Third trimester-equivalent ethanol exposure does not alter complex spikes and climbing fiber long-term depression in cerebellar Purkinje neurons from juvenile rats.
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Studies indicate that exposure to ethanol (EtOH) during fetal development damages cerebellar Purkinje cells (PCs). PC proximal dendrites receive glutamatergic input from climbing fibers (CFs) originating at the inferior olive. CF input produces a characteristic response in PCs known as the complex spike (CS). During the first 2 weeks of life in rodents (equivalent to the human third trimester of pregnancy), CF-PC synapses undergo profound refinement. Here, we characterized the impact of EtOH exposure during this period on CF-evoked responses in PCs.Using vapor chambers, neonatal rat pups and their mothers were exposed to air or EtOH for 4 h/d between postnatal day 2 (P2) and P12 (pup serum EtOH concentration, 0.16 g/dl). The function of CF-PC synapses was characterized using patch-clamp electrophysiological techniques in acute slices from the cerebellar vermis. Experiments were performed soon after EtOH withdrawal, when perisomatic CFs are still being eliminated (P15 to P17), and after weaning when CF dendritic translocation is almost complete (P21 to P34).Neither the baseline characteristics of the CS (Na(+) spike amplitude, area, coastline index, and afterhyperpolarization [AHP] amplitude) nor the type-1 metabotropic glutamate receptor (mGluR1)-mediated component of both the CS and AHP were significantly affected by EtOH exposure at P15 to P17 or P21 to P34. The mGluR1-dependent long-term depression (LTD) of CF-evoked excitatory postsynaptic currents was not significantly affected by EtOH exposure at P21 to P34.EtOH exposure during the third trimester equivalent neither affected basal characteristics of the CS nor CF-LTD at rat cerebellar PCs from juvenile rats.Copyright © 2014 by the Research Society on Alcoholism.