Involvement of β-adrenergic receptors in protein synthesis-dependent late long-term potentiation (LTP) in the dentate gyrus of freely moving rats: the critical role of the LTP induction strength

Abstract

We have investigated the requirement of β-adrenergic receptor activation and protein synthesis for the induction and specifically for the maintenance of long-term potentiation (LTP) in the dentate gyrus of freely moving rats in dependency on different LTP-induction procedures. Three tetanization paradigms were used: a relatively weak protocol A (10 bursts of 15 biphasic pulses at 200 Hz; 10-s interburst interval; 0.2-ms pulse width per phase), a stronger protocol B (as protocol A but 20 bursts and 0.25-ms pulse width) and, as the strongest condition, protocol C (2 times protocol B; inter-tetanus interval: 5 min). All protocols led to robust late-LTP in control animals. Late- but not early-LTP was protein synthesis-dependent under all tetanization conditions as indicated by the absence of long-lasting LTP when the protein synthesis inhibitor anisomycin was applied before tetanization. Application of the β-adrenergic receptor antagonist propranolol before LTP induction prevented late-LTP when either protocol A or B but not when protocol C was used. Thus, repeated strong tetanization can compensate for the loss of β-adrenergic receptor activation. We suggest that the results could provide a link to cellular mechanisms of memory consolidation in respect to the strength and relevance of the incoming sensory information during learning.