Cocaine enhancement of long-term potentiation in the CA1 region of rat hippocampus: lamina-specific mechanisms of action.

There is an expanding body of work characterizing dopaminergic modulation of synaptic plasticity in the hippocampus CA1 region, an area known to be involved in learning and memory. However, in vitro studies to date have focused almost exclusively on the proximal and distal apical dendritic layers (strata radiatum and lacunosum moleculare, respectively). In this report, we establish that dopaminergic activity can enhance long-term potentiation (LTP) in the basal dendritic layer (stratum oriens) of CA1 in the rat hippocampal slice preparation. Application of the D(1/5) agonist SKF38393 (20 microM) significantly increased the magnitude of basal LTP of the fEPSP response following high-frequency stimulation of the Schaffer collateral/commissural inputs in the stratum oriens layer. In addition, endogenous dopamine (DA) activity facilitated by the presence of cocaine (6 muM) was also capable of enhancing the magnitude of basal LTP. Prior application of the D(1/5) antagonist SKF83566 (2 muM) prevented this effect of cocaine, indicating that endogenously released dopamine was exerting its LTP-enhancing effect in stratum oriens via activation of D(1/5) receptors. This final result stands in contrast with the previously characterized effects of cocaine on apical LTP in the stratum radiatum, which instead have been shown to require D(3) receptor activation. These observations demonstrate that dopaminergic mechanisms resulting in the enhancement of hippocampal LTP are lamina specific at Schaffer collateral/commissural synapses in the CA1 region. Synapse 2010. (c) 2010 Wiley-Liss, Inc.