CORTICOTROPIN-RELEASING HORMONE MICROINFUSION IN THE CENTRAL AMYGDALADIMINISHES A CARDIAC PARASYMPATHETIC OUTFLOW UNDER STRESS-FREE CONDITIONS

The central nucleus of the amygdala (CeA) is known to be involved in t he regulation of autonomic, neuroendocrine and behavioural responses i n stress situations. The CeA contains large numbers of corticotropin-r eleasing hormone (CRH) cell bodies. Neuroanatomical studies revealed t hat the majority of the CRH fibres from the CeA have direct connection s with autonomic regulatory nuclei in the brainstem. In the present st udy, the effects of locally infused CRH (30 ng) into the CeA, in freel y moving male Wistar rats under stress-free conditions, were examined. Heart rate, endocrine parameters and behavioural activity were repeat edly measured before, during and after local administration of CRH, pr etreated with either artificial CSF or the CRH-receptor antagonist, al pha-helical CRH (alpha-hCRH). CRH infusion alone caused a long-lasting increase in heart rate without affecting plasma adrenaline and noradr enaline as indicators of sympathetic activity. This CRH-induced tachyc ardia was effectively blocked by pretreatment with a high dose (I mug) alpha-hCRH locally into the CeA, while the pretreatment with low dose (0.1 mug) of the alpha-hCRH caused a minor blockade of the CRH-induce d tachycardia. The results suggest that CRH mechanisms in the CeA regu late the autonomic changes probably only by affecting parasympathetic but not sympathetic output systems. Because CRH is given at the level of the cell body of the CRH neurons in the CeA, we suggest that the re duction of the parasympathetic output may be explained as an autorecep tor-mediated inhibition of CRH neurons from the CeA with parasympathet ic-regulating brainstem nuclei.