IONIC AND HEMODYNAMIC-CHANGES INFLUENCE THE RELEASE OF THE EXCITATORYAMINO-ACID GLUTAMATE IN THE POSTERIOR HYPOTHALAMUS

The push-pull technique was used to investigate the release of the exc itatory amino acid glutamate in the posterior hypothalamic area of the conscious rat. The hypothalamus was superfused through the push-pull cannula with artificial cerebrospinal fluid (CSF), and the superfusate was collected in time periods of 10 min when ionic conditions in the CSF were changed, or in short periods of 3 min when blood pressure cha nges were evoked. The mean glutamate release rate was 2.8 +/- 0.7 pmol /min. Depolarization by hypothalamic superfusion with CSF containing 5 0 mM K+ enhanced the release of glutamate in the presence of Ca2+. The K+-induced release was attenuated by 40% when the hypothalamus was su perfused with Ca2+-free CSF. Replacement of Ca2+ by Mg2+ abolished the K+-induced release of glutamate. Hypovolaemia elicited by haemorrhage enhanced the release rate of glutamate. Similarly, a hypotension elic ited by i.v. injection of chlorisondamine (3 mg/kg) led to a pronounce d and permanent enhancement in glutamate release. The effects of hypov olaemia and chlorisondamine on glutamate release were abolished in aor tic denervated rats, indicating that this response is due to a decreas e of impulse generation in baroreceptors. A hypervolaemia elicited by blood infusion did not affect the release of glutamate. Similarly, a p ronounced presser response to phenylephrine (15 mu g/kg per minute) in fused intravenously for 9 min was ineffective. The results show that t he K+-induced release of glutamate in the hypothalamus is dependent on the presence of Ca2+. The increase in glutamate release rate by hypov olaemia or chlorisondamine suggests that the glutamatergic neurons in the posterior hypothalamic area respond to unloading of aortic barorec eptors and possess a counteracting, hypertensive function.