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At least 19 recordsLinked to original sources
PubMed1994

Distribution of nitric oxide synthase-immunoreactive interneurons in the spinal trigeminal nucleus.

The spinal trigeminal nucleus is involved in the transmission of orofacial sensory information. Neither the distribution of the neuromessenger, nitric oxide, within the trigeminal system nor the possible relationship of this simple gas with trigeminothalamic neurons has been carefully studied. Using immunocytochemical (against nitric oxide synthase) and histochemical (NADPH-diaphorase staining) techniques, we have found that nitric oxide neurons and processes are more prominent in the nucleus caudalis and the dorsomedial aspect of the nucleus oralis than in other spinal trigeminal regions. To study the relationship of nitric oxide to trigeminothalamic neurons and intertrigeminal interneurons of the spinal trigeminal nucleus, spinal trigeminal neurons were retrogradely labeled with fluorogold by thalamic injections or by injections into the junction of the nucleus interpolaris and nucleus caudalis. Medullary sections were subsequently processed with NADPH-diaphorase histochemistry. None of the diaphorase-stained neurons in the spinal trigeminal nucleus was found to contain fluorogold; however, some diaphorase-stained processes were found in close proximity to trigeminothalamic neurons. Following spinal trigeminal nucleus injections, many diaphorase-stained neurons were found to contain fluorogold, especially in the nucleus caudalis, suggesting that nitric oxide-containing neurons in the spinal trigeminal nucleus are intertrigeminal interneurons. Collectively, these data indicate that nitric oxide is most prominent in interneurons located in nucleus caudalis and that these interneurons give rise to processes that appose trigeminothalamic neurons, raising the possibility that they may indirectly influence orofacial nociceptive processing at the level of the spinal trigeminal nucleus via nitric oxide production.

Amino Acid Oxidoreductases↗
PubMedDate not supplied

[Ultrasonic destruction of the spinal trigeminal nucleus in the deafferentation orofacial pain syndrome].

Ultrasonic destruction of the trigeminal spinal nucleus was conducted in 12 patients with the deafferentation orofacial pain syndrome. The etiological factors and clinical manifestations of the deafferentation syndrome are analysed. The surgical techniques of destruction of the trigeminal spinal nucleus and the principles of intraoperative electrophysiological control are described. The length of the nucleus destruction and the clinical effect of the surgical intervention are compared. To relieve pain and dysesthesia in the peri- and intraoral areas the terminal nucleus must be destroyed at the level of the obex of the fourth ventricle.

Adult↗
PubMed1998

Morphine administered in the substantia gelatinosa of the spinal trigeminal nucleus caudalis inhibits nociceptive activities in the spinal trigeminal nucleus oralis.

The present study investigates the effects of morphine microinjection into the spinal trigeminal nucleus caudalis (Sp5C) or the spinal trigeminal nucleus oralis (Sp5O) on C-fiber-evoked activities of Sp5O convergent neurons, after supramaximal percutaneous electrical stimulation in halothane-anesthetized rats. When it was microinjected into the Sp5O, morphine (2.5 microg in 0. 25 microl) never depressed the C-fiber-evoked responses of Sp5O convergent neurons (n = 13), whereas these neurons were responsive to the inhibitory effects of systemic morphine (6 mg/kg, i.v.) in a naloxone-reversible manner. On the contrary, morphine microinjected into the Sp5C produced a naloxone-reversible inhibition of the C-fiber-evoked responses of Sp5O neurons (n = 14). The magnitude and the time course of this effect varied according to the location of the injection sites. After microinjection into the superficial laminae (n = 7), a strong depressive effect of morphine (7 +/- 5% of control) on the C-fiber-evoked responses was apparent as soon as 5 min after the injection and could always be reversed by naloxone, administered either intravenously (0.4 mg/kg) or locally (2.5 microg in 0.6 microl) at the same site as morphine. After microinjection into deeper laminae (V-VI), a significant depressive effect (34 +/- 5% of control) of morphine could be detected only 20 min after the injection and was reversed only by intravenous administration of naloxone. These results suggest that morphine exerts its antinociceptive action on Sp5O convergent neurons by blocking the C-fiber inputs that relay in the Sp5C substantia gelatinosa. The mechanisms that underlie the activation of Sp5O convergent neurons by C-fibers and the inhibition of C-fiber-evoked responses of Sp5O convergent neurons by morphine microinjected into the Sp5C are discussed.

Animals↗
PubMed1986

Anatomical evidence that the pontine lateral tegmental field projects to lamina I of the caudal spinal trigeminal nucleus and spinal cord and to the Edinger-Westphal nucleus in the cat.

Autoradiographical tracing results in the cat indicate that the lateral pontine tegmental field projects mainly contralaterally to the marginal layer of the spinal trigeminal nucleus, to laminae I and II and the lateral part of laminae V and VI of the spinal cord and the Edinger-Westphal nucleus. It is pointed out that the projections from the lateral pontine tegmentum are very similar to the ones derived from the Edinger-Westphal nucleus and that these two areas are reciprocally connected. It is postulated that both areas may play a role in supraspinal pain control.

Afferent Pathways↗
PubMed1987

A quantitative light microscopic analysis and ultrastructural description of cholecystokinin-like immunoreactivity in the spinal trigeminal nucleus of the rat.

The spinal trigeminal nucleus is involved in orofacial sensory transmission. Cholecystokinin octapeptide has been identified in axons in this nucleus and appears to play a role in the transmission of orofacial sensation from the trigeminal ganglia to the spinal trigeminal nucleus. Although cholecystokinin has been reported in axonal processes within the spinal trigeminal nucleus at the light microscopic level, nothing is known about the synaptic relationships of these cholecystokinin axons. The goals of this study were to quantitatively determine the volume fraction of cholecystokinin-like immunoreactive cell bodies and fibers in the three subnuclei of the spinal trigeminal nucleus, to provide the first ultrastructural description of cholecystokinin-like immunoreactive processes within these subnuclei and to analyse the synaptic relationships of cholecystokinin-like immunoreactive processes within the spinal trigeminal nucleus neuropil. Cholecystokinin-like immunoreactivity was localized by the peroxidase-antiperoxidase method or the peroxidase labeled, avidin-biotin technique and quantified at the light microscopic level by point counting. Immunoreactive fibers were present in all three subnuclei, but the greatest volume fraction of immunoreactive axons was obtained in laminae I and II of the nucleus caudalis. No immunoreactive cell bodies were evident in any of the subnuclei. The majority of immunoreactive profiles in all three subnuclei were identified ultrastructurally as axon terminals that contained both small and medium sized agranular vesicles and infrequently, large dense core vesicles. These immunoreactive terminals were usually found in close contact with non-immunoreactive dendrites with which they were observed to form asymmetric synapses. Immunoreactive terminals were occasionally observed to contact the cell bodies of large non-immunoreactive neurons on the border of laminae I and II in the nucleus caudalis. These results indicate that cholecystokinin-like immunoreactive processes are present throughout the spinal trigeminal nucleus, and in nucleus caudalis show a distribution similar to that reported for the spinal cord dorsal horn. Immunoreactive axons make synaptic contact with both the dendrites and perikarya of spinal trigeminal nucleus neurons. No axoaxonic synapses were observed. These findings suggest that cholecystokinin plays an important role in spinal trigeminal nucleus function. The possible colocalization of cholecystokinin and substance P in the spinal trigeminal nucleus, and the possible role of cholecystokinin in attenuating the action of opioids in the spinal trigeminal nucleus are also discussed.

Animals↗
PubMed1998

Substance P receptor (NK1)-immunoreactive neurons projecting to the periaqueductal gray: distribution in the spinal trigeminal nucleus and the spinal cord of the rat.

Substance P receptor (SPR)-immunoreactive neurons projecting to the periaqueductal gray (PAG) were examined in the rat spinal trigeminal nucleus and spinal cord by a retrograde tracing method combined with immunofluorescence histochemistry. After injection of Fluoro-gold (FG) into the PAG, SPR-immunoreactive neurons labeled with FG were observed mainly in the lateral spinal nucleus and lamina I of the medullary and spinal dorsal horns and additionally in laminae V and X of the spinal cord.

Animals↗
PubMed1999

Changes in c-Fos expression induced by noxious stimulation in the trigeminal spinal nucleus caudalis and C1 spinal neurons of rats after hyperbaric exposure.

The present study aims to test the hypothesis that hyperbaric exposure inhibits nociceptive processing in the trigeminal spinal nucleus caudalis and C1 spinal neurons. We investigated the c-Fos-like immunoreactivity of the brainstem and upper cervical spinal cord (C1 region) following an injection of mustard oil (15 microliters of 20%) into the nasal mucosa of pentobarbital anesthetized rats after exposure to hyperbaric (2-atmospheres, 1 h) and normobaric pressures. After the hyperbaric exposure, the mean number of Fos-immunoreactive neurons in the ipsilateral laminae I-II and III-IV of the trigeminal spinal nucleus caudalis were significantly lower than those in the normobaric condition. Similarly, the mean number of c-Fos positive neurons in the superficial layer (I-II) of the ipsilateral C1 segment were significantly reduced as compared with that in the normobaric condition. When treated with the vehicle alone, no significant difference was detected in the numbers of c-Fos positive neurons in the trigeminal spinal nucleus caudalis and C1 regions between hyperbaric and normobaric conditions. These results suggest that hyperbaric exposure may attenuate nociceptive signals from the area innervated by the trigeminal nerves at the level of both the trigeminal spinal nucleus caudalis and C1 dorsal horn.

Animals↗
PubMed1998

Morphine microinjected into the nucleus raphe magnus does not block the activity of spinal trigeminal nucleus oralis convergent neurons in the rat.

This study investigated the effects of morphine microinjection into the nucleus raphe magnus (RMg) on electrically evoked C-fiber activities of convergent neurons in the spinal trigeminal nucleus oralis (Sp5O), in halothane-anesthetized rats. Although the neurons could be depressed by systemic morphine (6 mg/kg, i.v.) in a naloxone-reversible fashion, morphine microinjected into the RMg (2. 5 microgram or 5 microgram) neither depressed their C-fiber-evoked responses, nor the diffuse noxious inhibitory controls acting on them. It is concluded that the RMg is not involved in reinforcing descending inhibitory controls that are tonic or triggered by noxious stimuli acting on Sp5O convergent neurons.

Animals↗
PubMed1996

Effects of systemic morphine on the activity of convergent neurons of spinal trigeminal nucleus oralis in the rat.

The spinal trigeminal nucleus oralis has been shown to relay nociceptive inputs mainly from the oral and perioral regions. In this study, we examined the effects of intravenous administration of morphine on C-fiber-evoked activities of spinal trigeminal nucleus oralis convergent neurons in halothane-anesthetized rats. Morphine depressed the C-fiber-evoked responses of spinal trigeminal nucleus oralis convergent neurons in a dose-related (3-12 mg/kg range) and naloxone-reversible fashion. The ED50 was 6.1 mg/kg, a dose similar to that found in the spinal horn. The observed strong depressive action of morphine on noxious-evoked activities of spinal trigeminal nucleus oralis neurons is consistent with our previous statement, based on electrophysiological studies, that this region plays an important role in the transmission of trigeminal nociceptive information. The effect of morphine on the spinal trigeminal nucleus oralis neurons is discussed in relation to its possible site and mechanism of action.

Animals↗
PubMed2002

Induction of Fos protein-like immunoreactivity in the trigeminal spinal nucleus caudalis and upper cervical cord following noxious and non-noxious mechanical stimulation of the whisker pad of the rat with an inferior alveolar nerve transection.

After transection of the inferior alveolar nerve (IAN: the third branch of the trigeminal nerve), the whisker pad area, which is innervated by the second branch of the trigeminal nerve, showed hypersensitivity to mechanical stimulation. Two days after IAN transection, the threshold intensity for escape behavior to mechanical stimulation of the ipsilateral whisker pad area was less than 1.0 g, a sign of allodynia, and returned to the preoperative level (preoperative threshold: 52.0 g) at 32 days after surgery. This decrement of escape threshold lasted for more than 3 weeks. The whisker pad area contralateral to the IAN transection also showed a decrease in escape threshold to non-noxious mechanical stimulation as compared with sham-operated rats. However, the change in threshold intensity for the side contralateral to transection was not as pronounced as that on the ipsilateral side. Fos protein-like immunoreactive (LI) cells were observed in the superficial laminae but not dominant in deeper laminae of the trigeminal spinal nucleus caudalis (Vc) and the first segment of the spinal cord (C1) after non-noxious mechanical stimulation of the whisker pad area in the rats with IAN transection. Fos protein-LI cells were expressed bilaterally in the Vc and C1, but were more numerous on the ipsilateral side to transection than on the contralateral side. The largest number of Fos protein-LI cells was observed at 2400 microm caudal from the trigeminal subnucleus interporalis (Vi)-Vc border both in ipsilateral and contralateral sides. The number of Fos protein-LI cells increased after application of 1, 4, and 16 g stimuli as compared to rats without mechanical stimulation. Furthermore, an extensively greater number of Fos protein-LI cells were expressed both in superficial and deep laminae of the bilateral Vc and C1 of the spinal cord after subcutaneous injection of mustard oil into the whisker pad. Fos protein expression after mustard oil injection was much stronger than that observed after any mechanical stimulation in the rats with IAN transection. These data suggest that the change in the numbers and spatial arrangement of nociceptive neurons in the Vc and C1 after IAN transection reflect the development of mechanical hyperalgesia in the area adjacent to the IAN innervated region.

Animals↗
PubMed1986

Effects of superfusion of morphine and enkephalins on the activity of single units in the spinal trigeminal nucleus and cuneate nucleus of cat.

The effects of superfusion of morphine, met-enkephalin and D-ala2-met5-enkephalinamide on the spontaneous neural discharge rates of units in the spinal trigeminal nucleus and cuneate nucleus of decerebrate cats were studied. The drugs were superfused onto the dorsum of the exposed surface of the caudal medulla overlying these nuclei. Some of these neurons were identified by their response to innocuous mechanical stimuli delivered to the skin. In the caudal spinal trigeminal nucleus, morphine caused a dose-dependent suppression of the spontaneous discharge rate in the majority of the neurons studied. Endogenous opiate peptide, met-enkephalin or its synthetic analogue, D-ala2-met5-enkephalinamide caused an initial reduction, followed by a rebound of the discharge rate to the control value. These depressant effects of morphine and enkephalins were antagonized by concomitant superfusion of the opiate antagonist naloxone. In the main cuneate nucleus, however, similar doses of morphine, met-enkephalin and D-ala2-met5-enkephalinamide have little if any significant effect on the spontaneous activity of the neurons studied. These results provide electrophysiological evidence for the presence of opiate receptors in the caudal spinal trigeminal nucleus and the relative lack of such receptors in the main cuneate nucleus.

Action Potentials↗
PubMed1987

The nuclei of origin of brainstem enkephalin and cholecystokinin projections to the spinal trigeminal nucleus of the rat.

The sites of origin of brain stem enkephalin and cholecystokinin projections to the rodent spinal trigeminal nucleus were studied utilizing the combined retrograde transport-peroxidase antiperoxidase immunohistochemical technique. Several brain stem areas were found to contain enkephalin-like immunoreactive double-labeled neurons following injection of wheat germ agglutinin-horseradish peroxidase or horseradish peroxidase into the spinal trigeminal nucleus. The largest numbers of enkephalin double-labeled neurons were identified in the nucleus pontis oralis, nucleus raphe medianis, medial vestibular nucleus and the midbrain periaqueductal gray. Enkephalin projections to the spinal trigeminal nucleus were also found to originate from the nucleus solitarius, nucleus raphe pallidus, nucleus raphe magnus, nucleus raphe dorsalis, nucleus reticularis paragigantocellularis, nucleus reticularis gigantocellularis pars alpha and the deep mesencephalic nucleus. In contrast to the numerous sources of enkephalin input to the spinal trigeminal nucleus, cholecystokinin projections to this region were limited to four brain stem nuclei. These included the nucleus solitarius, raphe obscurus, nucleus paragigantocellularis and the ventral reticular nucleus of the medulla. The finding that only a small number of brain stem cholecystokinin-like immunoreactive neurons project to the spinal trigeminal nucleus supports the hypothesis that most of the cholecystokinin input to the spinal trigeminal nucleus arises from primary afferent trigeminal fibers. The spinal trigeminal nucleus is known to play a role in processing sensory information and in the transmission of orofacial nociception. The present study identifies several brain stem sites which provide enkephalin and/or cholecystokinin input to the spinal trigeminal nucleus. Several of these nuclei have been implicated as components of the endogenous pain control system and the present results raise the possibility that they may modulate incoming orofacial nociception by releasing the endogenous opioid, enkephalin. Cholecystokinin, on the other hand, has been demonstrated in other studies to attenuate the action of opiates and thus may play an opposing role in the spinal trigeminal nucleus.

Animals↗
PubMed1994

NMDA receptor mRNA expression in NOS-containing neurons in the spinal trigeminal nucleus of the rat.

The spinal trigeminal nucleus (STN) is involved in the transmission of orofacial sensory information. Nitric oxide (NO), an important neuromessenger, and the glutamate receptor subtype, NMDA NR1, have been implicated in nociception in the STN. However, the anatomical relationship of NO and NMDA NR1 has not been investigated within this nucleus. Using both immunocytochemical (against NO synthase; NOS) and in situ hybridization studies of NMDA NR1 receptor mRNA, we found that NOS-containing neurons in the STN expressed more mRNA for NR1 than did non-NOS-containing neurons in the STN. These data suggest that NMDA activation may lead to NO production in the STN and is consistent with previous studies, implicating both NMDA and NO in nociception.

Amino Acid Oxidoreductases↗
PubMed1978

Synapse development within the spinal trigeminal nucleus.

Pars interpolaris of the spinal trigeminal nucleus of kittens has been studied with the electron microscope at birth and at several subsequent ages during the first month of life. Attention has been given to ultrastructural maturational changes that occur in this neuropil, especially events in synaptogenesis. The results of this investigation include the following observations: (1) the neuropil, even at the earliest ages studied (three-hour-old kittens), is strikingly mature, necessitating a quantitative assessment in order to determine subtle developmental changes in synaptic patterns; (2) the number of axoaxonic contacts at birth are few, and their emergence is essentially a postnatal phenomenon; (3) it appears that the immature Gray type II or symmetrical synapse possesses distinct cleft material and dense, parallel membrane specializations. Synaptic vesicle accumulation at this contact appears to occur after the membrane specializations have formed. A previous study by Kerr26 has shown a reduced potential for primary afferent reorganization with the spinal trigeminal nucleus when kittens are subjected to trigeminal rhizotomy after three days of age. Our observations on the development of axoaxonic synaptic arrangements in the neonatal period may provide an explanation for these earlier results.

Age Factors↗