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The Journal of Neuroscience, August 15, 2000, 20(16):6106-6116
A Critical Period for Nicotine-Induced Disruption of Synaptic Development in Rat Auditory Cortex
V. Bess Aramakis1, Candace Y. Hsieh1, Frances M. Leslie2, and Raju Metherate1 Departments of 1 Neurobiology and Behavior and 2 Pharmacology, University of California, Irvine, California 92697-4550
Cholinergic markers in the middle layers of rat auditory cortex are transiently upregulated during the second postnatal week, at which time
7 nicotinic acetylcholine receptors (nAChRs) selectively regulate NMDA receptor (NMDAR)-mediated EPSPs. To investigate the developmental role of this regulation, we determined whether manipulating nAChR function at specific times during the first 4 weeks after birth could alter subsequent neuronal function. Rat pups were injected twice daily with nicotine (1 or 2 mg/kg) or saline during approximately the first, second, or fourth postnatal week (i.e., before, during, or after the peak upregulation of nAChRs). Glutamate EPSPs and intrinsic membrane properties were measured during whole-cell recordings from visually identified pyramidal neurons in layers II-IV of brain slices prepared at least 15 hr after the last injection. Chronic nicotine exposure (CNE) had little effect on intrinsic membrane properties and during week 1 or 4 did not affect synaptic function. However, CNE during week 2 resulted in EPSPs with long durations, multiple peaks, and enhanced NMDAR components. These changes remained significant even 10 d after CNE. Rapid application of nicotine, which in control neurons selectively enhances NMDAR EPSPs during week 2, produced only weak effects after CNE. Receptor binding studies showed that CNE-induced EPSP alterations occurred in the absence of altered
Key words: acetylcholine; auditory; cortex; development; EPSP; glutamate; nicotine; NMDA; intrinsic properties; synaptic
Copyright © 2000 Society for Neuroscience 0270-6474/00/20166106-11$05.00/0
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