GABAergic mechanisms in the ventrolateral medulla alter vasopressor responses from the anterior hypothalamus

The facilitatory and inhibitory roles of the ventrolateral medulla in modulating cardiovascular responses elicited from the anterior hypothalamus were studied in urethane-anesthetized rats. Control pressor responses (35-50 mm Hg) were consistently evoked by electrically stimulating the anterior hypothalamic medial preoptic area (AH/POA). The ventrolateral medulla is divided into two functionally distinct neuron pools, namely a rostral ventrolateral vasopressor area (VLPA) and a caudal ventrolateral vasodepressor area (VLDA). In each experiment neuron pools in the VLDA or VLPA were identified with bilateral microinjections of the neuroexcitatory amino acid L-glutamate, and changes in AH/POA responses were determined before and after alterations in ventrolateral neuronal activity. Inhibition or excitation of neuronal activity was accomplished by bilaterally stimulating or blocking M-aminobutyric acid (GABA) receptors, respectively, in the VLPA or VLDA. Inhibition of neuronal activity by microinjecting the GABA agonist muscimol into the VLPA decreased the AH/POA response by 64 ± 10% and, in the VLDA, increased the AH/POA response by 57 ± 4%. Blockade of GABA receptors by microinjecting the GABA antagonist bicuculline methiodide into the VLPA caused a 68 ± 7% increase in the AH/POA response. Most surprising was a reversal of the AH/POA pressor response to a depressor response (150 + 2% decrease) following bicuculline microinjections in the VLDA. This finding suggests that GABA is released in the VLDA following AH/POA stimulation. It was concluded that neuron pools in the VLPA and VLDA determine the magnitude and direction of blood pressure responses elicited by electrical stimulation of the AH/ POA. GABAergic mechanisms in the VLPA and the VLDA may modulate blood pressure changes relayed from the hypothalamus. A hypothetical pathway is proposed.