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  • Title: Cardiac, neuroendocrine, and behavioral effects of central amygdaloid vasopressinergic and oxytocinergic mechanisms under stress-free conditions in rats.
    Author: Roozendaal B, Schoorlemmer GH, Koolhaas JM, Bohus B.
    Journal: Brain Res Bull; 1993; 32(6):573-9. PubMed ID: 8221155.
    Abstract:
    The central nucleus of the amygdala (CEA) is considered to play a major role in the expression of behavioral, autonomic, and neuroendocrine components of the stress response. The present study was designed to examine possible modulating effects of the neuropeptides arginine-8-vasopressin (AVP) and oxytocin (OXT) on functioning of the CEA in male Wistar rats. Heart rate, neuroendocrine parameters, and behavioral activity were repeatedly measured before, during, and after local administration of several doses of AVP and OXT under stress-free resting conditions. In comparison with control artificial-CSF infusion, AVP infusion in the lowest dose (20 pg) caused in a part of the animals a long-lasting decrease in heart rate, i.e., bradycardia, without affecting behavioral activity. In contrast, local infusion with high doses of AVP and OXT (2 ng) induced a transient cardioacceleration concomitant with an increase in behavioral activity. Moreover, these latter effects of AVP could effectively be blocked by pretreatment with a selective OXT receptor antagonist. These findings suggest that higher doses of AVP are effective via agonistic action on OXT receptors in the CEA. A strong correlation existed between the magnitudes of the tachycardiac response and behavioral activation. Thus, heart rate increase by OXT receptor stimulation is possibly due to somatic-autonomic coupling rather than genuine autonomic activation. Additionally, plasma corticosterone, but not epinephrine and norepinephrine, concentrations were elevated in response to AVP and OXT infusions. In conclusion, these results suggest that vasopressinergic influences on CEA function involve two receptor mechanisms possibly related to differential output systems.
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