title: Neurophysiological findings and drinking levels in high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) rats.
abstract: BACKGROUND
  Specific neurophysiological profiles, such as reduced P300 amplitude or altered spectral power in the EEG, have been associated with a risk for alcoholism in several clinical populations. In certain rodent models, high versus low alcohol consumption is associated with similar neurophysiological differences. For example, alcohol-preferring (P) rats have increased spectral power and decreased P300 amplitudes compared with alcohol-nonpreferring (NP) rats. In the present study, the neurophysiological profiles of high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) rats were assessed (1) to determine if their electrophysiological profiles are similar to P and NP rats and (2) to examine the relationship of these neurophysiological indices to ethanol drinking.
  
  
  METHODS
  Ethanol-naive HAD and LAD rats were implanted with cortical and amygdalar recording electrodes. Baseline EEG and event-related potentials (ERPs) then were assessed. Subsequently, all rats were trained to self-administer ethanol by using a sucrose-substitution procedure.
  
  
  RESULTS
  Baseline EEG and ERP (i.e., pre-ethanol exposure) were assessed based on line (HAD versus LAD) and actual ethanol consumption (high drinkers versus low drinkers). At baseline, ethanol-naive HAD rats displayed significantly greater power in the cortical EEG and decreased amygdala N1 ERP amplitude compared with ethanol-naive LAD rats. Similar EEG and ERP profiles have been observed when P and NP rats are compared. No differences in P300 between lines were observed, but high-drinking rats, independent of line, had significantly decreased P300 amplitude in the amygdala compared with low-drinking rats.
  
  
  CONCLUSIONS
  These data suggest there are some similarities in EEG and ERP profiles of P and HAD rats compared with NP and LAD rats. Furthermore, the data suggest that decreased P300 amplitude in the amygdala is associated with increased limited access ethanol drinking.
authors.affiliation: The Scripps Research Institute, Department of Neuropharmacoloy, La Jolla, California 92037, USA. cslawecki@scripps.edu
authors.forename: C J
authors.initials: CJ
authors.lastname: Slawecki
authors.forename: M
authors.initials: M
authors.lastname: Betancourt
authors.forename: T K
authors.initials: TK
authors.lastname: Li
authors.forename: C L
authors.initials: CL
authors.lastname: Ehlers
mesh_terms: D000428:Alcohol Drinking / Q000235:genetics / Q000503:physiopathology*; D000679:Amygdala / Q000503:physiopathology; D000818:Animals; D001835:Body Weight; D002540:Cerebral Cortex / Q000503:physiopathology; D004567:Electrodes, Implanted; D004569:Electroencephalography; D000431:Ethanol / Q000008:administration & dosage; D005071:Evoked Potentials; D008297:Male; D051381:Rats; D012646:Self Administration
chemical_list: D000431:Ethanol