Abstract
5-HT1A agonists given systemically are known to produce anxiolytic effects. In
addition, a growing body of research is showing that those compounds also have
central sympathoinhibitory properties. Since emotional arousal gives rise to
sympathetic activation, it is not clear if systemic treatment with a 5-HT1A agonist
reduces the sympathetic response to emotional stress primarily by a direct action on
sympathetic-related sites in the brain or indirectly through reducing anxiety. To test
this, we compared the effect of i.p. injections of 8-OH-DPAT (0.05 and 0.25 mg/kg), a
preferential 5-HT1A agonist, or vehicle, on the cardiovascular responses to four
stressors known to produce sympathetic activation, three of them emotional stressors,
and one physiological. In conscious rats, 30 min exposure to either a neutral context, a
fear-conditioned context or to restraint stress led to increases in heart rate and blood
pressure, which were attenuated by 8-OH-DPAT. In contrast, the same treatment did
not reduce the cardiovascular response to 30 min cold exposure (4°C). The results
suggest that 8-OH-DPAT acts preferentially on limbic, rather than central autonomic
sites. Hence, doses of 5-HT1A agonists which are just sufficient to produce anxiolysis
are not enough to cause true sympathoinhibition.