Abstract:The preoptic area regulates body temperature. GABA-ergic terminals and receptors are present in this area. Local microinjection studies have shown that GABA, its agonist, and its antagonist in this area may modulate body temperature. However, there are warm and cold sensitive neurons, and they are known to be affected by local and peripheral temperatures. In order to understand the mechanism of action of GABA in temperature regulation at the cellular level it was necessary to study the effect of GABA on indivi… Show more
“…Concentrations of GABA and its antagonists were similar to those used in iontophoretic experiments (Caspary et al, 1994; Backoff et al, 1997, 1999; Jha, 2001; Gai and Carney, 2008). The neurite and the modified Schwann cells of the inner core are covered by at least 30 layers of outer lamellae that are joined by tight junctions, as well as an outer 5 layers of external capsule, making this preparation less readily accessible to drugs than cell-culture studies or other tactile receptor preparations, e.g., Panek et al (2002) or Fagan and Cahusac (2001).…”
Pacinian corpuscles (PCs) are tactile receptors composed of a nerve ending (neurite) that is encapsulated by layers of lamellar cells. PCs are classified as primary mechanoreceptors because there is no synapse between the transductive membrane and the site of actionpotential generation. These touch receptors respond in a rapidly adapting manner to sustained pressure (indentation or displacement), which until now was believed to be attributable solely to the mechanical properties of the capsule. However, evidence of positive immunoreactivity for GABA receptors on the neurite, as well as evidence for gene expression of synaptobrevin in the lamellar cells led to the hypothesis that GABAergic inhibition originating from the lamellar cells is involved in the rapid adaptation process of PCs. Electrophysiological data from isolated PCs demonstrates that, in the presence of either gabazine or picrotoxin (GABA receptor antagonists), many action potentials appear during the static portion of a sustained indentation stimulus (similar to slowly adapting receptors) and that these "static" spikes completely disappear in the presence of GABA. It was consequently hypothesized that glutamate, released by either the neurite itself or the lamellar cells, caused these action potentials. Indeed, the glutamate receptor blocker kynurenate either decreased or totally eliminated the static spikes. Together, these results suggest that GABA, emanating from the modified Schwann cells of the capsule, inhibits glutamatergic excitation during the static portion of sustained pressure, thus forming a "mechanochemical," rather than purely mechanical, rapid adaptation response. This glial-neuronal interaction is a completely novel finding for the PC.
“…Concentrations of GABA and its antagonists were similar to those used in iontophoretic experiments (Caspary et al, 1994; Backoff et al, 1997, 1999; Jha, 2001; Gai and Carney, 2008). The neurite and the modified Schwann cells of the inner core are covered by at least 30 layers of outer lamellae that are joined by tight junctions, as well as an outer 5 layers of external capsule, making this preparation less readily accessible to drugs than cell-culture studies or other tactile receptor preparations, e.g., Panek et al (2002) or Fagan and Cahusac (2001).…”
Pacinian corpuscles (PCs) are tactile receptors composed of a nerve ending (neurite) that is encapsulated by layers of lamellar cells. PCs are classified as primary mechanoreceptors because there is no synapse between the transductive membrane and the site of actionpotential generation. These touch receptors respond in a rapidly adapting manner to sustained pressure (indentation or displacement), which until now was believed to be attributable solely to the mechanical properties of the capsule. However, evidence of positive immunoreactivity for GABA receptors on the neurite, as well as evidence for gene expression of synaptobrevin in the lamellar cells led to the hypothesis that GABAergic inhibition originating from the lamellar cells is involved in the rapid adaptation process of PCs. Electrophysiological data from isolated PCs demonstrates that, in the presence of either gabazine or picrotoxin (GABA receptor antagonists), many action potentials appear during the static portion of a sustained indentation stimulus (similar to slowly adapting receptors) and that these "static" spikes completely disappear in the presence of GABA. It was consequently hypothesized that glutamate, released by either the neurite itself or the lamellar cells, caused these action potentials. Indeed, the glutamate receptor blocker kynurenate either decreased or totally eliminated the static spikes. Together, these results suggest that GABA, emanating from the modified Schwann cells of the capsule, inhibits glutamatergic excitation during the static portion of sustained pressure, thus forming a "mechanochemical," rather than purely mechanical, rapid adaptation response. This glial-neuronal interaction is a completely novel finding for the PC.
“…Potential regional differences in GABA B receptor expression may also play a role in the altered hypothermic or ataxic responses to baclofen in the different mouse strains. Body temperature is coordinated primarily by the anterior hypothalamus and preoptic area (Boulant 2000;Frosini et al 2004), and is mediated at least partially through GABA B receptors in these regions (Yakimova et al 1996;Pierau et al 1997;Jha et al 2001). The posterior hypothalamus and brainstem nuclei are also implicated in body temperature regulation.…”
There is differential genetic control on specific GABA B receptor populations that mediate hypothermia and ataxia. Further, these studies demonstrate that background strain is an important determinant of GABA B receptor mediated responses, and that hypothermic and ataxic responses may be influenced by independent genetic loci.
“…This region is known for its involvement in thermoregulation (Belugin et al, 1999;Ishiwata et al, 2001;Jha et al, 2001). The preoptic area contains thermosensitive neurons and is thought to influence body temperature via interconnections with related hypothalamic neuroendocrine systems and by descending projections to autonomic targets in the brainstem and spinal cord, which are then able to mobilize either metabolic thermogenesis or behavioral heat dissipation mechanisms (Belugin et al, 1999;Ishiwata et al, 2001;Jha et al, 2001).…”
Section: Expression Of Vglut Mrnas In Hypothalamic Integratorsmentioning
confidence: 99%
“…This region is known for its involvement in thermoregulation (Belugin et al, 1999;Ishiwata et al, 2001;Jha et al, 2001). The preoptic area contains thermosensitive neurons and is thought to influence body temperature via interconnections with related hypothalamic neuroendocrine systems and by descending projections to autonomic targets in the brainstem and spinal cord, which are then able to mobilize either metabolic thermogenesis or behavioral heat dissipation mechanisms (Belugin et al, 1999;Ishiwata et al, 2001;Jha et al, 2001). In addition to its role in thermogenesis, the preoptic area is implicated in the regulation of male and female reproductive function and behavior (Coolen et al, 1998;Etgen et al, 1999) and in regulation of the hypothalamo-pituitary-adrenocortical axis (Viau and Meaney, 1996).…”
Section: Expression Of Vglut Mrnas In Hypothalamic Integratorsmentioning
Two isoforms of the vesicular glutamate transporter, VGLUT1 and VGLUT2, were recently cloned and biophysically characterized. Both VGLUT1 and VGLUT2 specifically transport glutamate into synaptic vesicles, making them definitive markers for neurons using glutamate as a neurotransmitter. The present study takes advantage of the specificity of the vesicular transporters to afford the first detailed map of putative glutamatergic neurons in the rat hypothalamus. In situ hybridization analysis was used to map hypothalamic distributions of VGLUT1 and VGLUT2 mRNAs. VGLUT2 is clearly the predominant vesicular transporter mRNA found in the hypothalamus; rich expression can be documented in regions regulating energy balance (ventromedial hypothalamus), neuroendocrine function (preoptic nuclei), autonomic tone (posterior hypothalamus), and behavioral/homeostatic integration (lateral hypothalamus, mammillary nuclei). Expression of VGLUT1 is decidedly more circumspect and is confined to relatively weak labeling in lateral hypothalamic regions, neuroendocrine nuclei, and the suprachiasmatic nucleus. Importantly, dual-label analysis revealed no incidence of colocalization of VGLUT1 or VGLUT2 mRNAs in glutamic acid decarboxylase (GAD) 65-positive neurons, indicating that GABA neurons do not express either transporter. Our data support a major role for hypothalamic glutamatergic neurons in regulation of all aspects of hypothalamic function.
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