Requirement of β‐adrenergic receptor activation and protein synthesis for LTP‐reinforcement by novelty in rat dentate gyrus

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Abstract
Long‐term potentiation (LTP) is supposed to be a cellular mechanism involved in memory formation. Similar to distinct types of memory formation, LTP can be separated into a protein synthesis‐independent early phase (early‐LTP) and a protein synthesis‐dependent late phase (late‐LTP). An important question is whether the transformation from early‐ into late‐LTP can be elicited by behavioural conditions such as the attention to novel events. Therefore, we investigated the effect of exploration of a novel environment (novelty‐exploration) on subsequently induced early‐LTP in the dentate gyrus of freely moving rats. While a delay of 60 min between exploration onset and LTP induction had no effect, intervals of 30 or 15 min led to a reinforcement of early‐ to late‐LTP. Exploration of a familiar environment failed to prolong LTP maintenance. The novelty‐induced LTP reinforcement was blocked when the translation inhibitor anisomycin or the β‐adrenergic antagonist propranolol were applied intracerebroventricularly before exploration onset. These findings support the hypothesis that the synergistic interplay of novelty‐triggered noradrenergic activity and weak tetanic stimulation promotes the synthesis of certain proteins that are required for late‐LTP. Such a cellular mechanism may underlie novelty‐dependent enhancement of memory formation.