Different stressful conditions elicit a typical behavior called the defense reaction. Our aim was to determine whether 5-HT3 receptors in the nucleus tractus solitarius (NTS) are involved in 1) the inhibition of the baroreflex
bradycardia and 2) the rise in blood pressure, which are known to occur during the defense reaction. In
urethane-anesthetized rats, the defense reaction was elicited by electrical stimulation of the dorsomedial nucleus of the hypothalamus (
DMH) or the dorsal part of the periaqueductal gray (dPAG). Direct electrical stimulation of the aortic depressor nerve was used to trigger the typical baroreflex responses. Aortic stimulation at high (100-150 microA) and low (50-90 microA) intensity produced a decrease in heart rate of -39 to -44% (relative to baseline, Group 1 responses, n = 113) and -19 to -24% (Group 2 responses, n = 43), respectively. In spontaneously breathing rats, Group 1 and Group 2 bradycardiac responses were inhibited during
DMH (-75 +/- 4% and -96 +/- 4%, n = 38 and n = 11, respectively), as well as dPAG (-81 +/- 3% and -95 +/- 4%, n = 36 and n = 10, respectively) stimulation. The aortic baroreflex
bradycardia was hardly affected by
DMH or dPAG stimulation when
bicuculline (5 pmol), a specific GABAA receptor antagonist, had previously been microinjected into the NTS. Likewise, NTS microinjections of
granisetron, a specific
5-HT3 receptor antagonist, prevented, in a dose-dependent manner, the baroreflex
bradycardia inhibition. In addition, intra-NTS
granisetron did not affect the rise in blood pressure induced by either site stimulation. These data show that 5-HT3 receptors in the NTS are involved in the GABAergic inhibition of the aortic baroreflex
bradycardia, but not in the rise in blood pressure, occurring during the defense reaction elicited by
DMH or dPAG stimulation.