LAUSR

Graphical abstract Figure. No caption available. Highlights&bgr;‐adrenergic receptors (&bgr;‐ARs) modulate synaptic plasticity and emotional memory.LTP was induced at dorsal and ventral hippocampal slices (DH‐VH) by theta‐bursts.We found that the &bgr;‐AR modulation of LTP is strikingly higher in VH than in DH.&bgr;‐AR‐induced increase in excitability may underlie the VH‐DH difference in LTP.&bgr;‐AR may be a basic cellular mechanism for VH‐DH diversification in emotionality. ABSTRACT The hippocampus is a functionally heterogeneous structure with the cognitive and emotional signal processing ascribed to the dorsal (DH) and the ventral hippocampus (VH) respectively. However, the underlying mechanisms are poorly understood. Noradrenaline is released in hippocampus during emotional arousal modulating synaptic plasticity and memory consolidation through activation of &bgr; adrenergic receptors (&bgr;‐ARs). Using recordings of field excitatory postsynaptic potentials from the CA1 field of adult rat hippocampal slices we demonstrate that long‐term potentiation (LTP) induced either by theta‐burst stimulation (TBS) that mimics a physiological firing pattern of hippocampal neurons or by high‐frequency stimulation is remarkably more sensitive to &bgr;‐AR activation in VH than in DH. Thus, pairing of subthreshold primed burst stimulation with activation of &bgr;‐ARs by their agonist isoproterenol (1 &mgr;M) resulted in a reliable induction of NMDA receptor‐dependent LTP in the VH without affecting LTP in the DH. Activation of &bgr;‐ARs by isoproterenol during application of intense TBS increased the magnitude of LTP in both hippocampal segments but facilitated voltage‐gated calcium channel‐dependent LTP in VH only. Endogenous &bgr;‐AR activation contributed to the stabilization and the magnitude of LTP in VH but not DH as demonstrated by the effects of the &bgr;‐ARs antagonist propranolol (10 &mgr;M). Exogenous (but not endogenous) &bgr;‐AR activation strongly increased TBS‐induced facilitation of postsynaptic excitability in VH. In DH, isoproterenol only produced a moderate and GABAergic inhibition‐dependent enhancement in the facilitation of synaptic burst responses. Paired‐pulse facilitation did not change with LTP at any experimental condition suggesting that expression of LTP does not involve presynaptic mechanisms. These findings suggest that &bgr;‐AR may act as a switch that selectively promotes synaptic plasticity in VH through multiple ways and provide thus a first clue to mechanisms that underlie VH involvement in emotionality.