Abstract
BackgroundTransient hyperthermic shifts in body temperature have been linked to the endogenous hormone calcitonin gene-related peptide (CGRP), which can increase sympathetic activation and metabolic heat production. Recent studies have demonstrated that these centrally mediated responses may result from CGRP dependent changes in the activity of thermoregulatory neurons in the preoptic and anterior regions of the hypothalamus (POAH).ResultsUsing a tissue slice preparation, we recorded the single-unit activity of POAH neurons from the adult male rat, in response to temperature and CGRP (10 μM). Based on the slope of firing rate as a function of temperature, neurons were classified as either warm sensitive or temperature insensitive. All warm sensitive neurons responded to CGRP with a significant decrease in firing rate. While CGRP did not alter the firing rates of some temperature insensitive neurons, responsive neurons showed an increase in firing rate.ConclusionWith respect to current models of thermoregulatory control, these CGRP dependent changes in firing rate would result in hyperthermia. This suggests that both warm sensitive and temperature insensitive neurons in the POAH may play a role in producing this hyperthermic shift in temperature.
Highlights
Transient hyperthermic shifts in body temperature have been linked to the endogenous hormone calcitonin gene-related peptide (CGRP), which can increase sympathetic activation and metabolic heat production
Our results clearly show that CGRP can alter the activity of thermoregulatory neurons in the preoptic and anterior regions of the hypothalamus (POAH), by decreasing the firing rates of warm sensitive neurons and increasing the firing rates of the majority of temperature insensitive neurons (Table 1)
While we do not yet know the functional role these neurons have in the neural pathways responsible for regulating specific thermoregulatory effector systems, we have clearly shown a selective effect for thermoregulatory neurons to CGRP that may lead to the initiation of an increase in body temperature
Summary
Transient hyperthermic shifts in body temperature have been linked to the endogenous hormone calcitonin gene-related peptide (CGRP), which can increase sympathetic activation and metabolic heat production. Recent studies have demonstrated that these centrally mediated responses may result from CGRP dependent changes in the activity of thermoregulatory neurons in the preoptic and anterior regions of the hypothalamus (POAH). Stimulation of specific sites in the brainstem may selectively activate thermoregulatory responses, local warming of the POAH results in a general heat loss, while cooling initiates heat production [1]. Within this region, in vivo and in vitro electrophysiologic studies have identified thermally classified populations of neurons. Warm sensitive neurons in the POAH appear to function as integrators of both central and peripheral thermal information, producing an (page number not for citation purposes)
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