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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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Oxygen‐Sensitive Potassium Channels in Chemoreceptor Cell Physiology
Annals of the New York Academy of Sciences, 2009Co-Authors: Constancio Gonzalez, José R. López-lópez, Luis M. Vaquero, M. Teresa Pérez-garcíaAbstract:The characterization of the molecular mechanisms involved in low-oxygen chemot ansduction has been an active field of research since the first description of an oxygen-sensitive K + channel in rabbit carotid body (CB) Chemoreceptor Cells. As a result, a large number of components of the transduction cascade, from O 2 sensors to 0 2 -sensitive ion channels, have been found. Although the endpoints of the process are analogous, the heterogeneity of the elements involved in the different Chemoreceptor tissues precludes a unifying theory of hypoxic signaling, and it has been a source of controversy. However, when these molecular constituents of the hypoxic cascade are brought back to their physiological context, it becomes clear that the diversity of mechanisms is necessary to build up an integrated Cellular response that demands the concerted action of several O 2 sensors and several effectors.
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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.
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Low glucose effects on rat carotid body Chemoreceptor Cells' secretory responses and action potential frequency in the carotid sinus nerve
The Journal of Physiology, 2007Co-Authors: Silvia V Conde, Ana Obeso, Constancio GonzalezAbstract:Glucose deprivation (hypoglycaemia) is counterbalanced by a neuroendocrine response in order to induce fast delivery of glucose to blood. Some central neurons can sense glucose, but nevertheless the most important glucose sensors/glycaemia regulators are located outside the brain. Some recent experimental evidence obtained in carotid body (CB) slices and isolated Chemoreceptor Cells in culture supports a role for the CB in glucose sensing and presumably glucose homeostasis, but this role has been questioned on the basis of a lack of effect of low glucose on the carotid sinus nerve activity. This work was performed in an attempt to clarify if low glucose is or is not a stimulus for the rat CB Chemoreceptors. Using freshly isolated intact CB preparations we have monitored the release of catecholamines (CAs) and ATP from Chemoreceptor Cells in response to several concentrations of glucose, as indices of Chemoreceptor Cell sensitivity to glycaemia, and the electrical activity in the carotid sinus nerve (CSN), as an index of reflex-triggering output of the CB. We have observed that basal (20% O2) and hypoxia (7 and 10% O2)-evoked release of CAs was identical in the presence of normal (5.55 mm) and low (3, 1 and 0 mm) glucose concentrations. 0 mm glucose did not activate the release of ATP from the CB, while hypoxia (5% O2) did. Basal and hypoxia (5% O2)-induced CSN action potential frequency was identical with 5.55 and 1 mm glucose. Our results indicate that low glucose is not a direct stimulus for the rat carotid body Chemoreceptors.
Ana Obeso - 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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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.
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Low glucose effects on rat carotid body Chemoreceptor Cells' secretory responses and action potential frequency in the carotid sinus nerve
The Journal of Physiology, 2007Co-Authors: Silvia V Conde, Ana Obeso, Constancio GonzalezAbstract:Glucose deprivation (hypoglycaemia) is counterbalanced by a neuroendocrine response in order to induce fast delivery of glucose to blood. Some central neurons can sense glucose, but nevertheless the most important glucose sensors/glycaemia regulators are located outside the brain. Some recent experimental evidence obtained in carotid body (CB) slices and isolated Chemoreceptor Cells in culture supports a role for the CB in glucose sensing and presumably glucose homeostasis, but this role has been questioned on the basis of a lack of effect of low glucose on the carotid sinus nerve activity. This work was performed in an attempt to clarify if low glucose is or is not a stimulus for the rat CB Chemoreceptors. Using freshly isolated intact CB preparations we have monitored the release of catecholamines (CAs) and ATP from Chemoreceptor Cells in response to several concentrations of glucose, as indices of Chemoreceptor Cell sensitivity to glycaemia, and the electrical activity in the carotid sinus nerve (CSN), as an index of reflex-triggering output of the CB. We have observed that basal (20% O2) and hypoxia (7 and 10% O2)-evoked release of CAs was identical in the presence of normal (5.55 mm) and low (3, 1 and 0 mm) glucose concentrations. 0 mm glucose did not activate the release of ATP from the CB, while hypoxia (5% O2) did. Basal and hypoxia (5% O2)-induced CSN action potential frequency was identical with 5.55 and 1 mm glucose. Our results indicate that low glucose is not a direct stimulus for the rat carotid body Chemoreceptors.
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Function of the rat carotid body Chemoreceptors in ageing.
Journal of Neurochemistry, 2006Co-Authors: Silvia V Conde, Emília C. Monteiro, R. Rigual, Ana Obeso, Constancio GonzalezAbstract:Some age-related deficits in the ventilatory responses have been attributed to a decline in the functionality of the carotid body (CB) arterial Chemoreceptors, but a systematic study of the CB function in ageing is lacking. In rats aged 3-24 months, we have performed quantitative morphometry on specific Chemoreceptor tissue, assessed the function of Chemoreceptor Cells by measuring the content, synthesis and release of catecholamines (a Chemoreceptor Cell neurotransmitter) in normoxia and hypoxia, and determined the functional activity of the intact organ by measuring chemosensory activity in the carotid sinus nerve (CSN) in normoxia, hypoxia and hypercapnic acidosis. We found that with age CBs enlarge, but at the same time there is a concomitant decrease in the percentage of Chemoreceptor tissue. CB content and turnover time for their catecholamines increase with age. Hypoxic stimulation of Chemoreceptor Cells elicits a smaller release of catecholamines in rats after 12 months of age, but a non-specific depolarizing stimulus elicits a comparable release at all ages. In parallel, there was a marked decrease in the responsiveness to hypoxia, but not to an acidic-hypercapnic stimulus, assessed as chemosensory activity in the CSN. We conclude that in aged mammals Chemoreceptor Cells become hypofunctional, leading to a decreased peripheral drive of ventilation.
Thomas E Finger - One of the best experts on this subject based on the ideXlab platform.
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nasal solitary Chemoreceptor Cell responses to bitter and trigeminal stimulants in vitro
Journal of Neurophysiology, 2008Co-Authors: Brian D. Gulbransen, Thomas E Finger, Tod R Clapp, Sue C KinnamonAbstract:Nasal trigeminal chemosensitivity in mice and rats is mediated in part by epithelial solitary Chemoreceptor (chemosensory) Cells (SCCs), but the exact role of these Cells in chemoreception is uncle...
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SOLITARY Chemoreceptor Cell SURVIVAL IS INDEPENDENT OF INTACT TRIGEMINAL INNERVATION
The Journal of Comparative Neurology, 2008Co-Authors: Brian D. Gulbransen, Wayne L. Silver, Thomas E FingerAbstract:Nasal solitary Chemoreceptor Cells (SCCs) are a population of specialized chemosensory epithelial Cells presumed to broaden trigeminal chemoreceptivity in mammals (Finger et al., 2003). SCCs are innervated by peptidergic trigeminal nerve fibers (Finger et al., 2003) but it is currently unknown if intact innervation is necessary for SCC development or survival. We tested the dependence of SCCs on innervation by eliminating trigeminal nerve fibers during development with neurogenin-1 knockout mice, during early postnatal development with capsaicin desensitization, and during adulthood with trigeminal lesioning. Our results demonstrate that elimination of innervation at any of these times does not result in decreased SCC numbers. In conclusion, neither SCC development nor mature Cell maintenance is dependent on intact trigeminal innervation.
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Solitary Chemoreceptor Cell proliferation in adult nasal epithelium
Journal of Neurocytology, 2005Co-Authors: Brian D. Gulbransen, Thomas E FingerAbstract:Nasal trigeminal chemosensitivity in mice and rats is mediated in part by solitary Chemoreceptor Cells (SCCs) in the nasal epithelium (Finger et al., 2003). Many nasal SCCs express the G-protein α-gustducin as well as other elements of the bitter-taste signaling cascade including phospholipase Cβ2, TRPM5 and T2R bitter-taste receptors. While some populations of sensory Cells are replaced throughout life (taste and olfaction), others are not (hair Cells and carotid body Chemoreceptors). These experiments were designed to test whether new SCCs are generated within the epithelium of adult mice. Wild type C57/B6 mice were injected with the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) to label dividing Cells. At various times after injection (1–40 days), the mice were perfused with 4% paraformaldehyde and prepared for dual-label immunocytochemistry. Double labeled Cells were detected as early as 3 days post BrdU injection and remained for as long as 12 days post-injection suggesting that SCCs do undergo turnover like the surrounding nasal epithelium. No BrdU labeled Cells were detected after 24 days suggesting relatively rapid replacement of the SCCs.
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Solitary Chemoreceptor Cell proliferation in adult nasal epithelium.
Journal of Neurocytology, 2005Co-Authors: Brian D. Gulbransen, Thomas E FingerAbstract:Nasal trigeminal chemosensitivity in mice and rats is mediated in part by solitary Chemoreceptor Cells (SCCs) in the nasal epithelium (Finger et al., 2003). Many nasal SCCs express the G-protein alpha-gustducin as well as other elements of the bitter-taste signaling cascade including phospholipase Cbeta2, TRPM5 and T2R bitter-taste receptors. While some populations of sensory Cells are replaced throughout life (taste and olfaction), others are not (hair Cells and carotid body Chemoreceptors). These experiments were designed to test whether new SCCs are generated within the epithelium of adult mice. Wild type C57/B6 mice were injected with the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) to label dividing Cells. At various times after injection (1-40 days), the mice were perfused with 4% paraformaldehyde and prepared for dual-label immunocytochemistry. Double labeled Cells were detected as early as 3 days post BrdU injection and remained for as long as 12 days post-injection suggesting that SCCs do undergo turnover like the surrounding nasal epithelium. No BrdU labeled Cells were detected after 24 days suggesting relatively rapid replacement of the SCCs.
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Evolution of taste and solitary Chemoreceptor Cell systems.
Brain Behavior and Evolution, 1997Co-Authors: Thomas E FingerAbstract:Vertebrates possess four distinct chemosensory systems distinguishable on the basis of structure, innervation and utilization: olfaction, taste, solitary Chemoreceptor Cells (SCC) and the common chemi
M. Teresa Pérez-garcía - One of the best experts on this subject based on the ideXlab platform.
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Oxygen‐Sensitive Potassium Channels in Chemoreceptor Cell Physiology
Annals of the New York Academy of Sciences, 2009Co-Authors: Constancio Gonzalez, José R. López-lópez, Luis M. Vaquero, M. Teresa Pérez-garcíaAbstract:The characterization of the molecular mechanisms involved in low-oxygen chemot ansduction has been an active field of research since the first description of an oxygen-sensitive K + channel in rabbit carotid body (CB) Chemoreceptor Cells. As a result, a large number of components of the transduction cascade, from O 2 sensors to 0 2 -sensitive ion channels, have been found. Although the endpoints of the process are analogous, the heterogeneity of the elements involved in the different Chemoreceptor tissues precludes a unifying theory of hypoxic signaling, and it has been a source of controversy. However, when these molecular constituents of the hypoxic cascade are brought back to their physiological context, it becomes clear that the diversity of mechanisms is necessary to build up an integrated Cellular response that demands the concerted action of several O 2 sensors and several effectors.
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Molecular identification of Kvalpha subunits that contribute to the oxygen-sensitive K+ current of Chemoreceptor Cells of the rabbit carotid body.
The Journal of physiology, 2002Co-Authors: Diego Sanchez, Ana Obeso, Gloria Sanz-alfayate, José R. López-lópez, M. Teresa Pérez-garcía, Maria D Ganfornina, Constancio GonzalezAbstract:Rabbit carotid body (CB) Chemoreceptor Cells possess a fast-inactivating K+ current that is specifically inhibited by hypoxia. We have studied the expression of Kvalpha subunits, which might be responsible for this current. RT-PCR experiments identified the expression of Kv1.4, Kv3.4, Kv4.1 and Kv4.3 mRNAs in the rabbit CB. There was no expression of Kv3.3 or Kv4.2 transcripts. Immunocytochemistry with antibodies to tyrosine hydroxylase (anti-TH) and to specific Kv subunits revealed the expression of Kv3.4 and Kv4.3 in Chemoreceptor Cells, while Kv1.4 was only found in nerve fibres. Kv4.1 mRNA was also found in Chemoreceptor Cells following in situ hybridization combined with anti-TH antibody labelling. Kv4.1 and Kv4.3 appeared to be present in all Chemoreceptor Cells, but Kv3.4 was only expressed in a population of them. Electrophysiological experiments applying specific toxins or antibodies demonstrated that both Kv3.4 and Kv4.3 participate in the oxygen-sensitive K+ current of Chemoreceptor Cells. However, toxin application experiments confirmed a larger contribution of members of the Kv4 subfamily. [Ca2+]i measurements under hypoxic conditions and immunocytochemistry experiments in dispersed CB Cells demonstrated the expression of Kv3.4 and Kv4.3 in oxygen-sensitive Cells; the presence of Kv3.4 in the Chemoreceptor Cell membrane was not required for the response to low PO2. In summary, three Kv subunits (Kv3.4, Kv4.1 and Kv4.3) may be involved in the fast-inactivating outward K+ current of rabbit CB Chemoreceptor Cells. The homogeneous distribution of the Kv4 subunits in Chemoreceptor Cells, along with their electrophysiological properties, suggest that Kv4.1, Kv4.3, or their heteromultimers, are the molecular correlate of the oxygen-sensitive K+ channel.
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Molecular identification of Kvα subunits that contribute to the oxygen-sensitive K+ current of Chemoreceptor Cells of the rabbit carotid body
The Journal of Physiology, 2002Co-Authors: Diego Sanchez, Ana Obeso, Gloria Sanz-alfayate, José R. López-lópez, M. Teresa Pérez-garcía, Maria D Ganfornina, Constancio GonzalezAbstract:Rabbit carotid body (CB) Chemoreceptor Cells possess a fast-inactivating K+ current that is specifically inhibited by hypoxia. We have studied the expression of Kvα subunits, which might be responsible for this current. RT-PCR experiments identified the expression of Kv1.4, Kv3.4, Kv4.1 and Kv4.3 mRNAs in the rabbit CB. There was no expression of Kv3.3 or Kv4.2 transcripts. Immunocytochemistry with antibodies to tyrosine hydroxylase (anti-TH) and to specific Kv subunits revealed the expression of Kv3.4 and Kv4.3 in Chemoreceptor Cells, while Kv1.4 was only found in nerve fibres. Kv4.1 mRNA was also found in Chemoreceptor Cells following in situ hybridization combined with anti-TH antibody labelling. Kv4.1 and Kv4.3 appeared to be present in all Chemoreceptor Cells, but Kv3.4 was only expressed in a population of them. Electrophysiological experiments applying specific toxins or antibodies demonstrated that both Kv3.4 and Kv4.3 participate in the oxygen-sensitive K+ current of Chemoreceptor Cells. However, toxin application experiments confirmed a larger contribution of members of the Kv4 subfamily. [Ca2+]i measurements under hypoxic conditions and immunocytochemistry experiments in dispersed CB Cells demonstrated the expression of Kv3.4 and Kv4.3 in oxygen-sensitive Cells; the presence of Kv3.4 in the Chemoreceptor Cell membrane was not required for the response to low PO2. In summary, three Kv subunits (Kv3.4, Kv4.1 and Kv4.3) may be involved in the fast-inactivating outward K+ current of rabbit CB Chemoreceptor Cells. The homogeneous distribution of the Kv4 subunits in Chemoreceptor Cells, along with their electrophysiological properties, suggest that Kv4.1, Kv4.3, or their heteromultimers, are the molecular correlate of the oxygen-sensitive K+ channel.
Brian D. Gulbransen - One of the best experts on this subject based on the ideXlab platform.
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nasal solitary Chemoreceptor Cell responses to bitter and trigeminal stimulants in vitro
Journal of Neurophysiology, 2008Co-Authors: Brian D. Gulbransen, Thomas E Finger, Tod R Clapp, Sue C KinnamonAbstract:Nasal trigeminal chemosensitivity in mice and rats is mediated in part by epithelial solitary Chemoreceptor (chemosensory) Cells (SCCs), but the exact role of these Cells in chemoreception is uncle...
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SOLITARY Chemoreceptor Cell SURVIVAL IS INDEPENDENT OF INTACT TRIGEMINAL INNERVATION
The Journal of Comparative Neurology, 2008Co-Authors: Brian D. Gulbransen, Wayne L. Silver, Thomas E FingerAbstract:Nasal solitary Chemoreceptor Cells (SCCs) are a population of specialized chemosensory epithelial Cells presumed to broaden trigeminal chemoreceptivity in mammals (Finger et al., 2003). SCCs are innervated by peptidergic trigeminal nerve fibers (Finger et al., 2003) but it is currently unknown if intact innervation is necessary for SCC development or survival. We tested the dependence of SCCs on innervation by eliminating trigeminal nerve fibers during development with neurogenin-1 knockout mice, during early postnatal development with capsaicin desensitization, and during adulthood with trigeminal lesioning. Our results demonstrate that elimination of innervation at any of these times does not result in decreased SCC numbers. In conclusion, neither SCC development nor mature Cell maintenance is dependent on intact trigeminal innervation.
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Solitary Chemoreceptor Cell proliferation in adult nasal epithelium
Journal of Neurocytology, 2005Co-Authors: Brian D. Gulbransen, Thomas E FingerAbstract:Nasal trigeminal chemosensitivity in mice and rats is mediated in part by solitary Chemoreceptor Cells (SCCs) in the nasal epithelium (Finger et al., 2003). Many nasal SCCs express the G-protein α-gustducin as well as other elements of the bitter-taste signaling cascade including phospholipase Cβ2, TRPM5 and T2R bitter-taste receptors. While some populations of sensory Cells are replaced throughout life (taste and olfaction), others are not (hair Cells and carotid body Chemoreceptors). These experiments were designed to test whether new SCCs are generated within the epithelium of adult mice. Wild type C57/B6 mice were injected with the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) to label dividing Cells. At various times after injection (1–40 days), the mice were perfused with 4% paraformaldehyde and prepared for dual-label immunocytochemistry. Double labeled Cells were detected as early as 3 days post BrdU injection and remained for as long as 12 days post-injection suggesting that SCCs do undergo turnover like the surrounding nasal epithelium. No BrdU labeled Cells were detected after 24 days suggesting relatively rapid replacement of the SCCs.
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Solitary Chemoreceptor Cell proliferation in adult nasal epithelium.
Journal of Neurocytology, 2005Co-Authors: Brian D. Gulbransen, Thomas E FingerAbstract:Nasal trigeminal chemosensitivity in mice and rats is mediated in part by solitary Chemoreceptor Cells (SCCs) in the nasal epithelium (Finger et al., 2003). Many nasal SCCs express the G-protein alpha-gustducin as well as other elements of the bitter-taste signaling cascade including phospholipase Cbeta2, TRPM5 and T2R bitter-taste receptors. While some populations of sensory Cells are replaced throughout life (taste and olfaction), others are not (hair Cells and carotid body Chemoreceptors). These experiments were designed to test whether new SCCs are generated within the epithelium of adult mice. Wild type C57/B6 mice were injected with the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) to label dividing Cells. At various times after injection (1-40 days), the mice were perfused with 4% paraformaldehyde and prepared for dual-label immunocytochemistry. Double labeled Cells were detected as early as 3 days post BrdU injection and remained for as long as 12 days post-injection suggesting that SCCs do undergo turnover like the surrounding nasal epithelium. No BrdU labeled Cells were detected after 24 days suggesting relatively rapid replacement of the SCCs.