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  • Title: GABAergic mechanisms in the ventrolateral medulla alter vasopressor responses from the anterior hypothalamus.
    Author: Willette RN, Gatti PA, Sapru HN.
    Journal: J Cardiovasc Pharmacol; 1984; 6(3):476-82. PubMed ID: 6202975.
    Abstract:
    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 gamma-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.
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