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Trigeminal Neurons (trigeminal + neuron)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Change of Excitability in Brainstem and Cortical Visual Processing in Migraine Exhibiting Allodynia

HEADACHE, Issue 10 2006
Koichi Shibata MD
Background.,Clinical and neurophysiological manifestations of information processing associated with central sensitization are little known. Allodynic migraine (AM) can be caused by the sensitization of trigeminal neuron, but no study has reported on AM between attacks using blink reflex (BR) and pattern-reversal visual evoked potentials (PVEPs). Objective.,We explored the characteristics of AM between attacks associated with central sensitization using BR and PVEP. Methods.,We recruited 13 patients with interictal AM and 15 patients with nonallodynic migraine (NA), and 30 healthy subjects (HS). BRs were obtained using paired pulses delivered at the interstimulus interval (ISI) of 150, 300, and 500 ms. The ratio of the area in the R2 of the second to R2 of the first shock was measured for each ISI. PVEP were recorded with 2 spatial frequencies (0.5 and 4.0 cpd) and 2 low and high contrasts (29% and 98%, respectively). Amplitudes of P100 were measured. Results.,For BR, there were no significant differences in the ratio of the area of the R2 between the sides of stimulation, and the sides of headache. AM patients had less suppression of the R2 at the ISI of 150 and 300 ms when compared with the NA patients and HS. For PVEP, at 0.5, there were significant differences of amplitude between AM patients and HS, and between NA patients and HS in low and high contrast. At 4.0 cpd, there were significant differences of amplitude between AM patients and HS in low contrast, and between AM patients and HS, and NA patients and HS in high contrast. In AM patients, there was a significant difference of amplitude ratio between 0.5 and 4.0 cpd. Conclusions.,Our BR and PVEP study showed that migraine patients exhibiting allodynia may show central sensitization of brainstem trigeminal neuron and have contrast modulating dysfunction during the cortical visual processing of striate and extrastriate on visual cortex in-between attacks. [source]

Referred Pain Elicited by Manual Exploration of the Lateral Rectus Muscle in Chronic Tension-Type Headache

PAIN MEDICINE, Issue 1 2009
César Fernández-de-las-Peñas PT
ABSTRACT Objective., To analyze the presence of referred pain elicited by manual examination of the lateral rectus muscle in patients with chronic tension-type headache (CTTH). Design., A case-control blinded study. Setting., It has been found previously that the manual examination of the superior oblique muscle can elicit referred pain to the head in some patients with migraine or tension-type headache. However, a referred pain from other extraocular muscles has not been investigated. Methods., Fifteen patients with CTTH and 15 healthy subjects without headache history were included. A blinded assessor performed a manual examination focused on the search for myofascial trigger points (TrPs) in the right and left lateral rectus muscles. TrP diagnosis was made when there was referred pain evoked by maintained pressure on the lateral corner of the orbit (anatomical projection of the lateral rectus muscle) for 20 seconds, and increased referred pain while the subject maintained a medial gaze on the corresponding side (active stretching of the muscle) for 15 seconds. On each side, a 10-point numerical pain rate scale was used to assess the intensity of referred pain at both stages of the examination. Results., Ten patients with CTTH (66.6%) had referred pain that satisfied TrPs diagnostic criteria, while only one healthy control (0.07%) reported referred pain upon the examination of the lateral rectus muscles (P < 0.001). The elicited referred pain was perceived as a deep ache located at the supraorbital region or the homolateral forehead. Pain was evoked on both sides in all subjects with TrPs, with no difference in pain intensity between the right and the left. The average pain intensity was significantly greater in the patient group (P < 0.001). All CTTH patients with referred pain recognized it as the frontal pain that they usually experienced during their headache attacks, which was consistent with active TrPs. Conclusion., In some patients with CTTH, the manual examination of lateral rectus muscle TrPs elicits a referred pain that extends to the supraorbital region or the homolateral forehead. Nociceptive inputs from the extraocular muscles may sustain the activation of trigeminal neuron, thus sensitizing central pain pathways and exacerbating headache. [source]

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]

Transient receptor potential A1 mediates acetaldehyde-evoked pain sensation

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2007
Sangsu Bang
Abstract Six transient receptor potential (TRP) ion channels expressed in the sensory afferents play an important role as body thermosensors and also as peripheral pain detectors. It is known that a number of natural compounds specifically activate those sensory neuronal TRP channels, and a well-known example is cinnamaldehyde for TRPA1. Here we show that human and mouse TRPA1 are activated by acetaldehyde, an intermediate substance of ethanol metabolism, in the HEK293T cell heterologous expression system and in cultured mouse trigeminal neurons. Acetaldehyde failed to activate other temperature-sensitive TRP channels expressed in sensory neurons. TRPA1 antagonists camphor and gadolinium, and a general TRP blocker ruthenium red inhibited TRPA1 activation by acetaldehyde. Camphor, gadolinium and ruthenium red also suppressed the acute nociceptive behaviors induced by the intradermal administration of acetaldehyde into the mouse footpads. Intradermal co-application of prostaglandin E2 and acetaldehyde greatly potentiated the acetaldehyde-induced nociceptive responses, and this effect was reversed by treatment with the TRPA1 antagonist camphor. These results suggest that acetaldehyde causes nociception via TRPA1 activation. Our data may also help elucidate the mechanisms underlying acetaldehyde-related pathological symptoms such as hangover pain. [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

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]