Does ethanol exposure in early adolescence inhibit intrinsic neuronal plasticity via sigma-1 receptor activation in hippocampal CA1 neurons?
Results here suggest that acute withdrawal from adolescent CIE exposure triggers sigma-1 receptors that act to depress the efficacy of excitatory inputs in triggering action potentials during LTP. Such withdrawal-induced depression of E-S plasticity in hippocampus probably entails sigma-1 receptor modulation of 1 or several voltage-gated ion channels controlling the neuronal input-output dynamics.
These results point to a conserved role of the neuroendocrine axis in growth control in multicellular organisms.