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Long-term potentiation (LTP) and long-term depression (LTD) are generally assumed to be cellular correlates for learning and memory. Different types of LTP induction protocols differing in severity of stimulation can be distinguished in CA1 of the hippocampus. To better understand signaling mechanisms and involvement of neuromodulators such as dopamine (DA) in synaptic plasticity, less severe and more physiological low frequency induction protocols should be used. In the study which is reviewed here, critical determinants of spike timing-dependent plasticity (STDP) at hippocampal CA3-CA1 synapses were investigated. We found that DA via D1 receptor signaling, but not adrenergic signaling activated by the β-adrenergic agonist isoproterenol, is important for successful expression of STDP at CA3-CA1 synapses. The DA effect on STDP is paralleled by changes in spike firing properties, thereby changing intrinsic excitability of postsynaptic CA1 neurons, and gating STDP. Whereas β-adrenergic signaling also leads to a similar (but not identical) regulation of firing pattern, it does not enable STDP. In this focused review we will discuss the current literature on dopaminergic modulation of LTP in CA1, with a special focus on timing dependent (t-)LTP, and we will suggest possible reasons for the selective gating of STDP by DA [but not noradrenaline (NA)] in CA1.

Dopamine regulates intrinsic excitability thereby gating successful induction of spike timing-dependent plasticity in CA1 of the hippocampus