EAA receptors in the dorsomedial hypothalamic area mediate the cardiovascular response to activation of the amygdala.

Abstract

The role of excitatory amino acid (EAA) receptors in the dorsomedial hypothalamus (DMH) in mediating the cardiovascular response to activation of the basolateral amygdala (BLA) was examined using conscious rats. Microinjection of the nonselective EAA receptor antagonist kynurenic acid (0.1-10 nmol) into the DMH blocked or reversed the increases in heart rate and arterial pressure resulting from injection of the GABAA receptor antagonists bicuculline methiodide (BMI; 100 pmol) and picrotoxin (100 pmol) into the BLA. Similar injections of kynurenic acid at sites lateral or dorsal to the DMH or injection of the inactive analog xanthurenic acid into the DMH were less effective in blocking the cardiovascular changes resulting from intra-amygdalar injection of BMI. Hypothalamic injection of the NMDA receptor antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (10 pmol) or the DL-alpha-amino-3-hydroxy-5-methylisoxazole-propionic acid receptor antagonist 1,2,3,4-tetrahydro-6-nitro-2, 3-dioxo-benzo[f]quinoxaline-7-sulfonamide (50 pmol) at doses shown to be selective for their respective EAA receptor subtypes attenuated the cardiovascular changes associated with intra-amygdalar injection of BMI. Therefore, EAA receptors in the area of the DMH appear to be involved in mediating the cardiovascular changes resulting from activation of the amygdala.