LTP in the lateral perforant path is β-adrenergic receptor-dependent

Abstract
NOREPINEPHRINE induces an activity-independent long-lasting depression of synaptic transmission in the lateral perforant path input to dentate granule cells, whereas high frequency stimulation induces activity-dependent long-term potentiation (LTP). We investigated the role of endogenous activation of β-adrenergic receptors in LTP of the lateral and medial perforant paths under conditions affording selective stimulation of these pathways in the rat hippo-campal slice. Propranolol (1 μM), a β-receptor antagonist, blocked LTP induction of both lateral and medial perforant path-evoked field excitatory postsynaptic potentials. The results indicate a broad requirement for norepinephrine in different types of synaptic plasticity, including activity-independent depression and activity-dependent LTP in the lateral perforant path.