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Constancio Gonzalez - One of the best experts on this subject based on the ideXlab platform.
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Experimental Observations on the Biological Significance of Hydrogen Sulfide in Carotid Body Chemoreception
Advances in Experimental Medicine and Biology, 2015Co-Authors: Teresa Gallego-martin, Ana Obeso, Asuncion Rocher, A. Gómez-niño, Teresa Agapito, M. C. Ramírez, Elena Olea, Sara Yubero, Constancio GonzalezAbstract:The cascade of transduction of hypoxia and hypercapnia, the natural stimuli to Chemoreceptor Cells, is incompletely understood. A particular gap in that knowledge is the role played by second messengers, or in a most ample term, of modulators. A recently described modulator of Chemoreceptor cell responses is the gaseous transmitter hydrogen sulfide, which has been proposed as a specific activator of the hypoxic responses in the carotid body, both at the level of the Chemoreceptor cell response or at the level of the global output of the organ. Since sulfide behaves in this regard as cAMP, we explored the possibility that sulfide effects were mediated by the more classical messenger. Data indicate that exogenous and endogenous sulfide inhibits adenyl cyclase finding additionally that inhibition of adenylyl cyclase does not modify Chemoreceptor cell responses elicited by sulfide. We have also observed that transient receptor potential cation channels A1 (TRPA1) are not regulated by sulfide in Chemoreceptor Cells.
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Effects of low glucose on carotid body Chemoreceptor cell activity studied in cultures of intact organs and in dissociated Cells.
American Journal of Physiology-Cell Physiology, 2012Co-Authors: Teresa Gallego-martin, Ana Obeso, R. Rigual, Silvia Fernandez-martinez, Constancio GonzalezAbstract:The participation of the carotid body (CB) in glucose homeostasis and evidence obtained in simplified cultured CB slices or dissociated Cells have led to the proposal that CB Chemoreceptor Cells ar...
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EPAC signalling pathways are involved in low PO2 chemoreception in carotid body Chemoreceptor Cells.
The Journal of physiology, 2009Co-Authors: Asuncion Rocher, Ana I Caceres, Laura Almaraz, Constancio GonzalezAbstract:Chemoreceptor Cells of the carotid bodies (CB) are activated by hypoxia and acidosis, responding with an increase in their rate of neurotransmitter release, which in turn increases the electrical activity in the carotid sinus nerve and evokes a homeostatic hyperventilation. Studies in isolated Chemoreceptor Cells have shown that moderate hypoxias ( 46 mmHg) produces smaller depolarisations and comparable Ca(2+) transients but a much higher catecholamine (CA) release response in intact CBs than intense acidic/hypercapnic stimuli (20% CO(2), pH 6.6). Similarly, intense hypoxia ( 20 mmHg) produces smaller depolarizations and Ca(2+) transients in isolated Chemoreceptor Cells but a higher CA release response in intact CBs than a pure depolarizing stimulus (30-35 mm external K(+)). Studying the mechanisms responsible for these differences we have found the following. (1) Acidic hypercapnia inhibited I(Ca) (60%; whole cell) and CA release (45%; intact CB) elicited by ionomycin and high K(+). (2) Adenylate cyclase inhibition (SQ-22536; 80 microm) inhibited the hypoxic release response (>50%) and did not affect acidic/hypercapnic release, evidencing that the high gain of hypoxia to elicit neurotransmitter release is cAMP dependent. (3) The last effect was independent of PKA activation, as three kinase inhibitors (H-89, KT 5720 and Rp-cAMP; 10 x IC(50)) did not alter the hypoxic release response. (4) The Epac (exchange protein activated by cAMP) activator (8-pCPT-2-O-Me-cAMP, 100 microm) reversed the effects of the cyclase inhibitor. (5) The Epac inhibitor brefeldin A (100 microm) inhibited (54%) hypoxic induced release. Our findings show for the first time that an Epac-mediated pathway mediates O(2) sensing/transduction in Chemoreceptor Cells.
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General redox environment and carotid body Chemoreceptor function.
American Journal of Physiology-Cell Physiology, 2009Co-Authors: M. T. Agapito, Constancio Gonzalez, Gloria Sanz-alfayate, A. Gómez-niño, Ana ObesoAbstract:Carotid body (CB) Chemoreceptor Cells detect physiological levels of hypoxia and generate a hyperventilation, homeostatic in nature, aimed to minimize the deleterious effects of hypoxia. Intimate m...
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Effects of mitochondrial poisons on glutathione redox potential and carotid body Chemoreceptor activity
Respiratory Physiology & Neurobiology, 2009Co-Authors: A. Gómez-niño, M. T. Agapito, Ana Obeso, Constancio GonzalezAbstract:Abstract Low oxygen sensing in Chemoreceptor Cells involves the inhibition of specific plasma membrane K + channels, suggesting that mitochondria-derived reactive oxygen species (ROS) link hypoxia to K + channel inhibition, subsequent cell depolarization and activation of neurotransmitter release. We have used several mitochondrial poisons, alone and in combination with the antioxidant N-acetylcysteine (NAC), and quantify their capacity to alter GSH/GSSG levels and glutathione redox potential ( E GSH ) in rat diaphragm. Selected concentrations of mitochondrial poisons with or without NAC were tested for their capacity to activate neurotransmitter release in Chemoreceptor Cells and to alter ATP levels in intact rat carotid body (CB). We found that rotenone (1 μM), antimycin A (0.2 μg/ml) and sodium azide (5 mM) decreased E GSH ; NAC restored E GSH to control values. At those concentrations mitochondrial poisons activated neurotransmitter release from CB Chemoreceptor Cells and decreased CB ATP levels, NAC being ineffective to modify these responses. Additional experiments with 3-nitroprionate (5 mM), lower concentrations of rotenone and dinitrophenol revealed variable relationships between E GSH and Chemoreceptor cell neurotransmitter release responses and ATP levels. These findings indicate a lack of correlation between mitochondrial-generated modifications of E GSH and Chemoreceptor Cells activity. This lack of correlation renders unlikely that alteration of mitochondrial production of ROS is the physiological pathway Chemoreceptor Cells use to signal hypoxia.
Asuncion Rocher - One of the best experts on this subject based on the ideXlab platform.
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Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells
Antioxidants, 2019Co-Authors: Teresa Gallego-martin, Asuncion Rocher, Jesus Prieto-lloret, Philip I. Aaronson, Ana ObesoAbstract:Carotid body (CB) Chemoreceptor Cells sense arterial blood PO2, generating a neurosecretory response proportional to the intensity of hypoxia. Hydrogen sulfide (H2S) is a physiological gaseous messenger that is proposed to act as an oxygen sensor in CBs, although this concept remains controversial. In the present study we have used the H2S scavenger and vitamin B12 analog hydroxycobalamin (Cbl) as a new tool to investigate the involvement of endogenous H2S in CB oxygen sensing. We observed that the slow-release sulfide donor GYY4137 elicited catecholamine release from isolated whole carotid bodies, and that Cbl prevented this response. Cbl also abolished the rise in [Ca2+]i evoked by 50 µM NaHS in enzymatically dispersed CB glomus Cells. Moreover, Cbl markedly inhibited the catecholamine release and [Ca2+]i rise caused by hypoxia in isolated CBs and dispersed glomus Cells, respectively, whereas it did not alter these responses when they were evoked by high [K+]e. The L-type Ca2+ channel blocker nifedipine slightly inhibited the rise in CB Chemoreceptor Cells [Ca2+]i elicited by sulfide, whilst causing a somewhat larger attenuation of the hypoxia-induced Ca2+ signal. We conclude that Cbl is a useful and specific tool for studying the function of H2S in Cells. Based on its effects on the CB Chemoreceptor Cells we propose that endogenous H2S is an amplifier of the hypoxic transduction cascade which acts mainly by stimulating non-L-type Ca2+ channels.
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Guinea Pig Oxygen-Sensing and Carotid Body Functional Properties
Frontiers Media S.A., 2017Co-Authors: Elvira Gonzalez-obeso, Ana Obeso, Elena Olea, Inmaculada Docio, Angel Cogolludo, Asuncion RocherAbstract:Mammals have developed different mechanisms to maintain oxygen supply to Cells in response to hypoxia. One of those mechanisms, the carotid body (CB) Chemoreceptors, is able to detect physiological hypoxia and generate homeostatic reflex responses, mainly ventilatory and cardiovascular. It has been reported that guinea pigs, originally from the Andes, have a reduced ventilatory response to hypoxia compared to other mammals, implying that CB are not completely functional, which has been related to genetically/epigenetically determined poor hypoxia-driven CB reflex. This study was performed to check the guinea pig CB response to hypoxia compared to the well-known rat hypoxic response. These experiments have explored ventilatory parameters breathing different gases mixtures, cardiovascular responses to acute hypoxia, in vitro CB response to hypoxia and other stimuli and isolated guinea pig Chemoreceptor Cells properties. Our findings show that guinea pigs are hypotensive and have lower arterial pO2 than rats, probably related to a low sympathetic tone and high hemoglobin affinity. Those characteristics could represent a higher tolerance to hypoxic environment than other rodents. We also find that although CB are hypo-functional not showing chronic hypoxia sensitization, a small percentage of isolated carotid body Chemoreceptor Cells contain tyrosine hydroxylase enzyme and voltage-dependent K+ currents and therefore can be depolarized. However hypoxia does not modify intracellular Ca2+ levels or catecholamine secretion. Guinea pigs are able to hyperventilate only in response to intense acute hypoxic stimulus, but hypercapnic response is similar to rats. Whether other brain areas are also activated by hypoxia in guinea pigs remains to be studied
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Experimental Observations on the Biological Significance of Hydrogen Sulfide in Carotid Body Chemoreception
Advances in Experimental Medicine and Biology, 2015Co-Authors: Teresa Gallego-martin, Ana Obeso, Asuncion Rocher, A. Gómez-niño, Teresa Agapito, M. C. Ramírez, Elena Olea, Sara Yubero, Constancio GonzalezAbstract:The cascade of transduction of hypoxia and hypercapnia, the natural stimuli to Chemoreceptor Cells, is incompletely understood. A particular gap in that knowledge is the role played by second messengers, or in a most ample term, of modulators. A recently described modulator of Chemoreceptor cell responses is the gaseous transmitter hydrogen sulfide, which has been proposed as a specific activator of the hypoxic responses in the carotid body, both at the level of the Chemoreceptor cell response or at the level of the global output of the organ. Since sulfide behaves in this regard as cAMP, we explored the possibility that sulfide effects were mediated by the more classical messenger. Data indicate that exogenous and endogenous sulfide inhibits adenyl cyclase finding additionally that inhibition of adenylyl cyclase does not modify Chemoreceptor cell responses elicited by sulfide. We have also observed that transient receptor potential cation channels A1 (TRPA1) are not regulated by sulfide in Chemoreceptor Cells.
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EPAC signalling pathways are involved in low PO2 chemoreception in carotid body Chemoreceptor Cells.
The Journal of physiology, 2009Co-Authors: Asuncion Rocher, Ana I Caceres, Laura Almaraz, Constancio GonzalezAbstract:Chemoreceptor Cells of the carotid bodies (CB) are activated by hypoxia and acidosis, responding with an increase in their rate of neurotransmitter release, which in turn increases the electrical activity in the carotid sinus nerve and evokes a homeostatic hyperventilation. Studies in isolated Chemoreceptor Cells have shown that moderate hypoxias ( 46 mmHg) produces smaller depolarisations and comparable Ca(2+) transients but a much higher catecholamine (CA) release response in intact CBs than intense acidic/hypercapnic stimuli (20% CO(2), pH 6.6). Similarly, intense hypoxia ( 20 mmHg) produces smaller depolarizations and Ca(2+) transients in isolated Chemoreceptor Cells but a higher CA release response in intact CBs than a pure depolarizing stimulus (30-35 mm external K(+)). Studying the mechanisms responsible for these differences we have found the following. (1) Acidic hypercapnia inhibited I(Ca) (60%; whole cell) and CA release (45%; intact CB) elicited by ionomycin and high K(+). (2) Adenylate cyclase inhibition (SQ-22536; 80 microm) inhibited the hypoxic release response (>50%) and did not affect acidic/hypercapnic release, evidencing that the high gain of hypoxia to elicit neurotransmitter release is cAMP dependent. (3) The last effect was independent of PKA activation, as three kinase inhibitors (H-89, KT 5720 and Rp-cAMP; 10 x IC(50)) did not alter the hypoxic release response. (4) The Epac (exchange protein activated by cAMP) activator (8-pCPT-2-O-Me-cAMP, 100 microm) reversed the effects of the cyclase inhibitor. (5) The Epac inhibitor brefeldin A (100 microm) inhibited (54%) hypoxic induced release. Our findings show for the first time that an Epac-mediated pathway mediates O(2) sensing/transduction in Chemoreceptor Cells.
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RT-PCR and Pharmacological Analysis of L-and T-Type Calcium Channels in Rat Carotid Body
Advances in Experimental Medicine and Biology, 2009Co-Authors: Ana Isabel Caceres, Constancio Gonzalez, Elvira Gonzalez-obeso, Asuncion RocherAbstract:Mechanisms involved in carotid body (CB) Chemoreceptor Cells O2-sensing and responses are not fully understood. So far, it is known that hypoxia depolarizes Chemoreceptor Cells via O2-sensitive K+-channel inhibition; calcium influx via voltage-gated channels and neurotransmitter secretion follow. Presence of high voltage activated (HVA) calcium channels in rat CB Chemoreceptor Cells is well documented, but the presence of low voltage activated (LVH) or T-type calcium channels has not been reported to date. The fact that O2-sensitive PC12 Cells express T-type channels and that they are inducible by chronic hypoxia (CH) lead us to hypothesize they could be present and play a role in the genesis of the hypoxic response in rat CB Chemoreceptor Cells. We have analyzed the expression of the three isoforms of T-type calcium channels (α1G, α1H and α1I) and the isoforms α1C and α1D of L-type calcium channels in rat CB by RT-PCR. We found that rat CB expresses α1G and α1C subunits. After chronic hypoxic treatment of adult rats (10° O2, 8 days), expression of α1G seems to be down-regulated whereas α1C expression is up-regulated. Functionally, it was found that the release of catecholamine induced by hypoxia and high external K{+} from CB Chemoreceptor Cells was fully sensitive to L-type channel inhibition (nisoldipine, 2 μM), while specific inhibition of T-channels (mibefradil, 2 μM) inhibited exclusively hypoxia-induced release (50°). As a whole, present findings demonstrate the presence of T-type as well as L-type calcium channels in rat CB and suggest a selective participation of the T-type channels in the hypoxic activation of Chemoreceptor Cells.
Jelle Atema - One of the best experts on this subject based on the ideXlab platform.
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The olfactory pathway for individual recognition in the American lobster Homarus americanus.
Journal of Experimental Biology, 2005Co-Authors: Meg E. Johnson, Jelle AtemaAbstract:Individual recognition in the lobster Homarus americanus (Milne-Edwards), is based on detection of urine pheromones via Chemoreceptors of the lateral antennular flagellum. The specific sensory pathway mediating this recognition is not known. Most of the Chemoreceptor Cells of this flagellum are found in the unimodal aesthetasc sensilla and project specifically to the glomeruli of the olfactory lobe in the brain. Additional Chemoreceptor Cells are located among mechanoreceptor Cells in bimodal sensilla, including the guard hairs; they do not project to the olfactory lobe. This neuroanatomy suggested that aesthetascs were essential to all complex chemosensory tasks until it was shown that spiny lobsters Panulirus argus can still perform complex food odor discrimination and localization tasks without aesthetascs. Here, we demonstrate that the aesthetascs of H. americanus contain the Chemoreceptors necessary for individual recognition of familiar opponents. In contrast to intact and guard hair-shaved animals, lobsters with aesthetascs removed did not recognize previous opponents as shown by second encounters statistically similar in length and aggression to first-encounter fights. Non-aesthetasc chemosensory pathways were incapable of rescuing opponent recognition. Subsequent lesion of all remaining Chemoreceptor Cells (by immersion in distilled water) abolished recognition and renewed fighting.
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Temporal resolution in olfaction III: flicker fusion and concentration-dependent synchronization with stimulus pulse trains of antennular Chemoreceptor Cells in the American lobster
Journal of Comparative Physiology A: Sensory Neural and Behavioral Physiology, 1999Co-Authors: George Gomez, Rainer Voigt, Jelle AtemaAbstract:To understand how Chemoreceptor organs may extract temporal information from odor plumes, we investigated the frequency filter properties of lobster Chemoreceptor Cells. We used rapid stimulation and high-resolution stimulus measurement for accurate stimulus control and recorded extracellular responses from Chemoreceptors in the lobster lateral antennule in situ. We tested 16 hydroxyproline-sensitive Cells with a series of ten 100-ms pulses at 10, 100 and 1000 μmol l−1 at stimulation frequencies from 0.5 Hz to 4 Hz. Receptor cell responses could accurately encode 10 μmol l−1, but not 100 or 1000 μmol l−1 pulses, delivered at rates of 4 Hz. Flicker-fusion frequency and synchronization with the stimulus pulse train were concentration dependent: performance rates above 1 Hz became poorer both with increasing pulse amplitude and frequency. Flicker fusion frequency was 3 Hz for 100 μmol l−1 pulses and 2 Hz for 1000 μmol l−1 pulses. Individual Cells showed differences in their stimulus pulse following capabilities, as measured by the synchronization coefficient. These individual differences may form a basis for coding temporal features of an odor plume in an across-fiber pattern.
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Spectral tuning of Chemoreceptor Cells in the lateral antennules of the American lobster,Homarus Americanus
Marine and Freshwater Behaviour and Physiology, 1997Co-Authors: Rainer Voigt, Anna Margriet Weinstein, Jelle AtemaAbstract:Chemoreceptor Cells in the lateral flagellum of the first antennae (lateral antennule) of the American lobster, Homarus americanus, serve, among other functions, in long distance orientation and mediate chemical recognition of food and chemical information used in social interactions. Based upon extracellular recordings of action potentials, we report on 60 Cells identified with a 15‐compound equimolar mixture of mostly amino acids and a few other compounds used in previous studies of lobster Chemoreceptors. Subsequently, all Cells were tested with each compound separately. Forty‐three percent of all Cells responded strongest to hydroxyproline, 13% to taurine, and 10% to glutamate. These Cells were generally narrowly tuned and had no consistent second best stimulus. Other Cells were more broadly tuned and responded strongest to valine, arginine, leucine, glutamine, serine, glycine, alanine and ammonium. Most Chemoreceptor Cells responded less to a mixture containing their best compound than to the best co...
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Temporal resolution in olfaction II: time course of recovery from adaptation in lobster Chemoreceptor Cells.
Journal of Neurophysiology, 1996Co-Authors: George Gomez, Jelle AtemaAbstract:1. Adaptation and disadaptation rates determine the temporal response properties of sensory receptor Cells. In chemoreception, temporal filter properties of receptor Cells are poorly understood. We studied the time course of disadaptation in lobster antennular Chemoreceptor Cells by using in situ high-resolution stimulus measurement and extracellularly recorded spike responses. Fifteen receptor Cells were each tested with two series (one at 10 microM, one at 100 microM) of three odor (hydroxyproline) pulses: a 200-ms test pulse, a 5-s adapting pulse, and a 200-ms probe pulse after time intervals ranging from 1 to 60 s. After complete adaptation by the adapting pulse, individual Cells recovered at different rates. After 1 s, a third of the Cells responded with a mean response of 3 spikes/cell, representing approximately 20% recovery. All Cells fully recovered between 10 and 30 s. Mean full recovery was within 25 s, with a time constant of 14 s, independent of stimulus concentration.
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temporal resolution in olfaction stimulus integration time of lobster Chemoreceptor Cells
The Journal of Experimental Biology, 1996Co-Authors: George Gomez, Jelle AtemaAbstract:The stimulus integration time of lobster olfactory receptor Cells in situ was determined using extracellularly recorded spiking responses from receptor Cells and on-line high-resolution measurement of odor square pulses. At a fixed odor concentration, odor steps of 200 ms duration elicited maximum responses; shorter odor steps did not drive the Cells to their maximum response and longer odor steps added spikes but did not result in higher firing rates. Excitatory processes peaked within 220 ms of stimulus onset. At 160300 ms, stimulus intensity discrimination was most evident. Adaptation processes reduced response magnitude to near-zero levels within 1000 ms of stimulus onset. Olfactory receptor Cells thus resolve odor peak onsets within the first few hundred milliseconds: this time window corresponds to the 45 Hz frequency of olfactory sampling (i.e. 'sniffing') as well as the rapid fluctuations in odor concentration that are common in natural odor plumes. The stimulus integration time of 200 ms may play a role in the filtering of information used by lobsters to orient to distant odor sources.
Ana Obeso - One of the best experts on this subject based on the ideXlab platform.
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Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells
Antioxidants, 2019Co-Authors: Teresa Gallego-martin, Asuncion Rocher, Jesus Prieto-lloret, Philip I. Aaronson, Ana ObesoAbstract:Carotid body (CB) Chemoreceptor Cells sense arterial blood PO2, generating a neurosecretory response proportional to the intensity of hypoxia. Hydrogen sulfide (H2S) is a physiological gaseous messenger that is proposed to act as an oxygen sensor in CBs, although this concept remains controversial. In the present study we have used the H2S scavenger and vitamin B12 analog hydroxycobalamin (Cbl) as a new tool to investigate the involvement of endogenous H2S in CB oxygen sensing. We observed that the slow-release sulfide donor GYY4137 elicited catecholamine release from isolated whole carotid bodies, and that Cbl prevented this response. Cbl also abolished the rise in [Ca2+]i evoked by 50 µM NaHS in enzymatically dispersed CB glomus Cells. Moreover, Cbl markedly inhibited the catecholamine release and [Ca2+]i rise caused by hypoxia in isolated CBs and dispersed glomus Cells, respectively, whereas it did not alter these responses when they were evoked by high [K+]e. The L-type Ca2+ channel blocker nifedipine slightly inhibited the rise in CB Chemoreceptor Cells [Ca2+]i elicited by sulfide, whilst causing a somewhat larger attenuation of the hypoxia-induced Ca2+ signal. We conclude that Cbl is a useful and specific tool for studying the function of H2S in Cells. Based on its effects on the CB Chemoreceptor Cells we propose that endogenous H2S is an amplifier of the hypoxic transduction cascade which acts mainly by stimulating non-L-type Ca2+ channels.
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Guinea Pig Oxygen-Sensing and Carotid Body Functional Properties
Frontiers Media S.A., 2017Co-Authors: Elvira Gonzalez-obeso, Ana Obeso, Elena Olea, Inmaculada Docio, Angel Cogolludo, Asuncion RocherAbstract:Mammals have developed different mechanisms to maintain oxygen supply to Cells in response to hypoxia. One of those mechanisms, the carotid body (CB) Chemoreceptors, is able to detect physiological hypoxia and generate homeostatic reflex responses, mainly ventilatory and cardiovascular. It has been reported that guinea pigs, originally from the Andes, have a reduced ventilatory response to hypoxia compared to other mammals, implying that CB are not completely functional, which has been related to genetically/epigenetically determined poor hypoxia-driven CB reflex. This study was performed to check the guinea pig CB response to hypoxia compared to the well-known rat hypoxic response. These experiments have explored ventilatory parameters breathing different gases mixtures, cardiovascular responses to acute hypoxia, in vitro CB response to hypoxia and other stimuli and isolated guinea pig Chemoreceptor Cells properties. Our findings show that guinea pigs are hypotensive and have lower arterial pO2 than rats, probably related to a low sympathetic tone and high hemoglobin affinity. Those characteristics could represent a higher tolerance to hypoxic environment than other rodents. We also find that although CB are hypo-functional not showing chronic hypoxia sensitization, a small percentage of isolated carotid body Chemoreceptor Cells contain tyrosine hydroxylase enzyme and voltage-dependent K+ currents and therefore can be depolarized. However hypoxia does not modify intracellular Ca2+ levels or catecholamine secretion. Guinea pigs are able to hyperventilate only in response to intense acute hypoxic stimulus, but hypercapnic response is similar to rats. Whether other brain areas are also activated by hypoxia in guinea pigs remains to be studied
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Experimental Observations on the Biological Significance of Hydrogen Sulfide in Carotid Body Chemoreception
Advances in Experimental Medicine and Biology, 2015Co-Authors: Teresa Gallego-martin, Ana Obeso, Asuncion Rocher, A. Gómez-niño, Teresa Agapito, M. C. Ramírez, Elena Olea, Sara Yubero, Constancio GonzalezAbstract:The cascade of transduction of hypoxia and hypercapnia, the natural stimuli to Chemoreceptor Cells, is incompletely understood. A particular gap in that knowledge is the role played by second messengers, or in a most ample term, of modulators. A recently described modulator of Chemoreceptor cell responses is the gaseous transmitter hydrogen sulfide, which has been proposed as a specific activator of the hypoxic responses in the carotid body, both at the level of the Chemoreceptor cell response or at the level of the global output of the organ. Since sulfide behaves in this regard as cAMP, we explored the possibility that sulfide effects were mediated by the more classical messenger. Data indicate that exogenous and endogenous sulfide inhibits adenyl cyclase finding additionally that inhibition of adenylyl cyclase does not modify Chemoreceptor cell responses elicited by sulfide. We have also observed that transient receptor potential cation channels A1 (TRPA1) are not regulated by sulfide in Chemoreceptor Cells.
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Effects of low glucose on carotid body Chemoreceptor cell activity studied in cultures of intact organs and in dissociated Cells.
American Journal of Physiology-Cell Physiology, 2012Co-Authors: Teresa Gallego-martin, Ana Obeso, R. Rigual, Silvia Fernandez-martinez, Constancio GonzalezAbstract:The participation of the carotid body (CB) in glucose homeostasis and evidence obtained in simplified cultured CB slices or dissociated Cells have led to the proposal that CB Chemoreceptor Cells ar...
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General redox environment and carotid body Chemoreceptor function.
American Journal of Physiology-Cell Physiology, 2009Co-Authors: M. T. Agapito, Constancio Gonzalez, Gloria Sanz-alfayate, A. Gómez-niño, Ana ObesoAbstract:Carotid body (CB) Chemoreceptor Cells detect physiological levels of hypoxia and generate a hyperventilation, homeostatic in nature, aimed to minimize the deleterious effects of hypoxia. Intimate m...
Yoshihiro Yoshihara - One of the best experts on this subject based on the ideXlab platform.
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genetic tracing of the gustatory and trigeminal neural pathways originating from t1r3 expressing taste receptor Cells and solitary Chemoreceptor Cells
Molecular and Cellular Neuroscience, 2008Co-Authors: Makoto Ohmoto, Ichiro Matsumoto, Akihito Yasuoka, Yoshihiro YoshiharaAbstract:We established transgenic mouse lines expressing a transneuronal tracer, wheat germ agglutinin (WGA), under the control of mouse T1R3 gene promoter/enhancer. In the taste buds, WGA transgene was faithfully expressed in T1R3-positive sweet/umami taste receptor Cells. WGA protein was transferred not laterally to the synapse-bearing, sour-responsive type III Cells in the taste buds but directly to a subset of neurons in the geniculate and nodose/petrosal ganglia, and further conveyed to a rostro-central region of the nucleus of solitary tract. In addition, WGA was expressed in solitary Chemoreceptor Cells in the nasal epithelium and transferred along the trigeminal sensory pathway to the brainstem neurons. The solitary Chemoreceptor Cells endogenously expressed T1R3 together with bitter taste receptors T2Rs. This result shows an exceptional signature of receptor expression. Thus, the t1r3-WGA transgenic mice revealed the sweet/umami gustatory pathways from taste receptor Cells and the trigeminal neural pathway from solitary Chemoreceptor Cells.