Adolescent ethanol exposure: does it produce long-lasting electrophysiological effects?
ABSTRACT This review discusses evidence for long-lasting neurophysiological changes that may occur following exposure to ethanol during adolescent development in animal models. Adolescence is the time that most individuals first experience ethanol exposure, and binge drinking is not uncommon during adolescence. If alcohol exposure is neurotoxic to the developing brain during adolescence, not unlike it is during fetal development, then understanding how ethanol affects the developing adolescent brain becomes a major public health issue. Adolescence is a critical time period when cognitive, emotional, and social maturation occurs and it is likely that ethanol exposure may affect these complex processes. To study the effects of ethanol on adolescent brain, animal models where the dose and time of exposure can be carefully controlled that closely mimic the human condition are needed. The studies reviewed provide evidence that demonstrates that relatively brief exposure to high levels of ethanol, via ethanol vapors, during a period corresponding to parts of adolescence in the rat is sufficient to cause long-lasting changes in functional brain activity. Disturbances in waking electroencephalogram and a reduction in the P3 component of the event-related potential (ERP) have been demonstrated in adult rats that were exposed to ethanol vapor during adolescence. Adolescent ethanol exposure was also found to produce long-lasting reductions in the mean duration of slow-wave sleep (SWS) episodes and the total amount of time spent in SWS, a finding consistent with a premature aging of sleep. Further studies are necessary to confirm these findings, in a range of strains, and to link those findings to the neuroanatomical and neurochemical mechanisms potentially underlying the lasting effects of adolescent ethanol exposure.
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ABSTRACT: Abnormal or borderline electroencephalograms are commonly observed in cases of gross mental retardation. However, fewer studies have focused on the use of event-related responses to aid in the differential diagnosis of developmental cognitive disorders. Fetal alcohol syndrome (FAS) and Down syndrome represent the most common known causes of mental retardation in the Western world. Although Down syndrome is easily diagnosed with a chromosome assay, FAS can be more difficult to diagnose since the diagnostic features are more subjectively based. The present study is the first to characterize auditory event-related potentials (ERPs) in children with FAS and contrast them to subjects with Down syndrome and controls. A passive auditory "oddball-plus-noise" paradigm was utilized to elicit ERPs. Parietal P300 latencies in response to the noise-burst stimuli for the FAS children were significantly longer, as were the P300s from all cortical sites in Down syndrome subjects in response to the both the infrequent tone and noise-burst stimuli when compared with the controls. Frontal P300s in Down syndrome children were significantly larger in amplitude compared to the controls and FAS children in response to the infrequent tone. A discriminant function analysis also revealed that these children could be correctly classified as being either Down syndrome, FAS, or normal controls using measures of latency and amplitude of the P300. These data suggest that an evaluation of ERP characteristics may provide a better understanding of the differences between FAS and Down syndrome children, and prove to be an aid in the early identification of children with FAS. These results demonstrate neurophysiological differences between FAS and Down syndrome, and suggest that P300 amplitude and latency data collected from a passive ERP task may be helpful in the discrimination of developmental cognitive disorders.Alcoholism Clinical and Experimental Research 03/1996; 20(1):35-42. · 3.34 Impact Factor
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ABSTRACT: Ca(2+)-activated non-selective cation (CAN) channels are activated by cytoplasmic Ca(2+) and I(CAN) underlies many slow depolarizing processes in neurons including a putative role in excitotoxicity. CAN channels in many non-neuronal cells are blocked by non-steroidal antiinflammatory drugs that are derivatives of diphenylamine-2-carboxylate (DPC). The DPC derivative flufenamate (FFA) has a complex effect on certain neurons, whereby it blocks CAN channels and increases [Ca(2+)](i). We report here that FFA, but not the parent compound, DPC, blocks CAN channels in hippocampal CA1 neurons. As was the case in other neurons, the effects of FFA are complex and include a maintained rise in [Ca(2+)](i). Furthermore, the CAN channel blocking ability of FFA persists even when the channels have been potentiated by a Ca(2+)-dependent process. The use of a CAN channel-blocking drug is important for delineating CAN channel-dependent processes and may provide a basis for therapy for CAN channel-dependent events in ischemia.Brain Research 07/2000; 867(1-2):143-8. · 2.73 Impact Factor
Article: Magnitude and ethanol sensitivity of tonic GABAA receptor-mediated inhibition in dentate gyrus changes from adolescence to adulthood.[show abstract] [hide abstract]
ABSTRACT: Ethanol consumption by adolescents is a public health problem of striking importance. Educational and clinical efforts to address this problem have been aided by recent neurobehavioral studies indicating that ethanol disrupts memory and memory-related brain functions more powerfully in adolescent animals than in adults. Still, the mechanisms underlying this developmental sensitivity remain unclear. GABA(A) receptor (GABA(A)R)-mediated neurotransmission in the hippocampal formation, particularly that which is driven by extrasynaptic GABA(A)Rs, is enhanced by pharmacologically relevant concentrations of ethanol, and may be, in part, responsible for the modulation of memory and memory-related circuit plasticity. Using hippocampal slices from adolescent and adult rats, we have shown that tonic current mediated by extrasynaptic GABA(A)Rs is larger in dentate gyrus granule cells from adult animals than in those from adolescents and that 30 mM ethanol enhances inhibitory tonic current more in cells from adolescent rats than in those from adults. It is possible that more powerful promotion of tonic GABA(A)R-mediated inhibition by ethanol in the dentate gyrus of adolescent rats, compared with adults, contributes to the developmental differences that have previously been observed with respect to ethanol-induced memory impairment and reduction of synaptic plasticity.Journal of Neurophysiology 06/2007; 97(5):3806-11. · 3.32 Impact Factor