Augmented neuronal activity in the hypothalamus of spontaneously hypertensive rats.

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). The purpose of this study was to determine if the spontaneous neuronal activity in the posterior hypothalamus of spontaneously hypertensive rats differs from that of age-matched normotensive Wistar-Kyoto rats (WKY). Single unit, extracellular recordings of posterior hypothalamic neurons were performed on both in vivo and in vitro preparations. The spontaneous firing rate of posterior hypothalamic neurons in the anesthetized adult SHR was significantly higher (3.66 +/- 0.55 Hz) compared to that of the anesthetized adult WKY rat (2.11 +/- 0.29 Hz). Moreover, more of the neurons in the anesthetized SHR (38%) had a bursting discharge pattern than in the WKY (16%). In order to exclude inputs from peripheral receptors or other brain areas, an in vitro preparation was used. Neurons from both young and adult SHRs also had an increased spontaneous discharge rate and higher percentage of burster-type cells in the posterior hypothalamus compared to neurons from age-matched WKYs in the brain slice preparation. Both the in vivo and in vitro findings support the possibility that an elevated neuronal activity in the posterior hypothalamus, a known pressor area, of the SHR contributes to the development and/or maintenance of hypertension in this animal model.