The Experts below are selected from a list of 216 Experts worldwide ranked by ideXlab platform
Marta Bianciardi - One of the best experts on this subject based on the ideXlab platform.
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probabilistic template of the lateral parabrachial Nucleus medial parabrachial Nucleus vestibular nuclei complex and medullary viscero sensory motor nuclei complex in living humans from 7 tesla mri
Frontiers in Neuroscience, 2020Co-Authors: Kavita Singh, I Indovina, Jean C Augustinack, Kimberly Nestor, Maria G Garciagomar, Jeffrey P Staab, Marta BianciardiAbstract:The lateral parabrachial Nucleus, medial parabrachial Nucleus, vestibular nuclei complex and medullary viscero-sensory-motor nuclei complex (the latter including among others the Solitary Nucleus, vagus nerve Nucleus, and hypoglossal Nucleus) are anatomically and functionally connected brainstem gray-matter structures that convey signals across multiple modalities between the brain and the spinal cord to regulate vital bodily functions. It is remarkably difficult to precisely extrapolate the location of these nuclei from ex vivo atlases to conventional 3 Tesla in vivo images; thus, a probabilistic brainstem template in stereotaxic neuroimaging space in living humans is needed. We delineated these nuclei using single-subject high contrast 1.1 mm isotropic resolution 7 Tesla MRI images. After precise coregistration of nuclei labels to stereotaxic space, we generated a probabilistic template of their anatomical locations. Finally, we validated the nuclei labels in the template by assessing their inter-rater agreement, consistency across subjects and volumes. We also performed a preliminary comparison of their location and microstructural properties to histologic sections of a postmortem human brainstem specimen. In future, the resulting probabilistic template of these brainstem nuclei in stereotaxic space may assist researchers and clinicians in evaluating autonomic, vestibular and viscero-sensory-motor nuclei structure, function and connectivity in living humans using conventional 3 Tesla MRI scanners.
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probabilistic atlas of the lateral parabrachial Nucleus medial parabrachial Nucleus vestibular nuclei complex and medullary viscero sensory motor nuclei complex in living humans from 7 tesla mri
bioRxiv, 2019Co-Authors: Kavita Singh, I Indovina, Jean C Augustinack, Kimberly Nestor, Maria G Garciagomar, Jeffrey P Staab, Marta BianciardiAbstract:Abstract The lateral parabrachial Nucleus, medial parabrachial Nucleus, vestibular nuclei complex and medullary viscero-sensory-motor nuclei complex (the latter including among others the Solitary Nucleus, vagus nerve Nucleus, and hypoglossal Nucleus) are anatomically and functionally connected brainstem gray-matter structures that convey signals across multiple modalities between the brain and the spinal cord to regulate vital bodily functions. It is remarkably difficult to precisely extrapolate the location of these nuclei from ex vivo atlases to conventional 3 Tesla in vivo images; thus, a probabilistic brainstem atlas in stereotaxic neuroimaging space in living humans is needed. We delineated these nuclei using single-subject high contrast 1.1 mm isotropic resolution 7 Tesla MRI images. After precise coregistration of nuclei labels to stereotaxic space, we generated a probabilistic atlas of their anatomical locations. Finally, we validated the nuclei labels in the atlas by assessing their inter-rater agreement, consistency across subjects and volumes. We also performed a preliminary comparison of their location and microstructural properties to histologic sections of a postmortem human brainstem specimen. In future, the resulting probabilistic atlas of these brainstem nuclei in stereotaxic space may assist researchers and clinicians in evaluating autonomic, vestibular and viscero-sensory-motor nuclei structure, function and connectivity in living humans using conventional 3 Tesla MRI scanners.
Gerlinda E. Hermann - One of the best experts on this subject based on the ideXlab platform.
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CXCL12 sensitizes vago-vagal reflex neurons in the dorsal medulla.
Brain Research, 2012Co-Authors: Richard C. Rogers, Edouard Viard, Gerlinda E. HermannAbstract:Previous studies from our laboratory illustrated the potential for stromal cell-derived factor one [CXCL12; also referred to as SDF-1] to act on its receptor [CXCR4] within the dorsal vagal complex [DVC] of the hindbrain to suppress gastric motility (Hermann et al., 2008). While CXCR4 receptors are essential for normal brain development, they also play a critical role in the proliferation of the HIV virus and initiation of metastatic cell growth in the brain. Anorexia, nausea, and failed autonomic regulation of gastrointestinal function are significant causes of morbidity and are contributory factors in the mortality associated with these disease states. The implication of our previous study was that CXCL12 caused gastric stasis by acting on gastric reflex circuit elements in the DVC. This hindbrain complex includes vagal afferent terminations in the Solitary Nucleus, neurons in the Solitary Nucleus (NST) and visceral efferent motorneurons in the dorsal motor Nucleus (DMN) that are responsible for the regulation of digestive functions from the oral cavity to the transverse colon. In the current study, in vivo single-unit neurophysiological recordings from physiologically-identified NST and DMN components of the gastric accommodation reflex show that while injection of femtomole doses of CXCL12 onto NST or DMN neurons has no effect on their basal activity, CXCL12 amplifies the effect of gastric vagal mechanosensory input to activate the NST and, in turn, inhibit DMN motor activity.
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Leptin amplifies the action of thyrotropin-releasing hormone in the Solitary Nucleus: an in vitro calcium imaging study.
Brain Research, 2011Co-Authors: Richard C. Rogers, David H. Mcdougal, Gerlinda E. HermannAbstract:Abstract Leptin exerts a powerful permissive influence on neurogenic thermogenesis. During starvation and an absence of leptin, animals cannot produce thermogenic reactions to cold stress. However, thermogenesis is rescued by restoring leptin. We have previously observed a highly cooperative interaction between leptin and thyrotropin-releasing hormone [TRH] to activate hindbrain-generated thermogenic responses (Hermann et al., 2006). In vivo physiological studies (Rogers et al., 2009) suggested that the thermogenic impact of TRH in the hindbrain is amplified by the action of leptin through a leptin receptor-mediated production of phosphoinositol-trisphosphate [PIP3]. In turn, PIP3 can activate a tyrosine kinase whose target is the Src–SH2 regulatory site on the phospholipase C [PLC] complex. The TRH receptor signals through the PLC complex. Our immunohistochemical studies (Barnes et al., 2010) suggest that this transduction interaction between leptin and TRH occurs within neurons of the Solitary Nucleus [NST], though this interaction had not been verified. The present in vitro live cell calcium imaging study shows that while medial NST neurons are rarely activated by leptin alone, leptin pre-treatment significantly augments NST neurons′ responsiveness to TRH. This leptin-mediated priming of NST neurons was uncoupled by pre-treatment with the phosphoinositide 3-kinase [PI3K] inhibitor [wortmannin], the phospholipase C inhibitor [U73122] and the Src–SH2 antagonist [PP2]. TTX did not eliminate the synergistic response of the agonists, thus the sensitization cannot be attributed to pre-synaptic mechanisms. It seems likely that NST neurons are involved in the leptin-mediated increase in BAT temperature by sensitizing the TRH–PLC–IP3-calcium release mechanism.
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TNF activates astrocytes and catecholaminergic neurons in the Solitary Nucleus: implications for autonomic control.
Brain Research, 2009Co-Authors: Gerlinda E. Hermann, Richard C. RogersAbstract:Abstract Tumor necrosis factor [TNF] produces a profound anorexia associated with gastrointestinal stasis. Our work suggests that the principal site of action of TNF to cause this change in gastric function is via vagal afferents within the Nucleus of the Solitary tract [NST]. Excitation of these afferents presumably causes gastric stasis by activating downstream NST neurons that, in turn, suppress gastric motility via action on neurons in the dorsal motor Nucleus of the vagus that project to the stomach. Results from our parallel studies on gastric vago-vagal reflexes suggest that noradrenergic neurons in the NST are particularly important to the generation of reflex gastroinhibition. Convergence of these observations led us to hypothesize that TNF action in the NST may preferentially affect putative noradrenergic neurons. The current study confirms our observations of a dose-dependent TNF activation of cells [as indicated by cFOS production] in the NST. The phenotypic identity of these TNF-activated neurons in the NST was ∼ 29% tyrosine hydroxylase [TH]-positive [i.e., presumably noradrenergic neurons]. In contrast, less than 10% of the nitrergic neurons were activated after TNF exposure. Surprisingly, another 54% of the cFOS-activated cells in the NST were phenotypically identified to be astrocytes. Taken together with previous observations, the present results suggest that intense or prolonged vagal afferent activity [induced by visceral pathway activity, action of gut hormones or cytokines such as TNF] can alter local astrocyte immediate early gene expression that, in turn, can provoke long-term, perhaps permanent changes in the sensitivity of vagal-reflex circuitry.
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Mechanisms of action of CCK to activate central vagal afferent terminals.
Peptides, 2008Co-Authors: Richard C. Rogers, Gerlinda E. HermannAbstract:Cholecystokinin [CCK] is a peptide released as a hormone by the proximal gut in response to the presence of peptones and fatty acid in the gut. Considerable evidence suggests that CCK inhibits feeding behavior and gastric function by acting as a paracrine modulator of vagal afferents in the periphery, especially in the duodenum. CCK is also widely distributed throughout the mammalian brain and appears to function as a neurotransmitter and neuromodulator. More recent studies have suggested that CCK may act directly within the CNS to activate central vagal afferent terminal inputs to the Solitary Nucleus. We have developed an in vitro calcium imaging method that reveals, for the first time, the direct effects of this peptide on vagal terminals in the Solitary Nucleus. In vitro imaging reveals that CCK provokes increases in intracellular calcium in vagal afferent terminals as a consequence of a complex interaction between protein kinase A [PKA] and phospholipase C [PLC] transduction mechanisms that open L-type calcium channels and causes endoplasmic reticular [ER] calcium release. The subsequent activation of PKC may be responsible for initiating calcium spiking which is dependent on a TTX-sensitive mechanism. Thus, imaging of the isolated but spatially intact hindbrain slice has allowed a more complete appreciation of the interdependent transduction mechanisms used by CCK to excite identified central vagal afferent fibers and varicosities.
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TNFα -p55 receptors: medullary brainstem immunocytochemical localization in normal and vagus nerve-transected rats
Brain Research, 2004Co-Authors: Gerlinda E. Hermann, Sadie L. Hebert, Montina J. Van Meter, Gregory M. Holmes, Richard C. RogersAbstract:Abstract Tumor necrosis factor alpha (TNFα) is a potent modulator of autonomic reflex mechanisms that control the stomach. Evidence suggests that TNFα action directly on vago-vagal reflex control circuits causes the autonomic misregulation of digestion manifested as gastrointestinal stasis, nausea, and emesis associated with illness. Neurophysiological studies indicated that TNFα may have effects on vagal afferents in the Solitary Nucleus, as well as neurons of the Solitary Nucleus (NST) and dorsal motor Nucleus (DMN) of the vagus. The aim of this study was to determine the location of the TNFR1 receptor (p55) in the medulla using immunocytochemical methods. We devised a technique for localizing the p55 receptor using heat-induced antigen recovery in fixed tissue sections. This protocol allowed us to demonstrate that dense p55-immunoreactivity (p55-ir) is constitutively present on central (but not peripheral) vagal afferents in the Solitary tract (ST) and Nucleus; p55-ir is also present on afferents entering the spinal trigeminal Nucleus. Unilateral supra-nodose vagotomy eliminated p55-ir from ipsilateral central vagal afferents. Virtually all neurons in the brainstem appeared to express p55-ir at a low level, i.e., just above background. However, vagotomy caused a dramatic up-regulation of p55-ir in vagal motor neurons. This increase in p55-ir in axotomized neurons may play a pivotal role in the connection between the occurrence of the injury and the initiation of apoptotic processes resulting in elimination of damaged neurons.
Richard C. Rogers - One of the best experts on this subject based on the ideXlab platform.
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CXCL12 sensitizes vago-vagal reflex neurons in the dorsal medulla.
Brain Research, 2012Co-Authors: Richard C. Rogers, Edouard Viard, Gerlinda E. HermannAbstract:Previous studies from our laboratory illustrated the potential for stromal cell-derived factor one [CXCL12; also referred to as SDF-1] to act on its receptor [CXCR4] within the dorsal vagal complex [DVC] of the hindbrain to suppress gastric motility (Hermann et al., 2008). While CXCR4 receptors are essential for normal brain development, they also play a critical role in the proliferation of the HIV virus and initiation of metastatic cell growth in the brain. Anorexia, nausea, and failed autonomic regulation of gastrointestinal function are significant causes of morbidity and are contributory factors in the mortality associated with these disease states. The implication of our previous study was that CXCL12 caused gastric stasis by acting on gastric reflex circuit elements in the DVC. This hindbrain complex includes vagal afferent terminations in the Solitary Nucleus, neurons in the Solitary Nucleus (NST) and visceral efferent motorneurons in the dorsal motor Nucleus (DMN) that are responsible for the regulation of digestive functions from the oral cavity to the transverse colon. In the current study, in vivo single-unit neurophysiological recordings from physiologically-identified NST and DMN components of the gastric accommodation reflex show that while injection of femtomole doses of CXCL12 onto NST or DMN neurons has no effect on their basal activity, CXCL12 amplifies the effect of gastric vagal mechanosensory input to activate the NST and, in turn, inhibit DMN motor activity.
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Leptin amplifies the action of thyrotropin-releasing hormone in the Solitary Nucleus: an in vitro calcium imaging study.
Brain Research, 2011Co-Authors: Richard C. Rogers, David H. Mcdougal, Gerlinda E. HermannAbstract:Abstract Leptin exerts a powerful permissive influence on neurogenic thermogenesis. During starvation and an absence of leptin, animals cannot produce thermogenic reactions to cold stress. However, thermogenesis is rescued by restoring leptin. We have previously observed a highly cooperative interaction between leptin and thyrotropin-releasing hormone [TRH] to activate hindbrain-generated thermogenic responses (Hermann et al., 2006). In vivo physiological studies (Rogers et al., 2009) suggested that the thermogenic impact of TRH in the hindbrain is amplified by the action of leptin through a leptin receptor-mediated production of phosphoinositol-trisphosphate [PIP3]. In turn, PIP3 can activate a tyrosine kinase whose target is the Src–SH2 regulatory site on the phospholipase C [PLC] complex. The TRH receptor signals through the PLC complex. Our immunohistochemical studies (Barnes et al., 2010) suggest that this transduction interaction between leptin and TRH occurs within neurons of the Solitary Nucleus [NST], though this interaction had not been verified. The present in vitro live cell calcium imaging study shows that while medial NST neurons are rarely activated by leptin alone, leptin pre-treatment significantly augments NST neurons′ responsiveness to TRH. This leptin-mediated priming of NST neurons was uncoupled by pre-treatment with the phosphoinositide 3-kinase [PI3K] inhibitor [wortmannin], the phospholipase C inhibitor [U73122] and the Src–SH2 antagonist [PP2]. TTX did not eliminate the synergistic response of the agonists, thus the sensitization cannot be attributed to pre-synaptic mechanisms. It seems likely that NST neurons are involved in the leptin-mediated increase in BAT temperature by sensitizing the TRH–PLC–IP3-calcium release mechanism.
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TNF activates astrocytes and catecholaminergic neurons in the Solitary Nucleus: implications for autonomic control.
Brain Research, 2009Co-Authors: Gerlinda E. Hermann, Richard C. RogersAbstract:Abstract Tumor necrosis factor [TNF] produces a profound anorexia associated with gastrointestinal stasis. Our work suggests that the principal site of action of TNF to cause this change in gastric function is via vagal afferents within the Nucleus of the Solitary tract [NST]. Excitation of these afferents presumably causes gastric stasis by activating downstream NST neurons that, in turn, suppress gastric motility via action on neurons in the dorsal motor Nucleus of the vagus that project to the stomach. Results from our parallel studies on gastric vago-vagal reflexes suggest that noradrenergic neurons in the NST are particularly important to the generation of reflex gastroinhibition. Convergence of these observations led us to hypothesize that TNF action in the NST may preferentially affect putative noradrenergic neurons. The current study confirms our observations of a dose-dependent TNF activation of cells [as indicated by cFOS production] in the NST. The phenotypic identity of these TNF-activated neurons in the NST was ∼ 29% tyrosine hydroxylase [TH]-positive [i.e., presumably noradrenergic neurons]. In contrast, less than 10% of the nitrergic neurons were activated after TNF exposure. Surprisingly, another 54% of the cFOS-activated cells in the NST were phenotypically identified to be astrocytes. Taken together with previous observations, the present results suggest that intense or prolonged vagal afferent activity [induced by visceral pathway activity, action of gut hormones or cytokines such as TNF] can alter local astrocyte immediate early gene expression that, in turn, can provoke long-term, perhaps permanent changes in the sensitivity of vagal-reflex circuitry.
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Mechanisms of action of CCK to activate central vagal afferent terminals.
Peptides, 2008Co-Authors: Richard C. Rogers, Gerlinda E. HermannAbstract:Cholecystokinin [CCK] is a peptide released as a hormone by the proximal gut in response to the presence of peptones and fatty acid in the gut. Considerable evidence suggests that CCK inhibits feeding behavior and gastric function by acting as a paracrine modulator of vagal afferents in the periphery, especially in the duodenum. CCK is also widely distributed throughout the mammalian brain and appears to function as a neurotransmitter and neuromodulator. More recent studies have suggested that CCK may act directly within the CNS to activate central vagal afferent terminal inputs to the Solitary Nucleus. We have developed an in vitro calcium imaging method that reveals, for the first time, the direct effects of this peptide on vagal terminals in the Solitary Nucleus. In vitro imaging reveals that CCK provokes increases in intracellular calcium in vagal afferent terminals as a consequence of a complex interaction between protein kinase A [PKA] and phospholipase C [PLC] transduction mechanisms that open L-type calcium channels and causes endoplasmic reticular [ER] calcium release. The subsequent activation of PKC may be responsible for initiating calcium spiking which is dependent on a TTX-sensitive mechanism. Thus, imaging of the isolated but spatially intact hindbrain slice has allowed a more complete appreciation of the interdependent transduction mechanisms used by CCK to excite identified central vagal afferent fibers and varicosities.
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TNFα -p55 receptors: medullary brainstem immunocytochemical localization in normal and vagus nerve-transected rats
Brain Research, 2004Co-Authors: Gerlinda E. Hermann, Sadie L. Hebert, Montina J. Van Meter, Gregory M. Holmes, Richard C. RogersAbstract:Abstract Tumor necrosis factor alpha (TNFα) is a potent modulator of autonomic reflex mechanisms that control the stomach. Evidence suggests that TNFα action directly on vago-vagal reflex control circuits causes the autonomic misregulation of digestion manifested as gastrointestinal stasis, nausea, and emesis associated with illness. Neurophysiological studies indicated that TNFα may have effects on vagal afferents in the Solitary Nucleus, as well as neurons of the Solitary Nucleus (NST) and dorsal motor Nucleus (DMN) of the vagus. The aim of this study was to determine the location of the TNFR1 receptor (p55) in the medulla using immunocytochemical methods. We devised a technique for localizing the p55 receptor using heat-induced antigen recovery in fixed tissue sections. This protocol allowed us to demonstrate that dense p55-immunoreactivity (p55-ir) is constitutively present on central (but not peripheral) vagal afferents in the Solitary tract (ST) and Nucleus; p55-ir is also present on afferents entering the spinal trigeminal Nucleus. Unilateral supra-nodose vagotomy eliminated p55-ir from ipsilateral central vagal afferents. Virtually all neurons in the brainstem appeared to express p55-ir at a low level, i.e., just above background. However, vagotomy caused a dramatic up-regulation of p55-ir in vagal motor neurons. This increase in p55-ir in axotomized neurons may play a pivotal role in the connection between the occurrence of the injury and the initiation of apoptotic processes resulting in elimination of damaged neurons.
Kavita Singh - One of the best experts on this subject based on the ideXlab platform.
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probabilistic template of the lateral parabrachial Nucleus medial parabrachial Nucleus vestibular nuclei complex and medullary viscero sensory motor nuclei complex in living humans from 7 tesla mri
Frontiers in Neuroscience, 2020Co-Authors: Kavita Singh, I Indovina, Jean C Augustinack, Kimberly Nestor, Maria G Garciagomar, Jeffrey P Staab, Marta BianciardiAbstract:The lateral parabrachial Nucleus, medial parabrachial Nucleus, vestibular nuclei complex and medullary viscero-sensory-motor nuclei complex (the latter including among others the Solitary Nucleus, vagus nerve Nucleus, and hypoglossal Nucleus) are anatomically and functionally connected brainstem gray-matter structures that convey signals across multiple modalities between the brain and the spinal cord to regulate vital bodily functions. It is remarkably difficult to precisely extrapolate the location of these nuclei from ex vivo atlases to conventional 3 Tesla in vivo images; thus, a probabilistic brainstem template in stereotaxic neuroimaging space in living humans is needed. We delineated these nuclei using single-subject high contrast 1.1 mm isotropic resolution 7 Tesla MRI images. After precise coregistration of nuclei labels to stereotaxic space, we generated a probabilistic template of their anatomical locations. Finally, we validated the nuclei labels in the template by assessing their inter-rater agreement, consistency across subjects and volumes. We also performed a preliminary comparison of their location and microstructural properties to histologic sections of a postmortem human brainstem specimen. In future, the resulting probabilistic template of these brainstem nuclei in stereotaxic space may assist researchers and clinicians in evaluating autonomic, vestibular and viscero-sensory-motor nuclei structure, function and connectivity in living humans using conventional 3 Tesla MRI scanners.
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probabilistic atlas of the lateral parabrachial Nucleus medial parabrachial Nucleus vestibular nuclei complex and medullary viscero sensory motor nuclei complex in living humans from 7 tesla mri
bioRxiv, 2019Co-Authors: Kavita Singh, I Indovina, Jean C Augustinack, Kimberly Nestor, Maria G Garciagomar, Jeffrey P Staab, Marta BianciardiAbstract:Abstract The lateral parabrachial Nucleus, medial parabrachial Nucleus, vestibular nuclei complex and medullary viscero-sensory-motor nuclei complex (the latter including among others the Solitary Nucleus, vagus nerve Nucleus, and hypoglossal Nucleus) are anatomically and functionally connected brainstem gray-matter structures that convey signals across multiple modalities between the brain and the spinal cord to regulate vital bodily functions. It is remarkably difficult to precisely extrapolate the location of these nuclei from ex vivo atlases to conventional 3 Tesla in vivo images; thus, a probabilistic brainstem atlas in stereotaxic neuroimaging space in living humans is needed. We delineated these nuclei using single-subject high contrast 1.1 mm isotropic resolution 7 Tesla MRI images. After precise coregistration of nuclei labels to stereotaxic space, we generated a probabilistic atlas of their anatomical locations. Finally, we validated the nuclei labels in the atlas by assessing their inter-rater agreement, consistency across subjects and volumes. We also performed a preliminary comparison of their location and microstructural properties to histologic sections of a postmortem human brainstem specimen. In future, the resulting probabilistic atlas of these brainstem nuclei in stereotaxic space may assist researchers and clinicians in evaluating autonomic, vestibular and viscero-sensory-motor nuclei structure, function and connectivity in living humans using conventional 3 Tesla MRI scanners.
Hiroyuki Fukuda - One of the best experts on this subject based on the ideXlab platform.
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The Nucleus raphe magnus suppresses vomiting, and the Solitary Nucleus and 5-HT are not involved in this suppression.
Autonomic neuroscience : basic & clinical, 2009Co-Authors: Yuka Hattori, Tomoshige Koga, E Nakamura, Chie Hamaguchi, Yuko Yamada, Yukiko Urayama, Hiroyuki FukudaAbstract:In previous paper, we reported that stimulation of the Nucleus raphe magnus (stim-NRM) inhibits the induction of retching by afferent vagal fibers (VAs). We performed the present study to identity the transmitter of inhibition and then the site. The following results were obtained in decerebrated and paralyzed dogs. 1) The induction of fictive retching was suppressed by i.v. injection of 5-HT, and by 4th ventricular administration of 5-HT or a 5-HT3-receptor (R) agonist, 1-(m-chlorophenyl)-biguanade hydrochloride (m-CPBG). 2) Both forms of suppression were antagonized by i.v. injection of ondansetron, a 5-HT3-R antagonist. 3) Administration of the antagonist into the 4th ventricle did not affect the induction or its suppression by stim-NRM. These results suggest that the transmission from VAs to neurons in the Nucleus solitarius (NTS) is suppressed by 5-HT via 5-HT3-R. However, these results also suggest that both the transmitter and receptor are not involved in the induction of retching by VAs or in its suppression by the NRM. Next, we examined the site of suppression. Unitary firings of NTS neurons in response to pulse-train stimulation of VAs were not inhibited by NRM stimulation. Moreover, the firing of NTS neurons during the induction of retching by vagal stimulation did not significantly decrease with the superimposition of stim-NRM, although the induction of retching was completely suppressed. These results suggest that suppression of the induction of retching by the descending inhibitory system of pain did not occur in the synapse between afferent vagal fibers and NTS neurons. The site of suppression is discussed.
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Non-n-methyl-d-aspartate receptors may mediate the transmission of emetic signals between visceral vagal afferents and the Solitary Nucleus in dogs
Neuroscience Letters, 1998Co-Authors: Naohiro Furukawa, Hiroyuki Fukuda, Mizue Hatano, Tomoshige KogaAbstract:Abstract The effects of the N -methyl- d -aspartate (NMDA) and non-NMDA receptor antagonists MK-801 and NBQX, respectively, on salivary secretion and retching induced by vagal stimulation were studied in decerebrate dogs. Vagal stimulation induced an increase in salivary secretion and fictive retching. Intra-4th ventricular application of vehicle or MK-801 did not change either response, while NBQX completely abolished both responses. These results suggest that non-NMDA receptors mediate both responses in the Solitary Nucleus.
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The tachykinin NK1 receptor antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to Solitary Nucleus neurons in dogs
Brain Research, 1998Co-Authors: Hiroyuki Fukuda, Tomoshige Koga, Naohiro Furukawa, E Nakamura, Yasuteru ShiroshitaAbstract:Tachykinin NK1 receptor antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial Solitary Nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 receptor antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05–0.7 mg kg−1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml−1, 30 μl) into the 4th ventricle abolished retching, with latencies in excess of 120 min. These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.
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The tachykinin NK1 receptor antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to Solitary Nucleus neurons in dogs.
Brain research, 1998Co-Authors: Hiroyuki Fukuda, Tomoshige Koga, N Furukawa, E Nakamura, Yasuteru ShiroshitaAbstract:Tachykinin NK1 receptor antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial Solitary Nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK1 receptor antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05-0.7 mg kg-1, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml-1, 30 microliters) into the 4th ventricle abolished retching, with latencies in excess of 120 min These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.
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Capsaicin in the 4th ventricle abolishes retching and transmission of emetic vagal afferents to Solitary Nucleus neurons.
European Journal of Pharmacology, 1997Co-Authors: Yasuteru Shiroshita, Tomoshige Koga, Hiroyuki FukudaAbstract:Abstract Systemic tachykinin NK1 receptor antagonists and resiniferatoxin are known to abolish vomiting mediated by vagal afferents. Emetic vagal afferents have been shown to make synaptic contact with neurons in the medial Solitary Nucleus. These results suggest that substance P participates in the synapse as a mediator. To examine this possibility, the effects of 4th-ventricular application of capsaicin (0.033–33 mM, 20–30 μl) and resiniferatoxin (1.6–160 μM, 20–30 μl) on the activity of neurons in the medial Solitary Nucleus and fictive retching induced by vagal stimulation were observed in paralyzed decerebrate dogs. Capsaicin (33 mM) and resiniferatoxin (160 μM) initially increased the neuronal firing and occasionally produced retching, then abolished both neuronal and retching responses. However, stimulation of the medial Solitary Nucleus continued to provoke retching. Field potential changes in the medial Solitary Nucleus evoked by pulse-train vagal stimulation decreased in amplitude, but did not disappear. Latencies of neuronal firing and evoked potentials were about 300 ms. These results suggest that emetic vagal afferents are capsaicin-sensitive C fibers which may have substance P as an excitatory transmitter or modulator.