title: Role of nucleus tractus solitarius 5-HT3 receptors in the defense reaction-induced inhibition of the aortic baroreflex in rats.
abstract: 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.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, Unité 288, Faculté de Médecine Pitié-Salpêtrière, 75634 Paris Cedex 13, France. sevoz@ext.jussieu.fr
authors.forename: C
authors.initials: C
authors.lastname: Sévoz-Couche
authors.forename: M-A
authors.initials: MA
authors.lastname: Comet
authors.forename: M
authors.initials: M
authors.lastname: Hamon
authors.forename: R
authors.initials: R
authors.lastname: Laguzzi
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000502:physiology; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D004924:Escape Reaction / Q000187:drug effects / Q000502:physiology*; D017829:Granisetron / Q000494:pharmacology; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D044406:Receptors, Serotonin, 5-HT3 / Q000502:physiology*; D058831:Serotonin 5-HT3 Receptor Antagonists; D017552:Solitary Nucleus / Q000187:drug effects / Q000502:physiology*
chemical_list: D017829:Granisetron; D044406:Receptors, Serotonin, 5-HT3; D058831:Serotonin 5-HT3 Receptor Antagonists