The Experts below are selected from a list of 4668 Experts worldwide ranked by ideXlab platform
Kazuo Toda - One of the best experts on this subject based on the ideXlab platform.
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2005, Taste cell responses in the frog are modulated by parasympathetic Efferent Nerve fibers, Chem Senses 30
2015Co-Authors: Toshihide Sato, Yukio Okada, Toshihiro Miyazaki, Yuzo Kato, Kazuo TodaAbstract:We studied the anatomical properties of parasympathetic postganglionic neurons in the frog tongue and their modulatory effects on taste cell responses. Most of the parasympathetic ganglion cell bodies in the tongue were found in extremely small Nerve bundles running near the fungiform papillae, which originate from the lingual branches of the glossopharyngeal (GP) Nerve. The density of parasympathetic postganglionic neurons in the tongue was 8000–11,000/mm3 of the extremely small Nerve bundle. Themeanmajor axis of parasympathetic ganglion cell bodies was 21 lm, and themean length of parasympathetic postganglionic neurons was 1.45 mm. Electrical stimulation at 30 Hz of either the GP Nerve or the papillary Nerve produced slow hyperpolarizing potentials (HPs) in taste cells. After nicotinic acetyl choline receptors on the parasympathetic ganglion cells in the tongue had been blocked by intravenous (i.v.) injection of D-tubocurarine (1 mg/kg), stimulation of the GP Nerve did not induce any slow HPs in taste cells but that of the papillary Nerve did. A further i.v. injection of a substance P NK-1 antagonist, L-703,606, blocked the slow HPs induced by the papillary Nerve stimulation. This suggests that the parasympathetic postganglionic Efferent fibers innervate taste cells and are related to a generation of the slow HPs and that substance P is released from the parasympathetic postganglionic axon terminals. When the resting membrane potential of a taste cell was hyperpolarized by a prolonged slow HP, the gustatory receptor potentials for NaCl and sugar stimuli were enhanced in amplitude, but those for quinine-HCl and acetic acid stimuli remained unchanged. It is concluded that frog taste cell responses are modulated b
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Tonic Activity of Parasympathetic Efferent Nerve Fibers Hyperpolarizes the Resting Membrane Potential of Frog Taste Cells
2014Co-Authors: Toshihide Sato, Yukio Okada, Yuzo Kato, Kazuhisa Nishishita, Kazuo TodaAbstract:We investigated the relationship between the membrane potential of frog taste cells in the fungiform papillae and the tonic discharge of parasympathetic Efferent fibers in the glossopharyngeal (GP) Nerve. When the parasympathetic preganglionic fibers in the GP Nerve were kept intact, the mean membrane potential of Ringer-adapted taste cells was 40 mV but decreased to 31mVafter transecting the preganglionic fibers in theGPNerve and crushing the postganglionic fibers in the papillary Nerve. The same result occurred after blocking the nicotinic acetylcholine receptors on parasympathetic ganglion cells in the tongue and blocking the substance P neurokinin-1 (NK-1) receptors in the gustatory Efferent synapses. This indicates that the parasympathetic Nerve (PSN) hyperpolarizes the membrane potential of frog taste cells by 9 mV. Repetitive stimulation of a transected GP Nerve revealed that a9-mV hyperpolarization of taste cells maintained under the intact GP Nerve derives from an;10-Hz discharge of the PSN Efferent fibers. Themean frequency of tonic discharges extracellularly recorded from PSN Efferent fibers of the taste disks was 9.1 impulses/s. We conclude that the resting membrane potential of frog taste cells is continuously hyperpolarized by on average 9 mV by an;10-Hz tonic discharge from the parasympathetic preganglionic neurons in the medulla oblongata. Key words: gustatory Efferent synapse, membrane potential, parasympathetic Nerve, slow hyperpolarizing potential, taste receptor cel
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Tonic Activity of Parasympathetic Efferent Nerve Fibers Hyperpolarizes the Resting Membrane Potential of Frog Taste Cells
Chemical senses, 2006Co-Authors: Toshihide Sato, Yukio Okada, Yuzo Kato, Kazuhisa Nishishita, Kazuo TodaAbstract:We investigated the relationship between the membrane potential of frog taste cells in the fungiform papillae and the tonic discharge of parasympathetic Efferent fibers in the glossopharyngeal (GP) Nerve. When the parasympathetic preganglionic fibers in the GP Nerve were kept intact, the mean membrane potential of Ringer-adapted taste cells was -40 mV but decreased to -31 mV after transecting the preganglionic fibers in the GP Nerve and crushing the postganglionic fibers in the papillary Nerve. The same result occurred after blocking the nicotinic acetylcholine receptors on parasympathetic ganglion cells in the tongue and blocking the substance P neurokinin-1 (NK-1) receptors in the gustatory Efferent synapses. This indicates that the parasympathetic Nerve (PSN) hyperpolarizes the membrane potential of frog taste cells by -9 mV. Repetitive stimulation of a transected GP Nerve revealed that a -9-mV hyperpolarization of taste cells maintained under the intact GP Nerve derives from an approximately 10-Hz discharge of the PSN Efferent fibers. The mean frequency of tonic discharges extracellularly recorded from PSN Efferent fibers of the taste disks was 9.1 impulses/s. We conclude that the resting membrane potential of frog taste cells is continuously hyperpolarized by on average -9 mV by an approximately 10-Hz tonic discharge from the parasympathetic preganglionic neurons in the medulla oblongata.
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Taste cell responses in the frog are modulated by parasympathetic Efferent Nerve fibers.
Chemical senses, 2005Co-Authors: Toshihide Sato, Yukio Okada, Toshihiro Miyazaki, Yuzo Kato, Kazuo TodaAbstract:We studied the anatomical properties of parasympathetic postganglionic neurons in the frog tongue and their modulatory effects on taste cell responses. Most of the parasympathetic ganglion cell bodies in the tongue were found in extremely small Nerve bundles running near the fungiform papillae, which originate from the lingual branches of the glossopharyngeal (GP) Nerve. The density of parasympathetic postganglionic neurons in the tongue was 8000–11,000/mm 3 of the extremely small Nerve bundle. The mean major axis of parasympathetic ganglion cell bodies was 21lm, and the mean length of parasympathetic postganglionic neurons was 1.45 mm. Electrical stimulation at 30 Hz of either the GP Nerve or the papillary Nerve produced slow hyperpolarizing potentials (HPs) in taste cells. After nicotinic acetyl choline receptors on the parasympathetic ganglion cells in the tongue had been blocked by intravenous (i.v.) injection of D-tubocurarine (1 mg/kg), stimulation of the GP Nerve did not induce any slow HPs in taste cells but that of the papillary Nerve did. A further i.v. injection of a substance P NK-1 antagonist, L-703,606, blocked the slow HPs induced by the papillary Nerve stimulation. This suggests that the parasympathetic postganglionic Efferent fibers innervate taste cells and are related to a generation of the slow HPs and that substance P is released from the parasympathetic postganglionic axon terminals. When the resting membrane potential of a taste cell was hyperpolarized by a prolonged slow HP, the gustatory receptor potentials for NaCl and sugar stimuli were enhanced in amplitude, but those for quinine-HCl and acetic acid stimuli remained unchanged. It is concluded that frog taste cell responses are modulated by activities of parasympathetic postganglionic Efferent fibers innervating these cells.
Xiang Zhang - One of the best experts on this subject based on the ideXlab platform.
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A Brain-Melanocortin-Vagus Axis Mediates Adipose Tissue Expansion Independently of Energy Intake.
Cell reports, 2019Co-Authors: Jenna Holland, Joyce Sorrell, Emily Yates, Kathleen Smith, Shahriar Arbabi, Myrtha Arnold, Marita Rivir, Rachel L. Morano, Jenny Chen, Xiang ZhangAbstract:The melanocortin system is a brain circuit that influences energy balance by regulating energy intake and expenditure. In addition, the brain-melanocortin system controls adipose tissue metabolism to optimize fuel mobilization and storage. Specifically, increased brain-melanocortin signaling or negative energy balance promotes lipid mobilization by increasing sympathetic nervous system input to adipose tissue. In contrast, calorie-independent mechanisms favoring energy storage are less understood. Here, we demonstrate that reduction of brain-melanocortin signaling actively promotes fat mass gain by activating the lipogenic program and adipocyte and endothelial cell proliferation in white fat depots independently of caloric intake via Efferent Nerve fibers conveyed by the common hepatic branch of the vagus Nerve. Those vagally regulated obesogenic signals also contribute to the fat mass gain following chronic high-fat diet feeding. These data reveal a physiological mechanism whereby the brain controls energy stores that may contribute to increased susceptibility to obesity.
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A Brain-Melanocortin-Vagus Axis Mediates Adipose Tissue Expansion Independently of Energy Intake
'Elsevier BV', 2019Co-Authors: Jenna Holland, Joyce Sorrell, Emily Yates, Kathleen Smith, Shahriar Arbabi, Myrtha Arnold, Marita Rivir, Jenny Chen, Rachel Morano, Xiang ZhangAbstract:Summary: The melanocortin system is a brain circuit that influences energy balance by regulating energy intake and expenditure. In addition, the brain-melanocortin system controls adipose tissue metabolism to optimize fuel mobilization and storage. Specifically, increased brain-melanocortin signaling or negative energy balance promotes lipid mobilization by increasing sympathetic nervous system input to adipose tissue. In contrast, calorie-independent mechanisms favoring energy storage are less understood. Here, we demonstrate that reduction of brain-melanocortin signaling actively promotes fat mass gain by activating the lipogenic program and adipocyte and endothelial cell proliferation in white fat depots independently of caloric intake via Efferent Nerve fibers conveyed by the common hepatic branch of the vagus Nerve. Those vagally regulated obesogenic signals also contribute to the fat mass gain following chronic high-fat diet feeding. These data reveal a physiological mechanism whereby the brain controls energy stores that may contribute to increased susceptibility to obesity. : Brain-melanocortin signaling controls fat mass indirectly by regulating energy balance and by direct control of lipid mobilization from adipose tissue via sympathetic nervous system activity. Holland et al. show that reduced brain-melanocortin signaling promotes white adipose tissue expansion via signals conveyed by Efferent innervation of the vagus Nerve
Toshihide Sato - One of the best experts on this subject based on the ideXlab platform.
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2005, Taste cell responses in the frog are modulated by parasympathetic Efferent Nerve fibers, Chem Senses 30
2015Co-Authors: Toshihide Sato, Yukio Okada, Toshihiro Miyazaki, Yuzo Kato, Kazuo TodaAbstract:We studied the anatomical properties of parasympathetic postganglionic neurons in the frog tongue and their modulatory effects on taste cell responses. Most of the parasympathetic ganglion cell bodies in the tongue were found in extremely small Nerve bundles running near the fungiform papillae, which originate from the lingual branches of the glossopharyngeal (GP) Nerve. The density of parasympathetic postganglionic neurons in the tongue was 8000–11,000/mm3 of the extremely small Nerve bundle. Themeanmajor axis of parasympathetic ganglion cell bodies was 21 lm, and themean length of parasympathetic postganglionic neurons was 1.45 mm. Electrical stimulation at 30 Hz of either the GP Nerve or the papillary Nerve produced slow hyperpolarizing potentials (HPs) in taste cells. After nicotinic acetyl choline receptors on the parasympathetic ganglion cells in the tongue had been blocked by intravenous (i.v.) injection of D-tubocurarine (1 mg/kg), stimulation of the GP Nerve did not induce any slow HPs in taste cells but that of the papillary Nerve did. A further i.v. injection of a substance P NK-1 antagonist, L-703,606, blocked the slow HPs induced by the papillary Nerve stimulation. This suggests that the parasympathetic postganglionic Efferent fibers innervate taste cells and are related to a generation of the slow HPs and that substance P is released from the parasympathetic postganglionic axon terminals. When the resting membrane potential of a taste cell was hyperpolarized by a prolonged slow HP, the gustatory receptor potentials for NaCl and sugar stimuli were enhanced in amplitude, but those for quinine-HCl and acetic acid stimuli remained unchanged. It is concluded that frog taste cell responses are modulated b
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Tonic Activity of Parasympathetic Efferent Nerve Fibers Hyperpolarizes the Resting Membrane Potential of Frog Taste Cells
2014Co-Authors: Toshihide Sato, Yukio Okada, Yuzo Kato, Kazuhisa Nishishita, Kazuo TodaAbstract:We investigated the relationship between the membrane potential of frog taste cells in the fungiform papillae and the tonic discharge of parasympathetic Efferent fibers in the glossopharyngeal (GP) Nerve. When the parasympathetic preganglionic fibers in the GP Nerve were kept intact, the mean membrane potential of Ringer-adapted taste cells was 40 mV but decreased to 31mVafter transecting the preganglionic fibers in theGPNerve and crushing the postganglionic fibers in the papillary Nerve. The same result occurred after blocking the nicotinic acetylcholine receptors on parasympathetic ganglion cells in the tongue and blocking the substance P neurokinin-1 (NK-1) receptors in the gustatory Efferent synapses. This indicates that the parasympathetic Nerve (PSN) hyperpolarizes the membrane potential of frog taste cells by 9 mV. Repetitive stimulation of a transected GP Nerve revealed that a9-mV hyperpolarization of taste cells maintained under the intact GP Nerve derives from an;10-Hz discharge of the PSN Efferent fibers. Themean frequency of tonic discharges extracellularly recorded from PSN Efferent fibers of the taste disks was 9.1 impulses/s. We conclude that the resting membrane potential of frog taste cells is continuously hyperpolarized by on average 9 mV by an;10-Hz tonic discharge from the parasympathetic preganglionic neurons in the medulla oblongata. Key words: gustatory Efferent synapse, membrane potential, parasympathetic Nerve, slow hyperpolarizing potential, taste receptor cel
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Tonic Activity of Parasympathetic Efferent Nerve Fibers Hyperpolarizes the Resting Membrane Potential of Frog Taste Cells
Chemical senses, 2006Co-Authors: Toshihide Sato, Yukio Okada, Yuzo Kato, Kazuhisa Nishishita, Kazuo TodaAbstract:We investigated the relationship between the membrane potential of frog taste cells in the fungiform papillae and the tonic discharge of parasympathetic Efferent fibers in the glossopharyngeal (GP) Nerve. When the parasympathetic preganglionic fibers in the GP Nerve were kept intact, the mean membrane potential of Ringer-adapted taste cells was -40 mV but decreased to -31 mV after transecting the preganglionic fibers in the GP Nerve and crushing the postganglionic fibers in the papillary Nerve. The same result occurred after blocking the nicotinic acetylcholine receptors on parasympathetic ganglion cells in the tongue and blocking the substance P neurokinin-1 (NK-1) receptors in the gustatory Efferent synapses. This indicates that the parasympathetic Nerve (PSN) hyperpolarizes the membrane potential of frog taste cells by -9 mV. Repetitive stimulation of a transected GP Nerve revealed that a -9-mV hyperpolarization of taste cells maintained under the intact GP Nerve derives from an approximately 10-Hz discharge of the PSN Efferent fibers. The mean frequency of tonic discharges extracellularly recorded from PSN Efferent fibers of the taste disks was 9.1 impulses/s. We conclude that the resting membrane potential of frog taste cells is continuously hyperpolarized by on average -9 mV by an approximately 10-Hz tonic discharge from the parasympathetic preganglionic neurons in the medulla oblongata.
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Taste cell responses in the frog are modulated by parasympathetic Efferent Nerve fibers.
Chemical senses, 2005Co-Authors: Toshihide Sato, Yukio Okada, Toshihiro Miyazaki, Yuzo Kato, Kazuo TodaAbstract:We studied the anatomical properties of parasympathetic postganglionic neurons in the frog tongue and their modulatory effects on taste cell responses. Most of the parasympathetic ganglion cell bodies in the tongue were found in extremely small Nerve bundles running near the fungiform papillae, which originate from the lingual branches of the glossopharyngeal (GP) Nerve. The density of parasympathetic postganglionic neurons in the tongue was 8000–11,000/mm 3 of the extremely small Nerve bundle. The mean major axis of parasympathetic ganglion cell bodies was 21lm, and the mean length of parasympathetic postganglionic neurons was 1.45 mm. Electrical stimulation at 30 Hz of either the GP Nerve or the papillary Nerve produced slow hyperpolarizing potentials (HPs) in taste cells. After nicotinic acetyl choline receptors on the parasympathetic ganglion cells in the tongue had been blocked by intravenous (i.v.) injection of D-tubocurarine (1 mg/kg), stimulation of the GP Nerve did not induce any slow HPs in taste cells but that of the papillary Nerve did. A further i.v. injection of a substance P NK-1 antagonist, L-703,606, blocked the slow HPs induced by the papillary Nerve stimulation. This suggests that the parasympathetic postganglionic Efferent fibers innervate taste cells and are related to a generation of the slow HPs and that substance P is released from the parasympathetic postganglionic axon terminals. When the resting membrane potential of a taste cell was hyperpolarized by a prolonged slow HP, the gustatory receptor potentials for NaCl and sugar stimuli were enhanced in amplitude, but those for quinine-HCl and acetic acid stimuli remained unchanged. It is concluded that frog taste cell responses are modulated by activities of parasympathetic postganglionic Efferent fibers innervating these cells.
Jenna Holland - One of the best experts on this subject based on the ideXlab platform.
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A Brain-Melanocortin-Vagus Axis Mediates Adipose Tissue Expansion Independently of Energy Intake.
Cell reports, 2019Co-Authors: Jenna Holland, Joyce Sorrell, Emily Yates, Kathleen Smith, Shahriar Arbabi, Myrtha Arnold, Marita Rivir, Rachel L. Morano, Jenny Chen, Xiang ZhangAbstract:The melanocortin system is a brain circuit that influences energy balance by regulating energy intake and expenditure. In addition, the brain-melanocortin system controls adipose tissue metabolism to optimize fuel mobilization and storage. Specifically, increased brain-melanocortin signaling or negative energy balance promotes lipid mobilization by increasing sympathetic nervous system input to adipose tissue. In contrast, calorie-independent mechanisms favoring energy storage are less understood. Here, we demonstrate that reduction of brain-melanocortin signaling actively promotes fat mass gain by activating the lipogenic program and adipocyte and endothelial cell proliferation in white fat depots independently of caloric intake via Efferent Nerve fibers conveyed by the common hepatic branch of the vagus Nerve. Those vagally regulated obesogenic signals also contribute to the fat mass gain following chronic high-fat diet feeding. These data reveal a physiological mechanism whereby the brain controls energy stores that may contribute to increased susceptibility to obesity.
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A Brain-Melanocortin-Vagus Axis Mediates Adipose Tissue Expansion Independently of Energy Intake
'Elsevier BV', 2019Co-Authors: Jenna Holland, Joyce Sorrell, Emily Yates, Kathleen Smith, Shahriar Arbabi, Myrtha Arnold, Marita Rivir, Jenny Chen, Rachel Morano, Xiang ZhangAbstract:Summary: The melanocortin system is a brain circuit that influences energy balance by regulating energy intake and expenditure. In addition, the brain-melanocortin system controls adipose tissue metabolism to optimize fuel mobilization and storage. Specifically, increased brain-melanocortin signaling or negative energy balance promotes lipid mobilization by increasing sympathetic nervous system input to adipose tissue. In contrast, calorie-independent mechanisms favoring energy storage are less understood. Here, we demonstrate that reduction of brain-melanocortin signaling actively promotes fat mass gain by activating the lipogenic program and adipocyte and endothelial cell proliferation in white fat depots independently of caloric intake via Efferent Nerve fibers conveyed by the common hepatic branch of the vagus Nerve. Those vagally regulated obesogenic signals also contribute to the fat mass gain following chronic high-fat diet feeding. These data reveal a physiological mechanism whereby the brain controls energy stores that may contribute to increased susceptibility to obesity. : Brain-melanocortin signaling controls fat mass indirectly by regulating energy balance and by direct control of lipid mobilization from adipose tissue via sympathetic nervous system activity. Holland et al. show that reduced brain-melanocortin signaling promotes white adipose tissue expansion via signals conveyed by Efferent innervation of the vagus Nerve
Kanji Matsukawa - One of the best experts on this subject based on the ideXlab platform.
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central command control of cardiac sympathetic and vagal Efferent Nerve activity and the arterial baroreflex during spontaneous motor behaviour in animals
Experimental Physiology, 2012Co-Authors: Kanji MatsukawaAbstract:Feedforward control by higher brain centres (termed central command) plays a role in the autonomic regulation of the cardiovascular system during exercise. Over the past 20 years, workers in our laboratory have used the precollicular-premammillary decerebrate animal model to identify the neural circuitry involved in the CNS control of cardiac autonomic outflow and arterial baroreflex function. Contrary to the traditional idea that vagal withdrawal at the onset of exercise causes the increase in heart rate, central command did not decrease cardiac vagal Efferent Nerve activity but did allow cardiac sympathetic Efferent Nerve activity to produce cardiac acceleration. In addition, central command-evoked inhibition of the aortic baroreceptor-heart rate reflex blunted the baroreflex-mediated bradycardia elicited by aortic Nerve stimulation, further increasing the heart rate at the onset of exercise. Spontaneous motor activity and associated cardiovascular responses disappeared in animals decerebrated at the midcollicular level. These findings indicate that the brain region including the caudal diencephalon and extending to the rostral mesencephalon may play a role in generating central command. Bicuculline microinjected into the midbrain ventral tegmental area of decerebrate rats produced a long-lasting repetitive activation of renal sympathetic Nerve activity that was synchronized with the motor Nerve discharge. When lidocaine was microinjected into the ventral tegmental area, the spontaneous motor activity and associated cardiovascular responses ceased. From these findings, we conclude that cerebral cortical outputs trigger activation of neural circuits within the caudal brain, including the ventral tegmental area, which causes central command to augment cardiac sympathetic outflow at the onset of exercise in decerebrate animal models.
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central command does not decrease cardiac parasympathetic Efferent Nerve activity during spontaneous fictive motor activity in decerebrate cats
American Journal of Physiology-heart and Circulatory Physiology, 2011Co-Authors: Akito Kadowaki, Kanji Matsukawa, Rie Wakasugi, Tomoko Nakamoto, Nan LiangAbstract:To examine whether withdrawal of cardiac vagal Efferent Nerve activity (CVNA) predominantly controls the tachycardia at the start of exercise, the responses of CVNA and cardiac sympathetic Efferent...
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direct measurement of cardiac sympathetic Efferent Nerve activity during dynamic exercise
American Journal of Physiology-heart and Circulatory Physiology, 2002Co-Authors: Hirotsugu Tsuchimochi, Kanji Matsukawa, Hidehiko Komine, Jun MurataAbstract:The assumption that tachycardia during light to moderate exercise was predominantly controlled by withdrawal of cardiac parasympathetic Nerve activity but not by augmentation of cardiac sympathetic...
