Trigeminal Nuclear Complex Research Articles

Single axonal characterization of trigeminocerebellar projection patterns in the mouse.

The cerebellar projection from the trigeminal nuclear complex is one of the major populations of the cerebellar inputs. Although this projection is essential in cerebellar functional processing and organization, its morphological organization has not been systematically clarified. The present study addressed this issue by lobule-specific retrograde neuronal labeling and single axonal reconstruction with anterograde labeling. The cerebellar projection arose mainly from the interpolaris subdivision of the spinal trigeminal nucleus (Sp5I) and the principal trigeminal sensory nucleus (Pr5). Although crus II, paramedian lobule, lobule IX, and simple lobule were the major targets, paraflocculus, and other lobules received some projections. Reconstructed single trigeminocerebellar axons showed 77.8 mossy fiber terminals on average often in multiple lobules but no nuclear collaterals. More terminals were located in zebrin-negative or lightly-positive compartments than in zebrin-positive compartments. While Pr5 axons predominantly projected to ipsilateral crus II, Sp5I axons projected either predominantly to crus II and paramedian lobule often bilaterally, or predominantly to lobule IX always ipsilaterally. Lobule IX-predominant-type Sp5I neurons specifically expressed Gpr26. Gpr26-tagged neuronal labeling produced a peculiar mossy fiber distribution, which was dense in the dorsolateral lobule IX and extending transversely to the dorsal median apex in lobule IX. The projection to the cerebellar nuclei was observed in collaterals of ascending Sp5I axons that project to the diencephalon. In sum, multiple populations of trigeminocerebellar projections showed divergent projections to cerebellar lobules. The projection was generally complementary with the pontine projection and partly matched with the reported orofacial receptive field arrangement.

Proceedings #21: Specific Patterns of Current Flow Generated by Different tDCS Montages in the Midbrain and in the Trigeminal Brainstem Sensory Nuclear Complex

Proceedings #21: Specific Patterns of Current Flow Generated by Different tDCS Montages in the Midbrain and in the Trigeminal Brainstem Sensory Nuclear Complex

Lecture of the specialization cycle on reflexotherapy "Headache: Clinic, Diagnosis and Treatment"

In order to find out the mechanisms of headache, the issue of innervations of craniocervical site structures is important, as irritation of any of them may cause headache. The parenchyma of the brain and the skull bones have only a small amount of nerve fibers that carry nociceptive information, whereas in the walls of the arteries, vascular and solid brain sines and sinuses, there is the largest number of nociceptors. Nerves of the orophacial region transmit nociceptive information to the trunk of the brain (through thistles, cranial and stony nodes), where through the trigeminal nuclear complex and the dorsal lemniscus system the transmission of pain information to the back of the thalamus is carried out (in addition, it is transmitted by the spinothalamic pathway and thalamic projections from caudal abider of the trigeminal nuclear complex). Thus, the important role of the trigeminal nerve system in the transmission of information to the central nervous system has been proved, the fact of innervation of the brain vessels of the trigeminal nerves is confirmed, which confirms the activity of the trimeric and vascular system, which is the main system that perceives pain impulse and leads to changes in the tone of the vascular wall of the head . This mechanism has the maximum value in the case of migraines headache, which made it possible to put forward the trigeminal vascular theory of migraine pathogenesis. Thalamic pain is a consequence of lesions of the lateral thalamus, including its posterior lateral ventral nucleus, and on the opposite side of the lesion there is a constant burning pain that is unclearly localized, amplified by attacks with emotional stress, sharp acoustic, visual, olfactory stimuli. The study of pathogenetic and diagnostic criteria of pain is an important component in the differential diagnosis of nociception, since this component is an important component in the practice and treatment of reflexology therapists in the selection of diagnostic criteria and therapeutic tactics / Considering the classification, clinical subtype, special characteristics of the pathogenesis of pain development has an important diagnostic importance for preventive measures in the practice of doctors.

Trigeminal nerve stimulation induces Fos immunoreactivity in selected brain regions, increases hippocampal cell proliferation and reduces seizure severity in rats

Sites and mechanisms by which trigeminal nerve stimulation (TNS) exerts beneficial effects on symptoms of drug-resistant epilepsy and depression are still unknown. Effects of short-term TNS on brain regions involved in the physiopathology of these disorders were investigated in this study.Forty male rats were assigned to three groups: TNS (undergoing electrical stimulation of the left infraorbitary nerve via surgically implanted cuff electrodes); Sham (undergoing surgical procedure but without a stimulation); Naïve rats. The effects of TNS (3-hour session; 30-s ON, 5-min OFF; 30Hz; 500μs; 2mA) were evaluated on: (i) behavioral pattern of pentylenetetrazole (PTZ)-induced seizures as measured by the Racine scale; (ii) c-Fos-like immunoreactivity in discrete brain areas; (iii) hippocampal cell proliferation by bromodeoxyuridine (BrdU)-like immunoreactivity.In comparison with Sham groups, TNS significantly decreased the duration of PTZ-induced seizures (p<0.05) and promoted a faster recovery (p<0.001) by reducing the most severe seizure types. In the TNS group the number of c-Fos-labeled cells was significantly increased (p<0.001) in the trigeminal nuclear complex, nucleus of the solitary tract, locus coeruleus, dorsal raphe nucleus, hippocampus, amygdala, endopiriform nucleus, entorhinal cortex and sensorimotor cortex. In the TNS group the number of BrdU-positive cells in the dentate gyrus was significantly greater with respect to both Naïve and Sham groups.Data show that acute TNS effectively counteracted PTZ-induced seizures and boosted hippocampal cell proliferation in rats. TNS increased c-Fos-like immunoreactivity in brainstem and forebrain structures which play a pivotal role in the physiopathology of epilepsy and depression.

The role of trigeminal nucleus caudalis orexin 1 receptors in orofacial pain transmission and in orofacial pain-induced learning and memory impairment in rats

It is widely accepted that the spinal trigeminal nuclear complex, especially the subnucleus caudalis (Vc), receives input from orofacial structures. The neuropeptides orexin-A and -B are expressed in multiple neuronal systems. Orexin signaling has been implicated in pain-modulating system as well as learning and memory processes. Orexin 1 receptor (OX1R) has been reported in trigeminal nucleus caudalis. However, its roles in trigeminal pain modulation have not been elucidated so far. This study was designed to investigate the role of Vc OX1R in the modulation of orofacial pain as well as pain-induced learning and memory deficits. Orofacial pain was induced by subcutaneous injection of capsaicin in the right upper lip of the rats. OX1R agonist (orexin-A) and antagonist (SB-334867-A) were microinjected into Vc prior capsaicin administration. After recording nociceptive times, learning and memory was investigated using Morris water maze (MWM) test. The results indicated that, orexin-A (150pM/rat) significantly reduced the nociceptive times, while SB334867-A (80nM/rat) exaggerated nociceptive behavior in response to capsaicin injection. In MWM test, capsaicin-treated rats showed a significant learning and memory impairment. Moreover, SB-334867-A (80nM/rat) significantly exaggerated learning and memory impairment in capsaicin-treated rats. However, administration of orexin-A (100pM/rat) prevented learning and memory deficits. Taken together, these results indicate that Vc OX1R was at least in part involved in orofacial pain transmission and orexin-A has also a beneficial inhibitory effect on orofacial pain-induced deficits in abilities of spatial learning and memory.

Vessel diameter measurements at the medullary brainstem in vivo as an index of trigeminal activity

Activity within the CNS can be quantified by a variety of methods. Here, we present an indirect method utilizing the neuro-vascular coupling via a continuous measurement of the vessel diameter. In anaesthetized rats, induced neuronal activity in the trigeminal system could be detected via arterial diameter measurements at the back of the medullary brainstem. Building upon the previously described diameter plugin, in images aligned to compensate for ventilation and heart-rate associated movement, automated processing allowed an evaluation immediately after acquisition. Electrical stimulation of facial trigeminal areas or the cranial dura mater caused vasodilatation of arteries in the dorsal medullary brainstem, which was abolished after application of the CGRP receptor antagonist olcegepant. No change in diameter was observed in corresponding veins. Intravenous infusion of sodium sulfide, which induces nitroxyl formation, also induced vasodilatation of brainstem-supplying arteries. Both experiments show a functional role of CGRP in the trigeminal nuclear brainstem complex. The presented method allows estimating central activity at the spinal level by vascular responses.

Organization of the spinal trigeminal nucleus in star‐nosed moles

Somatosensory inputs from the face project to multiple regions of the trigeminal nuclear complex in the brainstem. In mice and rats, three subdivisions contain visible representations of the mystacial vibrissae, the principal sensory nucleus, spinal trigeminal subnucleus interpolaris, and subnucleus caudalis. These regions are considered important for touch with high spatial acuity, active touch, and pain and temperature sensation, respectively. Like mice and rats, the star-nosed mole (Condylura cristata) is a somatosensory specialist. Given the visible star pattern in preparations of the star-nosed mole cortex and the principal sensory nucleus, we hypothesized there were star patterns in the spinal trigeminal nucleus subnuclei interpolaris and caudalis. In sections processed for cytochrome oxidase, we found star-like segmentation consisting of lightly stained septa separating darkly stained patches in subnucleus interpolaris (juvenile tissue) and subnucleus caudalis (juvenile and adult tissue). Subnucleus caudalis represented the face in a three-dimensional map, with the most anterior part of the face represented more rostrally than posterior parts of the face. Multiunit electrophysiological mapping was used to map the ipsilateral face. Ray-specific receptive fields in adults matched the CO segmentation. The mean areas of multiunit receptive fields in subnucleus interpolaris and caudalis were larger than previously mapped receptive fields in the mole's principal sensory nucleus. The proportion of tissue devoted to each ray's representation differed between the subnucleus interpolaris and the principal sensory nucleus. Our finding that different trigeminal brainstem maps can exaggerate different parts of the face could provide new insights for the roles of these different somatosensory stations.

Cessation Of Migraine After Thalamic Infarction

The thalamus is a key center in migraine: nociceptive signals are conveyed there from the trigeminal brainstem nuclear complex. Not surprisingly, it is activated during the acute attack and some drugs like triptanss or propanolol elicit their pain-relief effect by locally activating thalamic neurons. By the same token, thalamic structural lesions could potentially modify the course of this disorder. We support this possibility by a clinical case. A 65 year-old woman suffered from migraine without aura and migraine with aura from her twenties. Her course was chronic and refractory to preventive and to sympomatic treatment, so that in the last four years she had abandoned neurological follow-up and drug intake. In this situation, she was affected by a painlees episode of right hemiparesis and paresthesias, without visual symtoms and clearly distinctive from her auras. An acute left thalamic infarction, localized in its anteromedial area, was disclosed. Motor recovery was good. In addition, 15 months later she remained completely free of headache and of aura, with no other intervening treatment. The interruption of the pain signals from the thalamus is the proposed mechanism for making the pain recedes. According to the lesion, a differentiation of the cingular, medial temporal and prefrontal cortex is suggested. It could be worth seeking the relationship between migraine and its evolution in larger series of thalamic infractions.

Distinct Development of the Trigeminal Sensory Nuclei in Platypus and Echidna

Both lineages of the modern monotremes have been reported to be capable of electroreception using the trigeminal pathways and it has been argued that electroreception arose in an aquatic platypus-like ancestor of both modern monotreme groups. On the other hand, the trigeminal sensory nuclear complex of the platypus is highly modified for processing tactile and electrosensory information from the bill, whereas the trigeminal sensory nuclear complex of the short-beaked echidna (Tachyglossus aculeatus) is not particularly specialized. If the common ancestor for both platypus and echidna were an electroreceptively and trigeminally specialized aquatic feeder, one would expect the early stages of development of the trigeminal sensory nuclei in both species to show evidence of structural specialization from the outset. To determine whether this is the case, we examined the development of the trigeminal sensory nuclei in the platypus and short-beaked echidna using the Hill and Hubrecht embryological collections. We found that the highly specialized features of the platypus trigeminal sensory nuclei (i.e. the large size of the principal nucleus and oral part of the spinal trigeminal nuclear complex, and the presence of a dorsolateral parvicellular segment in the principal nucleus) appear around the time of hatching in the platypus, but are never seen at any stage in the echidna. Our findings support the proposition that the modern echidna and platypus are derived from a common ancestor with only minimal trigeminal specialization and that the peculiar anatomy of the trigeminal sensory nuclei in the modern platypus emerged in the ornithorhynchids after divergence from the tachyglossids.

Differential activation of mitogen-activated protein kinases and glial cells in the trigeminal sensory nuclear complex following lingual nerve injury

Differential activation of mitogen-activated protein kinases and glial cells in the trigeminal sensory nuclear complex following lingual nerve injury

Amygdalotrigeminal projection in the rat: An anterograde tracing study

Previous neurophysiological studies have demonstrated that the amygdala has a direct influence upon trigeminal motoneuron activity. The existence of a direct amygdalotrigeminal pathway in rats was proved by anterograde tracing with the neuroanatomical tracer, biotinylated dextran amine (BDA). After ipsilateral BDA application to the central nucleus of the amygdala (AmCe), widespread ipsilateral projections emerging from its medial subnucleus were traced to the trigeminal brainstem nuclear complex, including the principal sensory (Pr5) and mesencephalic trigeminal nucleus (Me5), and their premotoneurons and interneurons, located in the supratrigeminal, intertrigeminal and peritrigeminal nuclei. Sparse BDA-labeled axons and their terminals were also distributed in the contralateral Pr5, interpolar and caudal subnuclei of the spinal trigeminal nucleus. The central lateral amygdaloid nucleus gives rise to a light ipsilateral projection to the pontine part of the Me5. The present data indicate that AmCe sends massive efferents to the trigeminal nuclei in the brainstem, wherein its medial subnucleus sends the major input to them. The medial amygdaloid nucleus sparsely innervates Me5 neurons, specifically those located in its mesencephalic portion, while basomedial and basolateral efferents do not target the trigeminal nuclear complex. These results suggest that the amygdaloid input may modulate the activity of trigeminal sensory and motor neurons and, thus, the amygdala is possibly involved in the control of masticatory behavior.

Intranasal TRPV1 agonist capsaicin challenge and its effect on c-fos expression in the guinea pig brainstem

Central neuronal interaction seems to play a role in pathogenesis of upper airway cough syndrome. In the guinea pig model we used the method c-fos expression to identify neurons involved in processing of nociceptive nasal stimuli and their contribution to enhancement of cough. 21 spontaneously breathing, urethane anaesthetized animals were used. The controls received intranasal saline, stimulation group received capsaicin (15 microl, 50 microM), and not-treated group was free of nasal challenge. After 2 h animals were deeply anaesthetized, exsanguinated and transcardially perfused with saline and paraformaldehyde. The brainstems were removed, post-fixed, and slices were processed immunohistochemically for c-fos. In capsaicin group the FLI was detected in the nTs 0.5 mm caudal, 1.5 mm lateral to the obex, the area postrema, LRN and VRG. Intensive FLI was identified in trigeminal nuclear complex. Mean number of FOS positive neurons per section was significantly higher in capsaicin group than that in no-treatment controls or saline controls at the level of obex (p<0.01). Neurons of nTs and VRG clearly activated after nasal provocation may participate in enhancement of cough.

Distinctive response of CNS glial cells in oro-facial pain associated with injury, infection and inflammation.

Oro-facial pain following injury and infection is frequently observed in dental clinics. While neuropathic pain evoked by injury associated with nerve lesion has an involvement of glia/immune cells, inflammatory hyperalgesia has an exaggerated sensitization mediated by local and circulating immune mediators. To better understand the contribution of central nervous system (CNS) glial cells in these different pathological conditions, in this study we sought to characterize functional phenotypes of glial cells in response to trigeminal nerve injury (loose ligation of the mental branch), infection (subcutaneous injection of lipopolysaccharide-LPS) and to sterile inflammation (subcutaneous injection of complete Freund's adjuvant-CFA) on the lower lip. Each of the three insults triggered a specific pattern of mechanical allodynia. In parallel with changes in sensory response, CNS glial cells reacted distinctively to the challenges. Following ligation of the mental nerve, both microglia and astrocytes in the trigeminal nuclear complex were highly activated, more prominent in the principal sensory nucleus (Pr5) and subnucleus caudalis (Sp5C) area. Microglial response was initiated early (days 3-14), followed by delayed astrocytes activation (days 7-28). Although the temporal profile of microglial and astrocyte reaction corresponded respectively to the initiation and chronic stage of neuropathic pain, these activated glial cells exhibited a low profile of cytokine expression. Local injection of LPS in the lower lip skin also triggered a microglial reaction in the brain, which started in the circumventricular organs (CVOs) at 5 hours post-injection and diffused progressively into the brain parenchyma at 48 hours. This LPS-induced microglial reaction was accompanied by a robust induction of IκB-α mRNA and pro-inflammatory cytokines within the CVOs. However, LPS induced microglial activation did not specifically occur along the pain signaling pathway. In contrast, CFA injection led to minor microglial morphological changes and an induction of IκB-α mRNA in the CVO regions; a significant increase in IL-1β and IL-6 mRNA started only at 48 hours post-injection, when the induced pain-related behavior started to resolve. Our detailed analysis of CNS glial response clearly revealed that both nerve injury and oro-facial infection/inflammation induced CNS glial activation, but in a completely different pattern, which suggests a remarkable plasticity of glial cells in response to dynamic changes in their microenvironment and different potential involvement of this non-neuronal cell population in pathological pain development.

How triggers trigger acute migraine attacks: A hypothesis

A trigger is an integral part of any acute migraine attack. In this article, the author argues that triggers, identifiable or not, must be present in all attacks of migraine headache. It is hypothesized that triggers, internal or external, induce the onset of cortical spreading depression (CSD) in a pre-existing hyper-excitable cortex of a migraine brain, initiating the process of pain generation. The author hypothesizes on a second site of action of triggers at the level of trigeminal nuclear complex (TNC) in brain stem, the cell station of second order neuron pathway for migraine pain transmission to the sensory cortex. The author suggests existence of a hypothetical 'gate' at TNC level where incoming trigeminal migraine pain impulses would 'compete' with descending inhibitory signals from brain stem pain modulatory neurons, to get entry into the central nervous system. The author draws analogy with the 'gate control' mechanism operative at the dorsal horn level for spinally transmitted somatic and visceral pain. It is suggested that the hypothetical 'gate' at TNC level is controlled by activity of 5HT receptors, thus supporting the concept of an additional site of action of triptans in aborting acute migraine pain. The suggested hypothesis on mechanism of action of triggers, offers theoretical basis for efficacy of currently available pharmacologic and non-pharmacologic therapies for abortive and prophylactic treatment of migraine.

Migraine‐related vertigo: a common and important disorder

Migraine-related vertigo (MRV) or vestibular migrainehas had a difficult history being understood as a dis-order. But now with better recognition, it may be givenits due in clinical assessments and research. Dizziness isthe second most common neurologic complaint andMRV is of the most common presenting causes ofvertigo in clinics for dizziness [1]. In the most simplisticview, MRV is a syndrome of recurrent vertigo attacksthat occur in people who have the diagnosis of migraineheadache or aura. While it is easy to assert that there isa disease of vertigo attacks on the basis of migraine, it ishard to prove. Migraine headache itself is well-knownto be difficult to precisely specify: even the InternationalHeadache Society criteria are a collection of mix-and-match symptom features that add up to a diagnosis [2].There has been no equivalent consensus on the diag-nosis of MRV, however, Neuhauser [3] has come upwith a reasonable check-list of determining that thevertigo symptoms that are not explained by other ver-tigo-causing disorders and then verifying that thediagnostic criteria for migraine headaches are met.Whilst we appear to be approaching more precisepathophysiologic mechanisms for migraine headaches[4], there is less such convergence for MRV. Indeed,studies of such patients fail in simplest mechanistic levelof neurological disorder description: central or periph-eral? A heroic study by Lempert!s group [5] examinedMRV patients for nystagmus during attacks. Thefindings were: some central, some peripheral, someboth. The pathophysiology of migraine headachesseems to localize to the trigeminal nuclear complex inthe brainstem, a region closely apposed to vestibularnuclei. However, there is the scientifically unfortunatefinding of reliably measurable peripheral damage in thevestibular system in MRV patients. Some 20–40% ofthem show attenuated unilateral responses to caloricstimuli [6]. Thus, while there may be some central braincomponent to MRV, these peripheral effects need to beexplained. Perhaps like the vascular phenomena ofmigraine HA, these findings are epiphenomena [4]. Thiswould explain the inconsistent finding of peripheralchanges.Further discouragement in the realm of MRV isfound in the search for definitive treatment and forprophylaxis. There have been a number of studies ofclassical migraine headache treatments used inmanagement of MRV and there is some cross-over ofeffectiveness. In my own experience, lifestyle man-agement (diet, sleep and exercise) and traditionalmigraine headache treatments, such as verapamil andpropranolol, work acceptably well. However, thereis much trial-and-error in the regular use of thesemedications.Most frustrating in MRV are patients who havedrastic impairments of their lives and who are resistantto therapy. I believe it is important to publicize thedevastation that MRV can cause patients throughemotional stress and life disruption that result from it.Neuhauser notes a group that I very frequentlyencounter in my vertigo disorders clinic: perimeno-pausal women who had migraine headaches earlier intheir lives [3]. Such patients seem to be particularly re-calcitrant to treatment. The recent recognition thatestrogen and progesterone are very active neuro–hu-moral and neurotransmitter modulators [7,8] re-en-forces the idea that like migraine headache, MRV mayhave a strong brain component that is directly affectedby reproductive hormones. I am optimistic that hor-monal management regimens will be found that willreduce triggering of migraine headaches and MRV.An important clinical experience I have is the resis-tance of patients to the diagnosis that they havemigraines. Perhaps with reason, they do not want to belabeled as having a genetically determined and thus life-long disorder that upsets many lives. The resistance isstrong in patients presenting with vertigo. Many com-plain they don!t really have a problem with headaches,how can they have migraine? In the minority who havemigraine visual aura, which is pathognomonic formigraine,theexplanationis easier.Especiallyin commonmigraine, a useful approach in discussing it withpatients is to do the appropriate medical diagnosticprocedure: rule out other vertigo causing disorders andthen consider migraine.Acceptance by patients and by clinicians of this com-mon disorder will lead to understanding of its life effectsandtorenewedeffortstounderstandandtreatthisdisease.

Differential activation of the human trigeminal nuclear complex by noxious and non‐noxious orofacial stimulation

There is good evidence from animal studies for segregation in the processing of non-nociceptive and nociceptive information within the trigeminal brainstem sensory nuclear complex. However, it remains unknown whether a similar segregation occurs in humans, and a recent tract tracing study suggests that this segregation may not exist. We used functional magnetic resonance imaging (fMRI) to define and compare activity patterns of the trigeminal brainstem nuclear complex during non-noxious and noxious cutaneous and non-noxious and noxious muscle orofacial stimulation in humans. We found that during cutaneous pain, signal intensity increased within the entire rostrocaudal extent of the spinal trigeminal nucleus (SpV), encompassing the ipsilateral oralis (SpVo), interpolaris (SpVi) and caudalis (SpVc) subdivisions. In contrast, muscle pain did not activate SpVi, but instead activated a discrete region of the ipsilateral SpVo and SpVc. Further, muscle noxious stimulation activated a region of the ipsilateral lateral pons in the region of the trigeminal principal sensory nucleus (Vp). Innocuous orofacial stimulation (lip brushing) also evoked a significant increase in signal intensity in the ipsilateral Vp; however, non-noxious muscle stimulation showed no increase in signal in this area. The data reveal that orofacial cutaneous and muscle nociceptive information and innocuous cutaneous stimulation are differentially represented within the trigeminal nuclear complex. It is well established that cutaneous and muscle noxious stimuli evoke different perceptual, behavioural and cardiovascular changes. We speculate that the differential activation evoked by cutaneous and muscle noxious stimuli within the trigeminal sensory complex may contribute to the neural basis for these differences.

Morphine Increases Acetylcholine Release in the Trigeminal Nuclear Complex

The trigeminal nuclear complex (V) contains cholinergic neurons and includes the principal sensory trigeminal nucleus (PSTN) which receives sensory input from the face and jaw, and the trigeminal motor nucleus (MoV) which innervates the muscles of mastication. Pain associated with pathologies of V is often managed with opioids but no studies have characterized the effect of opioids on acetylcholine (ACh) release in PSTN and MoV. Opioids can increase or decrease ACh release in brainstem nuclei. Therefore, the present experiments tested the 2-tailed hypothesis that microdialysis delivery of opioids to the PSTN and MoV significantly alters ACh release. Using a within-subjects design and isoflurane-anesthetized Wistar rats (n=53), ACh release in PSTN during microdialysis with Ringer's solution (control) was compared to ACh release during dialysis delivery of the sodium channel blocker tetrodotoxin, muscarinic agonist bethanechol, opioid agonist morphine, mu opioid agonist DAMGO, antagonists for mu (naloxone) and kappa (nor-binaltorphimine; nor-BNI) opioid receptors, and GABAA antagonist bicuculline. Tetrodotoxin decreased ACh, confirming action potential-dependent ACh release. Bethanechol and morphine caused a concentration-dependent increase in PSTN ACh release. The morphine-induced increase in ACh release was blocked by nor-BNI but not by naloxone. Bicuculline delivered to the PSTN also increased ACh release. ACh release in the MoV was increased by morphine, and this increase was not blocked by naloxone or nor-BNI. These data comprise the first direct measures of ACh release in PSTN and MoV and suggest synaptic disinhibition as one possible mechanism by which morphine increases ACh release in the trigeminal nuclei.

The Motor Atonia of REM Sleep: A Critical Topics Forum

The Motor Atonia of REM Sleep: A Critical Topics Forum

Unilateral ligature-induced periodontitis influences the expression of neuropeptides in the ipsilateral and contralateral trigeminal ganglion in rats

Objectives Expression of neuronal neuropeptides in inflammatory conditions is altered. The changes in expression of substance P (SP) and calcitonin gene-related peptide (CGRP) in ipsilateral and contralateral trigeminal ganglion (TG) neurons were investigated by immunohistochemistry one week after unilateral ligature-induced periodontitis in rats. Design A retrograde nerve tracer Fluorogold (FG) was applied into the gingival sulcus of the second maxillary molar to identify the neurons in TG that specifically innervate the inflamed gingivomucosa. In addition, neurons from the corresponding maxillary and the adjacent mandibular–ophthalmic regions in TG were analysed. Results Statistically significantly higher frequencies of CGRP-positive neurons, regardless of their size, were found in TG ipsilateral to the periodontitis (83% and 73% in FG-labelled and maxillary regions, respectively) than in the control group without periodontitis (52% and 42% in FG-labelled and maxillary regions, respectively). The frequency of small FG-labelled SP-positive neurons in the ipsilateral TG (60%) was significantly higher than in the control TG (25%). In the contralateral TG the frequency of CGRP-positive neurons in maxillary region (66%) was significantly higher than in the control group. Surprisingly, the number of SP-positive neurons in all regions of contralateral TG decreased when compared to control and ipsilateral TGs. Conclusions Taken together, these results implicate a role of neurogenic component in the pathogenesis of periodontitis. The contralateral response in the TG could be mediated through the transmedian neurological pathways crossing in the trigeminal nuclear complex or through the systemic inflammatory reaction and the activation of the so called “neuro-immune axis”.

Patterns of convergence in rat zona incerta from the trigeminal nuclear complex: light and electron microscopic study.

In contrast to the restricted receptive field (RF) properties of the ventral posteromedial nucleus (VPM), neurons of the ventral thalamus zona incerta (ZI) have been shown to exhibit multiwhisker responses that vary from the ventral (ZIv) to the dorsal (ZId) subdivision. Differences in activity may arise from the trigeminal nuclear complex (TNC) and result from subnucleus specific inputs via certain cells of origin, axon distribution patterns, fiber densities, bouton sizes, or postsynaptic contact sites. We tested this hypothesis by assessing circuit relationships among TNC, ZI, and VPM. Results from tracer studies show that, 1) relative to ZId, the trigeminal projection to ZIv is denser and arises predominantly from the principalis (PrV) and interpolaris (SpVi) subdivisions; 2) the incertal projection from TNC subnuclei overlaps and covers most of ZIv; 3) two sets of PrV axons terminate in ZI: a major subtype, possessing bouton-like swellings, and a few fine fibers, with minimal specialization; 4) both PrV and SpVi terminals exhibit asymmetric endings and preferentially target dendrites of ZI neurons; 5) small and large neurons in PrV are labeled after retrograde injections into ZI; 6) small PrV cells with incertal projections form a population that is distinct from those projecting to VPM; and 7) approximately 30-50% of large cells in PrV send collaterals to ZI and VPM. These findings suggest that, 1) although information to ZI and VPM is essentially routed along separate TNC circuits, streams of somatosensory code converge in ZI to establish large RFs, and 2) subregional differences in ZI response profiles are attributable in part to TNC innervation density.