Ethanol reduces neuronal excitability and excitatory synaptic transmission in the developing rat spinal cord.

Effects of acute ethanol (EtOH) exposure on motoneuron excitability and properties of synaptic transmission were examined in spinal cords of postnatal rats. Whole-cell patch clamp recordings and intracellular recordings with high-resistance electrodes were carried out in motoneurons of 1- to 4-day-old postnatal rats. To determine the effects of extracellular EtOH on action potential waveform, properties of current-evoked soma action potentials and motoneuron ability to generate repetitive action potential firing were examined. During a brief EtOH (70 mM) exposure, larger depolarizing current was required for action potential generation, the duration of the after hyperpolarizing potential increased, and fewer action potentials were produced during a prolonged intracellular current injection. These effects were reversed within 20 min of EtOH removal from the extracellular solution. To determine whether the reduced probability of action potential generation was associated with changes in synaptic transmission, properties of evoked synaptic potentials and spontaneous synaptic currents were investigated. In the presence of EtOH, the amplitude of dorsal root-evoked synaptic potentials was reduced, the frequency of spontaneous excitatory postsynaptic currents decreased, while the frequency of inhibitory postsynaptic currents increased. Our data suggested that acute EtOH exposure suppressed motoneuron electrical activity by decreasing motoneuron excitability and shifting the balance between excitatory and inhibitory synaptic transmission toward inhibition.