Abstract
The electronic parameters of nerve cells in the dentate gyrus following long-term ingestion of ethanol were studied in vitro. The ethanol was administered in a liquid diet for a period of 20 wk followed by a 3-wk withdrawal period. A control group received a similar diet with the ethanol replaced by maltose-dextrins. Intracellular recordings were obtained from 44 neurons, and the voltage decays following current injections were analyzed with a recent electrical model of granule cells to take into account a somatic shunt already detected in previous studies. The new model accurately accounted for the fast voltage transients and showed that the membrane time constant in the dendrites is, on average, five times larger than the somatic time constant. Injection of horseradish peroxidase into the neurons for the morphological analysis showed that neurons in the ethanol group have a longer dendritic tree than neurons in the control group. Estimation of the membrane surface area showed that the membrane area in the dendrites is at least 60% greater (in both control and ethanol groups) when the membrane foldings and irregularities are taken into account. The results of the modeling analysis showed that the membrane time constant and the input resistance are not affected by ethanol. However, the membrane resistance is significantly increased in the ethanol group (6,632 versus 18,460 omega X cm2), and the capacitance is significantly decreased (4.48 versus 1.71 microF/cm2). The electrotonic length is also increased by chronic ethanol treatment (0.85 versus 0.94). Higher values of membrane specific resistance (Rm) mean larger transmission coefficients. However, since the neurons from the ethanol group are on average longer than neurons in the control group, it is suggested that the change in Rm compensates for the increase in the length of the dendrites, thereby maintaining a value of the electrotonic length under 1.0. The observed changes in the passive parameters are in opposite direction from the recently measured effect of acute doses of ethanol on hippocampal neurons. These results support a model of chronic alcohol intake where homeostatic adaptive changes lead to the development of long-term changes in cellular physiology.
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