The effects of local application of ethanol in the n. accumbens on dopamine overflow and clearance.

The actions of ethanol on extracellular dopamine levels in the n. accumbens were examined in both anesthetized and unanesthetized rats using either in vivo voltammetry or microdialysis. In the voltammetry studies, ethanol was microinjected directly into the accumbens. For the microdialysis studies, the ethanol was injected systemically. The voltammetry studies failed to find any direct effect of local ethanol on extracellular dopamine levels. However, exposure to high ethanol concentrations directly injected into the n. accumbens showed the rise rate and the return to baseline rate to a n. accumbens KCl-stimulated dopamine release. In the microdialysis studies, increased levels of extracellular dopamine in the n. accumbens were found in unanesthetized rats, similar to those reported in the literature. However, in the anesthetized rats, the extracellular dopamine levels were not increased, even with similar local ethanol levels measured in the dialysate. Taken together, the data suggest that the actions of ethanol to increase extracellular dopamine levels in the n. accumbens are most likely not an effect of ethanol at the level of the accumbens but rather an action which increases neural activity within the mesoaccumbens pathway, perhaps via actions at the ventral tegmental area.

Effects of chronic ethanol ingestion on mid-latency auditory evoked potentials depend on length of exposure.

We hypothesized that chronic ethanol ingestion is associated with modifications in components of mid-latency auditory evoked potentials (MAEPs). To test this, male Long Evans rats were administered 10% ethanol in drinking water as the sole fluid source for 3, 6, or 9 months. MAEPs were obtained and compared to age-matched control groups. MAEPs were obtained from additional rats after 4 weeks of abstinence. Data were obtained for varying frequencies (4, 8, 16, 24, 32 kHz) and intensities (65, 75, 85 dB SPL). Three months of ethanol exposure was associated with increased latencies and amplitudes of Na and Pa. MAEP components recovered and returned to control values after 4 weeks' abstinence following 3 months of EtOH exposure. Few significant differences were observed in the ethanol-treated or abstinent group after 6 months' exposure. However, 9 months of ethanol exposure revealed a significant increase in latencies and decrease in amplitudes of both Na and Pa components. After 4 weeks of abstinence, the Na and Pa component peak latencies appeared earlier than age-matched controls. The Na and Pa peak amplitudes were slightly greater than the ethanol-treated group; however, they did not recover to control values. These findings suggest that chronic ethanol consumption may produce time-dependent structural and/or neurochemical alterations in substrates for cortical information processing, which may be irreversible. In the present paradigm, this irreversibility may occur after 6 or more months of ethanol intake, and may be detected with the use of MAEPs.

Chronic ethanol ingestion produces cholinergic hypofunction in rat brain.

Alterations in cholinergic function due to prolonged ethanol exposure (up to 9 months) were assessed by choline acetyltransferase (ChAT) activity and high-affinity choline uptake (HAChU) in three brain regions of the Long-Evans rat: frontal cortex, parietal cortex, and region of the nucleus basalis of Meynert (NbM). No statistically significant changes were found in ChAT activity in the 3-month group; however, ChAT activity was decreased in both the frontal cortex (-32%) and NbM region (-22%) after 6 months of ethanol exposure. ChAT activity in the parietal cortex was increased 30% after 6 months. Nine months of exposure significantly decreased ChAT activity in all three brain regions. No significant differences were observed in high-affinity choline uptake after 3 months of ethanol exposure. However, after 6 months of ethanol exposure HAChU was decreased to 51% of control values in the frontal cortex. There was a simultaneous increase in HAChU to 43% and 178% of control values in the NbM and parietal cortex, respectively. However, choline uptake was significantly decreased in the frontal cortex and NbM region after 9 months of exposure. The results indicate a neurotoxic effect of prolonged intake of ethanol on the basal forebrain cholinergic projection system, which may cause impairment of cholinergic innervation of target areas of the basal nucleus complex.

Chronic ethanol ingestion alters parameters of mid-latency auditory evoked potentials in male rats.

The purpose of this study was to determine the effects of chronic ethanol ingestion on components of mid-latency auditory evoked potentials (MAEPs). Male Sprague-Dawley rats were administered 10% ethanol in drinking water for 10 months. MAEPs were obtained and compared to age-matched controls provided tap water. Data were obtained for varying frequencies (4, 8, 16, 24, and 32 kHz) and intensities (65, 75, and 85 dB sound pressure level). Ethanol treatment was associated with increased latencies, as well as decreased amplitudes of Na and Pa. The effects were most prominent for MAEP component Pa, but also appear for component Na. We suggest that chronic alcohol consumption induces structural and/or neurochemical alterations in substrates for cortical information processing.