The Tachycardia Associated with the Defense Reaction Involves Activation of Both Gaba_A and Gaba_B receptors in the Nucleus Tractus Solitarii

Abstract

In urethane-anesthetized rats, the tachycardia associated with the defense reaction can be elicited by unilateral microinjections of the GABA_A-antagonist, bicuculline methyliodide (BMI, 20 pmol), into the dorsomedial nucleus (DMN) of the hypothalamus. This effect is thought to be mediated via a pathway that activates GABAergic interneurons in the medullary nucleus tractus solitarii (NTS) which, in turn, inhibit vagal outflow to the heart. Ipsilateral intra-NTS microinjection of BMI (10 pmol) or the GABA_B-antagonist, 2-OH-saclofen (400 pmol), attenuated the tachycardia elicited from the DMN. The tachycardia was also inhibited by intra-NTS administration of the NMDA-receptor channel blocker, MK-801 (30 pmol), or the non-NMDA antagonist, CNQX (400 pmol). These findings are interpreted to indicate that a) GABAergic control of heart rate at the level of the NTS is mediated by both GABA_A and GABA_B receptors, and b) descending input from the DMN to the NTS releases GABA via plutamate acting on ionotropic glutamate receptors located on GABAergic interneurons.

Key Words:

• glutamate
• baroreceptor reflex
• perifornical area
• dorsomedial nucleus
• GABAergic interneuron