title: In vitro effects of GABA and hypoxia on posterior hypothalamic neurons from spontaneously hypertensive and Wistar-Kyoto rats.
abstract: Recent studies from this laboratory have shown that neurons in this hypothalamic region are stimulated by hypoxia in vivo and in vitro. In addition, GABAergic activity is depressed in the posterior hypothalamus of the spontaneously hypertensive rat compared to the normotensive rat. The major purposes of the present study were to: a) evaluate if posterior hypothalamic neurons respond differently to GABA in the hypertensive rat compared to the normotensive rat; and b) examine the possibility that hypothalamic neurons from spontaneously hypertensive rats respond differently to hypoxia than those from normotensive rats. In addition, the effects of GABA on hypoxia-sensitive neurons was recorded. Extracellular single unit recordings of hypothalamic neurons were performed in a rat brain slice preparation. Neuronal responses to hypoxia (10% O2/5% CO2/85% N2) and to GABA were recorded from slices taken from both Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Administration of three different concentrations of GABA evoked a dose-related decrease in discharge rate in similar percentages of neurons from both SHR and WKY rats. The magnitude of the depression elicited by GABA did not differ significantly between the neurons from SHR and WKY rats. Hypoxia increased the firing rate of 75% and 69% of the SHR and WKY neurons, respectively; no differences (p > 0.05) were noted in the magnitude of the response or in the percentage of neurons responding to hypoxia between the two strains of rats. The discharge rate of most of these neurons fell to below control level following removal of the hypoxic stimulus. A significant percentage of SHR (75%) and WKY (75%) neurons that were stimulated by hypoxia were inhibited by exogenously applied GABA. These results indicate that a) an altered sensitivity of hypothalamic neurons to GABA does not contribute to hypertension in the SHR and b) the depressed respiratory response to hypoxia in the SHR is not due to a decreased responsiveness of hypothalamic neurons to hypoxia.
authors.affiliation: Department of Physiology & Biophysics, College of Medicine, University of Illinois, Urbana 61801, USA.
authors.forename: C A
authors.initials: CA
authors.lastname: Shonis
authors.forename: T G
authors.initials: TG
authors.lastname: Waldrop
mesh_terms: D000818:Animals; D004594:Electrophysiology; D007034:Hypothalamus, Posterior / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology*; D000860:Hypoxia / Q000473:pathology / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
chemical_list: D005680:gamma-Aminobutyric Acid