The mechanism underlying the enhancement of long-term potentiation (LTP) induced by the systemic administration of PB-2, an α(1-3)(1-4)glucan- containing fraction extracted from the lichen Flavoparmelia baltimorensis and a putative LTP-enhancing agent, was investigated in the rat dentate gyrus in vivo. Particular attention was paid to the role of adrenaline β-receptors. An intravenous (i.v.) injection of PB-2 enhanced the induction of LTP, which was in turn inhibited by an i.v. injection of the adrenaline β1- receptor antagonist atenolol. An intracerebroventricular injection of atenolol did not affect the induction of LTP, but completely suppressed the PB-2-induced enhancement of LTP. The infusion of atenolol into the recording site attenuated the PB-2-induced facilitation of LTP. These results suggest that the adrenaline β1-receptors contribute to the enhancement of LTP induced by the systemic administration of PB-2, and that the functional β1- receptors are located both centrally and peripherally.
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