Abstract

Beta-adrenergic receptor activity may play a key role in the interaction of corticosterone and noradrenaline signaling during stress and can mediate the therapeutic efficacy of propranolol in post-traumatic stress disorder. However, it is still unclear whether the pharmacological activity of propranolol is associated with changes in the corticosterone secretion, and what is the role of peripheral and central β-adrenergic receptors in this phenomenon. In this study, the intracerebral microdialysis was used to assess the effect of β-adrenergic receptor inhibitors with different blood-brain barrier permeability, propranolol and sotalol, on the stress-evoked corticosterone secretion in C57Bl/6N mice. The data prove that systemic administration of propranolol (10 mg/kg), not sotalol, slightly suppressed, but did not prevent, the increase in corticosterone secretion evoked by elevated platform stress. The data prove the involvement of the central β-adrenergic receptors is the tuning of stress-evoked corticosterone secretion in mice

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