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At least 19 recordsLinked to original sources
PubMed1988

[Effect of the stimulation of the central gray substance of the midbrain on the neuronal responses of the trigeminal caudal nucleus during peripheral excitations].

Experiment on cats under chloralose-nembutal anaesthesia has shown that 65% responses of caudal trigeminal nucleus neurons to the activation of the tooth pulp, A alpha and/or A delta infraorbital nerve afferents were completely suppressed by conditioning stimulation of the central grey matter (CGM) by a train of stimuli (10-20) that followed with the rate of 200-400/s, if the interval between conditioning and testing stimuli did not exceed 100 ms. Conditioning stimulation of the CGM inhibited responses of the "convergent" neurons to the activation of tooth pulp most efficiently (0.76) and those to the activation of A alpha afferents more weakly (0.6). Effectiveness of "high-threshold" neurons inhibition under the effect of CGM stimulation was 0.71 and that of "low-threshold" neurons--0.48. Ten caudal trigeminal nucleus neurons were activated by the CGM stimulation with the latency of 7.5-20 ms. These neurons did not respond to peripheral nerve stimulation for 200-450 ms after CGM activation. A possible role of caudal trigeminal nucleus neurons in the CGM inhibition of jaw opening reflexes is discussed.

Action Potentials↗
PubMed1983

Mechanisms regulating the activity of facial nucleus motoneurones--2. Synaptic activation from the caudal trigeminal nucleus.

Field and postsynaptic potentials of facial motoneurones evoked by stimulation of the caudal trigeminal nucleus were studied in cats by means of extra- and intracellular recording. Mono- and polysynaptic input onto facial motoneurones from the caudal trigeminal nucleus were shown. Four types of responses were distinguished: excitatory postsynaptic potentials generating a single action potential; a gradual shift of depolarization inducing multiple discharges; a rhythmic discharge of action potentials appearing at a low level of depolarization; excitatory postsynaptic potentials or a sequence of excitatory and inhibitory postsynaptic potentials. Multiple discharge was shown to appear as a result of effective summation of high frequency excitatory influences from efferent neurones of the caudal trigeminal nucleus projecting into the facial nucleus. Factors facilitating the development of gradual depolarization are: dendritic localization of synaptic terminals, dendritic origin of after-depolarizing processes and the high input resistance of the facial motoneurone membrane. It is thought that specific features of facial motoneurones and properties of afferent inputs are supposed to provide high sensitivity of neuronal organization of the facial nucleus to afferent signals as well as wide diversity in controlling its activity.

Animals↗
PubMed1980

[Synaptic processes in motor neurons of the nucleus of the facial nerve upon stimulation of the caudal trigeminal nucleus].

Focal and postsynaptic potentials of facial motoneurons evoked by stimulation of the caudal trigeminal nucleus were studied in cats using extra- and intracellular recording technique. Pre- and post-synaptic components of focal potentials are shown. Four types of motoneuron responses are distinguished: EPSP generating single action potentials; gradual shift of depolarization evoking multiple discharges; rhythmical discharge of action potentials appearing at a low level of depolarization; EPSP and a sequence of EPSP-IPSP. Mono- and predominantly polysynaptic origin of these responses is shown. Possible mechanisms of afferent control of facial motoneuron activity are discussed.

Action Potentials↗
PubMedDate not supplied

[Implication of the neuropeptides methionine enkephalin, neurotensin and somatostatin of the caudal trigeminal nucleus in the experimental migraine].

INTRODUCTION: Primary peptidergic sensory neurons of the trigeminal ganglion that innervate the cerebral dura have been involved in the pathogenesis of headache, including the migraine. In addition, it is known that nociceptive central processes of the trigeminal neurons terminate in the caudal trigeminal nucleus. Moreover, the electrical stimulation of the trigeminal ganglion has been used as an experimental model in order to study the vascular headache, including the migraine. AIM: To study whether there is or not a decrease of the immunoreactivity for methionine enkephalin, somatostatin and neurotensin in the caudal trigeminal nucleus after electrical stimulation of the trigeminal ganglion. MATERIAL AND METHODS: The trigeminal ganglia of Wistar albino rats of both sexes were electrically stimulated (frequency, 5 Hz; duration, 5 ms; intensity, 0,8 1.4 mA) and unilaterally for five minutes. Sections of the medulla oblongata containing the caudal trigeminal nucleus were obtained and processed for immunocytochemistry, in which specific antibodies were used against methionine enkephalin, neurotensin and somatostatin 28. RESULTS: In stimulated animals, we observed a decrease in the immunoreactivity for the three neuropeptides studied in the stimulated (ipsilateral) side, in comparison with the not stimulated side (contralateral). In control animals (not stimulated) the degree of the immunoreactivity was the same on both sides. CONCLUSIONS: 1. The decrease of the immunoreactivity in the ipsilateral side (stimulated) suggests that methionine enkephalin, neurotensin and somatostatin 28 are released in the caudal trigeminal nucleus after electrical stimulation of the trigeminal ganglion; 2. Methionine enkephalin and somatostatin 28 could act in the caudal trigeminal nucleus as inhibitors (with antinociceptive action) of another released exciters neuropeptides (with nociceptive action); and 3. These data will allow in the future to try new therapeutic strategies (e.g., the inhibition of the receptors implicated.), in order to alleviate certain headaches.

Animals↗
PubMed1998

Depletion of calcitonin gene-related peptide from the caudal trigeminal nucleus of the rat after electrical stimulation of the Gasserian ganglion.

Electrical stimulation of the Gasserian ganglion resulted in partial depletion of calcitonin gene-related peptide (CGRP) from ipsilateral central terminals of pseudounipolar primary sensory ganglion cells. Affected terminals exhibit decreased CGRP immunoreactivity as shown by cytophotometric densitometry of the caudal trigeminal nucleus. The decrease in CGRP immunoreactivity is statistically significant only in the medial one-third of the caudal trigeminal nucleus. Since earlier studies have shown that electrical stimulation of the Gasserian ganglion induces first accumulation then depletion of CGRP from perivascular sensory terminals in the dura mater, the present experiments suggest that CGRP is depleted also from central terminals of primary sensory trigeminal neurons, which might be of importance in the pathogenesis of migraine headache.

Animals↗
PubMed1982

An ionophoretic study of the responses of rat caudal trigeminal nucleus neurones to non-noxious mechanical sensory stimuli.

1. Extracellular recordings of the responses of single caudal trigeminal nucleus neurones to non-noxious and noxious facial stimuli and to ionophoretically applied L-glutamate, L-aspartate and acetylcholine were made in urethane anaesthetized rats. 2. Neurones excited by non-noxious mechanical stimuli were located primarily in the magnocellular part of nucleus caudalis, whereas neurones excited by both noxious and non-noxious stimuli were located either ventromedially to the magnocellular part of nucleus caudalis or superficially to the substantia gelatinosa. 3. Both L-aspartate and L-glutamate were found to excite all neurones tested in nucleus caudalis. In contrast, however, acetylcholine was found to excite only 31% of the neurones tested. 4. Responses of nucleus caudalis neurones to non-noxious sensory stimulation were not antagonized by the excitatory amino acid antagonist D-alpha-aminoadipate, but were antagonized by cis-2, 3-piperidine dicarboxylate and gamma-D-glutamylglycine, two excitatory amino acid antagonists with a broader spectrum of action. 5. It is concluded that the chemical synaptic transmitter of non-nociceptive mechanoreceptive primary afferent fibres to nucleus caudalis may be a ligand for an excitatory amino acid receptor other than a D-alpha-aminoadipate-sensitive receptor. The synaptic receptor may thus be of the kainate or quisqualate type, and the transmitter possibly L-glutamate, L-aspartate or an as yet unidentified substance.

Acetylcholine↗
PubMed2006

[The modulatory effect of estrogen on the caudal trigeminal nucleus of the rat in an animal model of migraine].

Migraine is one of the most common neurological disorder affecting up to 14% of the population. The disease shows sexual dimorphism, thus gonadal steroids may play an important role in its pathophysiology. One model of migraine headache is the systemic administration of nitric oxide (NO) donor nitroglycerin (NTG), which triggers a delayed attack without aura in many migraine patients but not in healthy volunteers. NTG is also able to activate the neurons of the caudal trigeminal nucleus in the rat. In our review we summarise the effect of NTG on the expression of some molecules, in the superficial laminae of the spinal portion of trigeminal nucleus caudalis, which play an important role in the pathomechanism of headaches, and the modulatory effect of chronic estradiol treatment. Our data show that NTG was able to modify all the examined substances in the caudal trigeminal nucleus, while chronic estradiol treatment abolished this effect. These data may help to understand the mechanisms by which estrogens influence trigeminal nociception and how nitric oxide triggers migraine attacks.

Animals↗
PubMed1980

[Electroacupuncture inhibition of nociceptive responses in the caudal trigeminal nucleus].

Acute experiments on cats showed that auricular electroacupuncture (AEAP)) produces significant inhibition of evoked potentials (EP) in the caudal trigeminal nucleus which occur under single stimulation of the tooth pulp. The inhibition of EP lasts for 60--80 min. Then gradual (over 30--40 min) recovery of EP is recorded. Acupuncture stimulation decreases insignificantly the amplitude of EP caused by irritation of mouth mucosa. This fact indicates that AEAP inhibits nociceptive responses but does not affect mediation of signals in other modalities. It was established that reacing of AEAP analgetic effect does not require that the classical scheme of acupuncture point localization be strictly followed.

Acupuncture Therapy↗
PubMedDate not supplied

[Effect of lithium gamma-hydroxybutyrate on evoked potentials in the caudal trigeminal nucleus and somatosensory cortex in rats with trigeminal neuropathy].

Lithium gamma-hydroxybutyrate (20 mg/kg, i.e.) was studied for effects on the evoked potentials (EP) in the caudal trigeminal nucleus (CTN) and somatosensory cortex (SSC) in acute tests on rats with trigeminal neuropathy induced by incomplete compression of the infraorbital nerve. Before drug administration, EPs in CTN on the side of nerve compression were characterized by the increased amplitude of presynaptic R1N1 and late postsynaptic P3N3-P4N4 components and by the reduction in the early postsynaptic P2N2 component. In the contralateral CTN, EP had higher amplitudes. Spontaneous epileptoid activity was recorded in CTN in a third of the animals and in SSC in a half. These changes are regarded as a result of A-delta-C-afferent entry due to attenuation of afferentation along A-beta fibers. After administration of the drug, there was suppression of EP in SSC, while in CTN there was a decrease in the amplitude of the EP presynaptic component with increases in the postsynaptic components. There was suppression of abnormally enhanced spontaneous activity in CT and SSC. The findings are under discussion in terms of the cortical action of the drug resulting in the suppression of the abnormally enhanced activity developed in the brain projectional regions in nerve compression lesion.

Animals↗
PubMed1983

Distribution of substance P-responsive and nociceptive neurones in relation to substance P-immunoreactivity within the caudal trigeminal nucleus of the rat.

Substance P is a peptide which is found in small diameter primary afferent fibres and may have a function in nociceptive afferent transmission. In order to study the role of substance P in sensory processes in depth, we have compared the distributions of nociceptive neurones and substance P-responsive neurones with the distribution of substance P in the caudal trigeminal nucleus of the rat. It was found that substance P-like immunoreactivity was located primarily in the superficial layers of nucleus caudalis (equivalent to laminae I and II of the dorsal horn) and in more ventromedially located areas (equivalent to laminae V and VI). The distribution was found to be in good agreement with the distribution of nociceptive neurones. Iontophoretically applied substance P had predominantly excitatory actions on both nociceptive and non-nociceptive nucleus caudalis neurones, although the peptide did appear to be slightly more likely to excite nociceptive neurones. Similarly, the peptide appeared slightly more likely to be excitatory in areas of nucleus caudalis showing substance P staining, but excitations were also predominantly seen in areas containing little or no apparent substance P staining. These results are consistent with the proposed role for substance P as a nociceptive afferent neurotransmitter. However, it is also possible that the peptide performs other functions in the processing of sensory information.

Animals↗
PubMed1999

Nociceptive neurons in the rat caudal trigeminal nucleus respond to blood plasma perfusion of the subarachnoid space: the involvement of complement.

The meninges of the brain are innervated by afferent nerve fibres containing SP and CGRP, two typical peptides found in sensory neurons. These fibres project to the trigeminal nuclear complex and the cervical dorsal horn. Discharge of the afferents may provide a physiological basis for some types of headaches. Considerable speculation surrounds the possible causes of meningeal afferent activation. Blood-borne substances released during subarachnoid haemorrhage are one possibility and there is a possibility that these also play a role in migraine. In the case of migraine, blood components, e.g. from platelets, cannot be excluded. To investigate the possible effects of platelets and plasma factors, the subarachnoid space of the rat was continuously perfused with artificial cerebrospinal fluid during extracellular recordings from single units of the caudal trigeminal nucleus. Washed and concentrated suspensions of adenosindiphosphate (ADP)--activated platelets and plasma, from which platelets had been removed--were introduced as a bolus into the continuous flow. Neurons in the caudal nucleus of the trigeminal complex receiving input from the meninges were stimulated. They did not respond to the activated platelet suspensions but showed intense responses to plasma. Plasma completely lost its ability to excite trigeminal neurons after heat inactivation (30 min, 56 degrees C). It is concluded that the complement system may be involved in the excitatory nociceptive effect of platelet-poor plasma.

Animals↗
PubMed1982

Facial thermal input in the caudal trigeminal nucleus of rats reared at 30 degrees C.

1. Rats reared from birth in air at 30 degrees C showed a decreased ability to maintain colonic temperature when exposed to 10 degrees C as compared with rats reared at 20 degrees C. This difference was not due to physical factors affecting heat loss, such as surface area or fur thickness. 2. In anaesthetized rats extracellular recordings were made in trigeminal nucleus caudalis from higher order neurones with input from facial cold and warm receptors. A systematic search on a grid pattern showed there was no difference between heat-reared and control rats in facial receptive fields or in the abundance, extent and somatotopic distribution of thermal neurones in the nucleus. In both groups almost all the neurones were excited only by facial cooling. 3. When single cold neurones were tested quantitatively by the application of controlled temperature changes to their receptive fields on the face there was no difference in the static temperature/discharge rate relationship between the two groups of rats. 4. The results suggest that the observed difference in ability to regulate body temperature is not attributable to differences in skin-temperature reception at the level of the trigeminal nucleus.

Animals↗
PubMed1981

[Neuronal analysis of the projection of the caudal trigeminal nucleus to the nucleus of the facial nerve in cats].

Peculiarities of the trigeminal nucleus caudalis neurons which are projected to the facial nucleus were studied by microelectrode recording in cats. It is shown that the mentioned neurons are localized predominantly in ventral parts of the trigeminal nucleus caudalis and adjacent lateral reticular formation. Mono- and polysynaptic activation of efferent trigeminal neurons to pyramidal impulsation is described. Repetitive discharges of these neurons to stimulation of their axons, direct stimulation of the trigeminal nucleus caudalis as well as to that of the pyramidal tract and facial nerve are recorded. The significance of the obtained data in the light for the understanding of the synaptic mechanisms of regulation of facial motoneurons activity is discussed.

Animals↗
PubMed2006

Kynurenine in combination with probenecid mitigates the stimulation-induced increase of c-fos immunoreactivity of the rat caudal trigeminal nucleus in an experimental migraine model.

Nitroglycerin, often used as a migraine model, results in increased number of c-fos immunoreactive secondary sensory neurons in the caudal trigeminal nucleus. Since synapses between first- and second-order trigeminal neurons are mediated by excitatory amino acids, NMDA receptors are presumably inhibited by kynurenic acid, the only known endogeneous NMDA receptor antagonist. Although kynurenic acid does not cross the BBB, its precursor, kynurenine, if combined with probenecid, crosses it readily. Systemic kynurenine + probenecid treatment significantly diminishes nitroglycerin-induced increase of c-fos immunoreactivity in the brainstem.

Animals↗
PubMed2003

Hippocampal spreading depression bilaterally activates the caudal trigeminal nucleus in rodents.

Spreading depression (SD) and migraine aura involve transiently altered (i.e., increased followed by decreased) electrophysiological activity that propagates at the distinctive rate of millimeters per minute (mm/min), leading to the suggestion that they (and perhaps pain from migraine) are causally related via changes in the same brain structure. Neocortex is considered the anatomical zone associated with migraine aura and is the sole area known to induce caudal trigeminal nucleus (TNC) activation from SD in rodents. However, classical evidence of SD in human neocortex is reported only with severe brain disease, while migraine is a common and comparatively benign disorder. Because SD occurs in human hippocampus, and memory dysfunction referable to hippocampus is seen in migraineurs, we determined whether recurrent SD confined to hippocampus in rat could induce TNC activation. Our work shows that recurrent hippocampal SD evoked a significant (P < 0.05-0.001) increase in bilateral c-fos immunostaining within TNC superficial laminae compared with sham controls. Furthermore, hippocampal SD occurred with a correlated and transient change in spontaneous activity and blood flow in the ipsilateral neocortex without spread of SD to that area. Thus, hippocampal SD may be a previously unrecognized, potential trigger for nociceptive activation of TNC perhaps associated with migraine.

Animals↗
PubMed2003

Effects of stimulation of the trigeminal caudal nucleus on microvascular permeability in the eye in normal and capsaicin-treated rats.

Electrical stimulation of the trigeminal caudal nucleus in rats evoked increases in the permeability of eye microvessels. The microvascular effect did not appear when the nucleus was stimulated after administration of capsaicin 10 days before surgery (total dose 150 mg/kg, s.c., on two sequential days, given as 20, 30, 50, and 50 mg/kg). It is suggested that capsaicin-sensitive neurons in the trigeminal ganglion mediate the microvascular effect of stimulation of the trigeminal caudal nucleus.

Animals↗