beta-adrenergic blockade in the dentate gyrus in vivo prevents high frequency-induced long-term potentiation of EPSP slope, but not long-term potentiation of population spike amplitude

High frequency (HF)-induced and norepinephrine (NE)induced long-term potent iation have been hypothesized to utilize common mechanisms of induction and expression in the dentate gyrus. In vitro data tend to support this hypoth esis, but few studies have been done in vivo. The present study records per forant path-evoked potentials simultaneously on two micropipettes, one fill ed with saline and the other with the beta -antagonist, timolol. Stimulatio n of the paragigantocellularis nucleus (PGI) was used as a method of produc ing NE release in the dentate gyrus, and thus, to assess the efficacy of be ta -receptor blockade on the timolol pipette. beta -blockade by timolol att enuated PGi-induced spike potentiation. HE-induced potentiation of the exci tatory post-synaptic potential (EPSP) slope was also blocked by timolol, bu t HE-induced spike amplitude potentiation was unaffected. These results are consistent with an earlier report examining HE-long-term potentiation (LTP ) following 6-OHDA-induced NE depletion, which showed that the EPSP slope L TP depended, for its full expression, on NE, but potentiation of the popula tion spike amplitude component of HE-induced LTP did not. In the present st udy, PGi-induced potentiation of spike amplitude on the saline pipette was normal after HE-induced saturation of spike amplitude potentiation, suggest ing that the mechanisms for expression of spike potentiation, as well as in duction of spike potentiation, are separate for HF and NE stimulation. Hipp ocampus 2001;11:322-328. (C) 2001 Wiley-Liss, Inc.