Altered GABA ergic system in the posterior hypothalamus of the spontaneously hypertensive rat
Shonis, Casey Ann
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Permalink
https://hdl.handle.net/2142/19464
Description
Title
Altered GABA ergic system in the posterior hypothalamus of the spontaneously hypertensive rat
Author(s)
Shonis, Casey Ann
Issue Date
1994
Doctoral Committee Chair(s)
Waldrop, Tony G.
Department of Study
Molecular and Integrative Physiology
Discipline
Physiology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Neuroscience
Biology, Animal Physiology
Health Sciences, General
Language
eng
Abstract
"Previous studies indicate a tonic GABAergic inhibitory mechanism in the posterior hypothalamus (PH) contributes to modulating cardiovascular activity. Blockade of GABA receptors on neurons in this area elicits an increase in sympathetic discharge, arterial pressure and heart rate. It has been proposed that a deficit in this inhibitory system may be responsible for the elevated pressure in the spontaneously hypertensive rat (SHR), a useful animal model for studying human essential hypertension. The purpose of this thesis was to determine if the level of neuronal activity in the PH is augmented in the SHR compared to normotensive Wistar-Kyoto rats (WKY) and if so, is the hyperactivity due to a malfunction in the hypothalamic GABAergic system. Single unit, extracellular recordings of posterior hypothalamic neurons were performed in both in vivo and in vitro preparations. The spontaneous firing rate of posterior hypothalamic neurons in anesthetized adult and young SHRs was significantly higher compared to age-matched WKYs. Moreover, this enhanced neuronal discharge in the SHR was due to neurons possessing cardiac-related rhythms. SHR posterior hypothalamic neurons retained their augmented activity in the in vitro preparation as well. Based on immunocytochemistry for glutamic acid decarboxylase, the synthesizing enzyme for GABA, this enhanced activity in the SHR is most likely due to a ""disinhibition"" of the PH resulting from a decreased number of GABA-synthesizing neurons in this area. Neuronal responses to GABA and hypoxia appear to be intact in this animal. Therefore, a reduction in the tonic inhibitory GABAergic influence on the PH may be contributing to the development and/or maintenance of hypertension in this animal model for essential hypertension."
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