evoked CGRP release. Treatment with NPY evoked an overall inhibitory effect, although of lesser magnitude. Similarly, [Leu31,Pro34]-NPY inhibited BK/PGE2 -evoked increases in intracellular calcium levels whereas PYY(3-36) increased responses. NPY inhibition of BK/PGE2 -evoked release of CGRP was reversed by the Y1 receptor antagonist, BIBO3304, and higher concentrations of BIBO3304 significantly facilitated CGRP release. The Y2 receptor antagonist, BIIE0246, enhanced the inhibitory NPY effects. Conclusions and implications: These results demonstrate that NPY modulation of peptidergic neurons is due to net activation of inhibitory Y1 and excitatory Y2 receptor systems. The relative expression or activity of these opposing receptor systems may mediate dynamic responses to injury and pain. British Journal of Pharmacology (2007) 150, 72,79. doi:10.1038/sj.bjp.0706967 [source]

1212: Herpes simplex and zoster keratitis

ACTA OPHTHALMOLOGICA, Issue 2010
M LABETOULLE
Herpes simplex virus (HSV) and varicella-zoster virus (VZV) are two leading causes of corneal infection with potential severely impaired visual acuity. These two viruses share multiple characteristics, including the ability to become latent in the trigeminal ganglia, before reactivation and migration along the trigeminal fibers innervating the cornea. The clinical settings of keratitis may vary from an epithelial defect (dendritic of geographic) to a more severe disease involving the stroma and/or the endothelium. Classically, HSV keratitis occurs from the second decade of life, and associated skin disease is not frequent and only involves the eyelids. In contrast, VZV keratitis mostly occurs after the sixth decade, as an associated finding of herpes zoster ophthalmicus (HZO). However, several studies recently highlighted that the rate of HSV keratitis increases with age, even in elderly, and some other studies reported VZV keratitis in children, either isolated or associated with HZO. Antiviral drugs currently available are highly efficient to reduce the severity on ongoing HSV- or VZV keratitis, but preventive treatments still have to be optimized. For HSV keratitis, the usual preventive treatment, as defined by the HEDS study, only reduces the rate of relapses in a two-fold manner, and the optimal dosage has not been settled for patient with severe herpetic disease. For VZV, the two vaccines against chickenpox and HZO probably will lead in the future to a reduction of the incidence of keratitis, but they are not widely used, even in most of developed countries. [source]

Trigeminal Trophic Syndrome,Report of Four Cases and Review of the Literature

DERMATOLOGIC SURGERY, Issue 5 2004
Parrish Sadeghi MD
Background. Trigeminal trophic syndrome is a unilateral, frequently crescent-shaped neurotrophic ulceration of the face occurring after injury to the trigeminal nerve. The appearance of the ulcers resembles other disease entities such as granulomatous disease, neoplasm, vasculitis, infection, and factitial dermatitis. Objectives. The objectives of this study are to increase awareness of this disorder and to emphasize the importance of eliciting a thorough neurologic history when evaluating facial ulcerations. Methods. Four cases are reported and, using MEDLINE, the English and non-English literature from 1982 to 2002 is reviewed. Results. Including this report, there have been 60 cases of trigeminal trophic syndrome reported from 1982 to 2002. The age at presentation ranged from 14 months to 93 years. Time of onset from injury to the trigeminal ganglion or its branches and the development of the ulcers ranged from 2 weeks to 30 years. One-third of the patients had undergone trigeminal nerve ablation for the treatment of trigeminal neuralgia and another third had a history of stroke. Other causes included craniotomy, head trauma, herpes infection. Conclusion. The majority of cases of trigeminal trophic syndrome are associated with a history of stroke or trigeminal nerve ablation. Successful surgical outcome can be achieved if the underlying neurologic pathology is addressed before the reconstructive procedure. [source]

Regulation of the Neurofibromatosis 2 gene promoter expression during embryonic development

DEVELOPMENTAL DYNAMICS, Issue 10 2006
Elena M. Akhmametyeva
Abstract Mutations in the Neurofibromatosis 2 (NF2) gene are associated with predisposition to vestibular schwannomas, spinal schwannomas, meningiomas, and ependymomas. Presently, how NF2 is expressed during embryonic development and in the tissues affected by neurofibromatosis type 2 (NF2) has not been well defined. To examine NF2 expression in vivo, we generated transgenic mice carrying a 2.4-kb NF2 promoter driving ,-galactosidase (,-gal) with a nuclear localization signal. Whole-mount embryo staining revealed that the NF2 promoter directed ,-gal expression as early as embryonic day E5.5. Strong expression was detected at E6.5 in the embryonic ectoderm containing many mitotic cells. ,-gal staining was also found in parts of embryonic endoderm and mesoderm. The ,-gal staining pattern in the embryonic tissues was corroborated by in situ hybridization analysis of endogenous Nf2 RNA expression. Importantly, we observed strong NF2 promoter activity in the developing brain and in sites containing migrating cells including the neural tube closure, branchial arches, dorsal aorta, and paraaortic splanchnopleura. Furthermore, we noted a transient change of NF2 promoter activity during neural crest cell migration. While little ,-gal activity was detected in premigratory neural crest cells at the dorsal ridge region of the neural fold, significant activity was seen in the neural crest cells already migrating away from the dorsal neural tube. In addition, we detected considerable NF2 promoter activity in various NF2-affected tissues such as acoustic ganglion, trigeminal ganglion, spinal ganglia, optic chiasma, the ependymal cell-containing tela choroidea, and the pigmented epithelium of the retina. The NF2 promoter expression pattern during embryogenesis suggests a specific regulation of the NF2 gene during neural crest cell migration and further supports the role of merlin in cell adhesion, motility, and proliferation during development. Developmental Dynamics 235:2771,2785, 2006. © 2006 Wiley-Liss, Inc. [source]

Regulation of FGF10 by POU transcription factor Brn3a in the developing trigeminal ganglion

Dose and age-dependent axonal responses of embryonic trigeminal neurons to localized NGF via p75NTR receptor

DEVELOPMENTAL NEUROBIOLOGY, Issue 2 2005
P. Hande Özdinler
Abstract Nerve growth factor (NGF) and related neurotrophins are target-derived survival factors for sensory neurons. In addition, these peptides modulate neuronal differentiation, axon guidance, and synaptic plasticity. We tested axonal behavior of embryonic trigeminal neurons towards localized sources of NGF in collagen gel assays. Trigeminal axons preferentially grow towards lower doses of localized NGF and grow away from higher concentrations at earlier stages of development, but do not show this response later. Dorsal root ganglion axons also show similar responses to NGF, but NGF-dependent superior cervical ganglion axons do not. Such axonal responses to localized NGF sources were also observed in Bax,/, mice, suggesting that the axonal effects are largely independent of cell survival. Immunocytochemical studies indicated that axons, which grow towards or away from localized NGF are TrkA-positive, and TrkA,/, TG axons do not respond to any dose of NGF. We further show that axonal responses to NGF are absent in TG derived from mice that lack the p75 neurotrophin receptor (p75NTR). Collectively, our results suggest that localized sources of NGF can direct axon outgrowth from trigeminal ganglion in a dose- and age-dependent fashion, mediated by p75NTR signaling through TrkA expressing axons. © 2004 Wiley Periodicals, Inc. J Neurobiol, 2005 [source]

The anatomy of the palatoquadrate in the Lower Triassic Proterosuchus fergusi (Reptilia, Archosauromorpha) and its morphological transformation within the archosauriform clade

ACTA ZOOLOGICA, Issue 3 2009
Jozef Klembara
Abstract The anatomy of the palatoquadrate ossifications of the Lower Triassic archosauromorph Proterosuchus fergusi from South Africa is described. It consists of two ossifications, the epipterygoid and the quadrate, which were joined by cartilage in life. The margins of the cartilage are clearly indicated by ridges and grooves on the dorsal surface of the pterygoid. The epipterygoid ossification consists of two structures: the anteroposteriorly expanded basal portion and, dorsally from it, an extending, slender, ascending process. From the anterior margin of the basal portion of the epipterygoid, a plate-like structure, herein called the lamina epipterygoidea anteromedialis, extends anteromedially to form the anterolateral wall of the cavum epiptericum. Comparisons with the similarly constructed embryonal and adult epipterygoid components of Sphenodon punctatus show that the anteromedial lamina of the epipterygoid of P. fergusi is an additional component of the epipterygoid of this species and that this lamina is absent in the former species. However, a structure in a topologically similar position to the anteromedial lamina of the epipterygoid of P. fergusi is present in the palatoquadrate of Alligator mississippiensis. In the latter species, the structure is called the lamina palatoquadrati anterior; it ossifies in membrane and forms the dorsolateral cover of the huge trigeminal ganglion. It is hypothesized here that the anteromedial lamina of the epipterygoid of P. fergusi and the anterior lamina of the palatoquadrate of A. mississippiensis are most probably homologous structures and are present in both the basal and one of the crown taxa of the archosauromorph clade, respectively. [source]

Lysosomal storage disease in Sida carpinifolia toxicosis: an induced mannosidosis in horses

Sensitization of meningeal nociceptors: inhibition by naproxen

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2008
Dan Levy
Abstract Migraine attacks associated with throbbing (manifestation of peripheral sensitization) and cutaneous allodynia (manifestation of central sensitization) are readily terminated by intravenous administration of a non-selective cyclooxygenase (COX) inhibitor. Evidence that sensitization of rat central trigeminovascular neurons was also terminated in vivo by non-selective COX inhibition has led us to propose that COX inhibitors may act centrally in the dorsal horn. In the present study, we examined whether COX inhibition can also suppress peripheral sensitization in meningeal nociceptors. Using single-unit recording in the trigeminal ganglion in vivo, we found that intravenous infusion of naproxen, a non-selective COX inhibitor, reversed measures of sensitization induced in meningeal nociceptors by prior exposure of the dura to inflammatory soup (IS): ongoing activity of A,- and C-units and their response magnitude to mechanical stimulation of the dura, which were enhanced after IS, returned to baseline after naproxen infusion. Topical application of naproxen or the selective COX-2 inhibitor N -[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS-398) onto the dural receptive field of A,- and C-unit nociceptors also reversed the neuronal hyper-responsiveness to mechanical stimulation of the dura. The findings suggest that local COX activity in the dura could mediate the peripheral sensitization that underlies migraine headache. [source]

Inflammation alters somatostatin mRNA expression in sensory neurons in the rat

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2005
Seham A. Abd El-Aleem
Abstract Proinflammatory neuropeptides, such as substance P and calcitonin gene-related peptide, are up-regulated in primary afferent neurons in acute and chronic inflammation. While these neuropeptides have been intensively studied, potentially anti-inflammatory and/or anti-nociceptive neuropeptides such as somatostatin (SS) have been less widely investigated. Endogenous somatostatin is thought to exert a tonic antinociceptive effect. Exogenous SS is anti-inflammatory and antinociceptive and is thought to exert these actions through inhibition of proinflammatory neuropeptide release. In this study we have compared the expression of somatostatin in two inflammatory models: arthritis, a condition associated with increased nociception, and periodontitis, in which there is little evidence of altered nociceptive thresholds. In acute arthritis (< 24 h) SS mRNA was down-regulated in ipsilateral dorsal root ganglia (DRG; 52 ± 7% of control, P < 0.05), and up-regulated in contralateral DRG (134 ± 10% of control; P < 0.05). In chronic arthritis (14 days) this pattern of mRNA regulation was reversed, with SS being up-regulated ipsilaterally and down-regulated contralaterally. In chronic mandibular periodontitis (7,10 days), SS mRNA was up-regulated in only the mandibular division of the ipsilateral trigeminal ganglion (TG) (day 7, 219 ± 9% and day 10, 217 ± 12% of control; P < 0.02) but showed no change in other divisions of the trigeminal ganglion or in the mesencephalic nucleus. These data show that antinociceptive and anti-inflammatory neuropeptides are also regulated in inflammation. It is possible that the degree of inflammation and nociception seen may depend on the balance of pro- and anti-inflammatory and nociceptive peptide expression in a particular condition. [source]

Afferent ingrowth and onset of activity in the rat trigeminal nucleus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2000
P. M. E. Waite
Abstract A novel in vitro preparation, consisting of the rat brainstem with the trigeminal ganglion attached, has been used to study the anatomical and functional development of the trigeminal nucleus from embryonic day (E)13 to postnatal day (P)6. Neurobiotin injections into the trigeminal ganglion showed that primary afferents had reached the trigeminal tract by E13 and had grown simple, mainly unbranched, collaterals into all levels of the nucleus by E15. By E17, these collaterals were extensively branched, with occasional boutons present. Patches of intense neurobiotin-labelled terminals, corresponding to whisker-related patterns, were first seen at E20 and became clearer over the next few days. Terminal arbours at this stage were relatively localized and densely branched, with many boutons. Responses from the trigeminal nucleus were recorded with suction electrodes, following stimulation of the trigeminal ganglion. Recordings from the main sensory nucleus showed a postsynaptic response was first present at E15. At E16, bath application of AP5 and DNQX showed that the response contained both NMDA and AMPA components, with NMDA predominating (75%). The NMDA : AMPA ratio remained high until P1, then gradually declined to 50% by P6. The postsynaptic response was also reduced by bath application of bicuculline, indicating the presence of a GABAA -mediated excitatory component. GABAergic excitation was present at all ages but was maximal from E20 to P1, the age at which whisker-related patterns are developing. It is hypothesized that both GABAergic excitation and NMDA receptor activation play a role in the consolidation of trigeminal connections, and are thus important in the development of whisker-related patterns. [source]

A new class of neurotoxin from wasp venom slows inactivation of sodium current

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2000
Yoshinori Sahara
Abstract The effects of ,-pompilidotoxin (,-PMTX), a new neurotoxin isolated from the venom of a solitary wasp, were studied on the neuromuscular synapses in lobster walking leg and the rat trigeminal ganglion (TG) neurons. Paired intracellular recordings from the presynaptic axon terminals and the innervating lobster leg muscles revealed that ,-PMTX induced long bursts of action potentials in the presynaptic axon, which resulted in facilitated excitatory and inhibitory synaptic transmission. The action of ,-PMTX was distinct from that of other known facilitatory presynaptic toxins, including sea anemone toxins and ,-scorpion toxins, which modify the fast inactivation of Na+ current. We further characterized the action of ,-PMTX on Na+ channels by whole-cell recordings from rat trigeminal neurons. We found that ,-PMTX slowed the Na+ channels inactivation process without changing the peak current,voltage relationship or the activation time course of tetrodotoxin (TTX)-sensitive Na+ currents, and that ,-PMTX had voltage-dependent effects on the rate of recovery from Na+ current inactivation and deactivating tail currents. The results suggest that ,-PMTX slows or blocks conformational changes required for fast inactivation of the Na+ channels on the extracellular surface. The simple structure of ,-PMTX, consisting of 13 amino acids, would be advantageous for understanding the functional architecture of Na+ channel protein. [source]

Neuron,Glia Signaling in Trigeminal Ganglion: Implications for Migraine Pathology

Masticatory problems after balloon compression for trigeminal neuralgia: a longitudinal study1

JOURNAL OF ORAL REHABILITATION, Issue 2 2007
S. R. D. T. DE SIQUEIRA
summary, Idiopathic trigeminal neuralgia (ITN) is a chronic neuropathic pain that affects the masticatory system. The objective of this study was to identify orofacial pain and temporomandibular characteristics, including temporomandibular disorder (TMD), in a sample of 105 ITN patients treated with compression of the trigeminal ganglion. The evaluations occurred before, 7, 30 (1 month), 120 (3 months) and 210 days (7 months) after surgery. The Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD), the Clinical Questionnaire (EDOF-HC) and Helkimo Indexes were used. Findings before neurosurgery were used as control for parameters. McNemar test and variance analysis for repetitive measurements were used for statistical analysis; 45·3% of the edentulous patients presented severe dental occlusion index; numbness was an important masticatory complaint in 42·6%; mastication became bilateral, but its discomfort continued during all period; headache and body pain reduced after surgery; TMD, present in 43·8% before surgery, increased but normalized after 7 months; jaw mobility compromise was still present, but daily activities improved after 7 months. We concluded that: (i) ITN relief reduced headache, body pain, depression and unspecific symptoms; and (ii) TMD before surgery and at 7 months suggests that this may be a contributory factor to patients' pain complaints. [source]

GDNF Expression in Terminal Schwann Cells Associated With the Periodontal Ruffini Endings of the Rat Incisors During Nerve Regeneration

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 8 2009
Megumi Ohishi
Abstract The terminal Schwann cells (TSCs) which play crucial roles in regeneration of the periodontal Ruffini endings (RE) exhibit immunoreaction for glial cell line-derived neurotrophic factor (GDNF). However, no information is available regarding the role of GDNF in the periodontal RE during nerve regeneration. This study was undertaken to examine the changes in GDNF expression in the rat periodontal RE following transection of the inferior alveolar nerve (IAN) using immunohistochemistry for GDNF and S-100 protein, a marker for the TSCs. We additionally investigated the changes in expression of GDNF in the trigeminal ganglion (TG) at protein and mRNA levels. A transection to IAN induced a disappearance of the TSCs from the alveolus-related part (ARP), followed by a migration of spindle-shaped cells with S-100 but without GDNF immunoreactions into the tooth-related part (TRP) by postoperative (PO) week 2. At PO week 2, GDNF immunoreacted cellular elements increased in number in the ARP although the spindle-shaped cells without GDNF reaction remained in the TRP. After PO week 4, many GDNF-positive TSCs appeared in the ARP though the spindle-shaped cells vanished from the TRP. A real time RT-PCR analysis demonstrated the highest elevation of GDNF mRNA in the TG at PO week 2. These findings suggested the involvement of this molecule in the maturation and maintenance of the periodontal RE during regeneration. Taken together with our previous and current studies, it appears that the regeneration of the periodontal RE is controlled by multiple neurotrophins in a stage-specific manner. Anat Rec, 2009. © 2009 Wiley-Liss, Inc. [source]

Characteristics and physiological role of hyperpolarization activated currents in mouse cold thermoreceptors

THE JOURNAL OF PHYSIOLOGY, Issue 9 2009
Patricio Orio
Hyperpolarization-activated currents (Ih) are mediated by the expression of combinations of hyperpolarization-activated, cyclic nucleotide-gated (HCN) channel subunits (HCN1,4). These cation currents are key regulators of cellular excitability in the heart and many neurons in the nervous system. Subunit composition determines the gating properties and cAMP sensitivity of native Ih currents. We investigated the functional properties of Ih in adult mouse cold thermoreceptor neurons from the trigeminal ganglion, identified by their high sensitivity to moderate cooling and responsiveness to menthol. All cultured cold-sensitive (CS) neurons expressed a fast activating Ih, which was fully blocked by extracellular Cs+ or ZD7288 and had biophysical properties consistent with those of heteromeric HCN1,HCN2 channels. In CS neurons from HCN1(,/,) animals, Ih was greatly reduced but not abolished. We find that Ih activity is not essential for the transduction of cold stimuli in CS neurons. Nevertheless, Ih has the potential to shape the excitability of CS neurons. First, Ih blockade caused a membrane hyperpolarization in CS neurons of about 5 mV. Furthermore, impedance power analysis showed that all CS neurons had a prominent subthreshold membrane resonance in the 5,7 Hz range, completely abolished upon blockade of Ih and absent in HCN1 null mice. This frequency range matches the spontaneous firing frequency of cold thermoreceptor terminals in vivo. Behavioural responses to cooling were reduced in HCN1 null mice and after peripheral pharmacological blockade of Ih with ZD7288, suggesting that Ih plays an important role in peripheral sensitivity to cold. [source]

2215: Animal models of herpetic retinitis

ACTA OPHTHALMOLOGICA, Issue 2010
M LABETOULLE
The Herpes simplex virus (HSV) is characterized its ability to replicate in the nervous system, before inducing a latent infection with potential reactivation. Most frequent ocular complications of recurrent HSV infection are keratitis and conjunctivitis. Less frequently, the iris and the ciliary body may also be involved (anterior uveitis). The most severe HSV ocular infection is retinitis, a rare but potentially blinding disease, due to frequent bilateral involvement. Studies on human post-mortem tissues showed that HSV is widely distributed in the population, with a preferential location within the trigeminal ganglions (innervating the cornea), but also in the superior cervical ganglions (innervating the iris) or in brain/medullar tissues (innervating the retina). Animal models have been developed to understand the pathogenic processes that lead to this rare but devastating retinal disease. Since human is the only natural host of HSV, it is difficult to obtain a perfect animal model that perfectly mimics the disease. Several animal models, based on different inoculation procedures, are thus necessary to circumscribe the anatomical, cellular and molecular aspects that lead to retinal infection. Finally, HSV retinitis appears as a clinical condition that is highly constrained by the relationships between the strain of the virus and the immune response of the host. [source]