EEG and ERP profiles in the high alcohol preferring (HAP) and low alcohol preferring (LAP) mice: relationship to ethanol preference.
Neurophysiological measures, such as decreased P300 amplitude and altered EEG alpha activity, have been associated with increased alcoholism risk. The purpose of the present study was to extend the assessment of the neurophysiological indices associated with alcohol consumption to a recently developed mouse model of high ethanol consumption, the first replicate line of high alcohol preferring (HAP-1) and low alcohol preferring (LAP-1) mice. Male HAP-1, LAP-1, and HS mice from the Institute for Behavioral Genetics at the University of Colorado Health Science Center (i.e., HS/Ibg mice) were implanted with cortical electrodes. EEG activity, and event related potentials (ERPs) were then examined. Following electrophysiological assessment, ethanol preference was assessed to examine the relationship between neurophysiological indices and ethanol consumption. EEG analyses revealed that HAPs and HS/Ibgs had greater peak frequency in the 2-4-Hz band and lower peak frequency in the 6-8- and 1-50-Hz bands of the cortical EEG compared to LAPs. Compared to HAPs, LAPs and HS/Ibgs had decreased peak EEG frequency in the 8-16-Hz band. Decreased parietal cortical power from 8 to 50 Hz was associated with high initial ethanol preference in HAP mice. In regards to ERPs, P1 amplitude was greater in HAPs compared to both LAPs and HS/Ibgs and the P3 latency in LAPs was decreased compared to both HAPs and HS/Ibgs. As expected, HAPs consumed more ethanol and had higher ethanol preference than LAPs and HS/Ibgs. There were no significant differences in ethanol intake or preference between HS/Ibgs and LAPs. These data indicate that selective breeding of the HAP and LAP lines has resulted in the divergence of EEG and ERP phenotypes. The differences observed suggest that increased cortical P1 amplitude and altered cortical EEG activity in the 8-50-Hz frequency range may be neurophysiological 'risk factors' associated with high ethanol consumption in mice. Decreased P3 latency in LAPs compared to HAPs and HS/Ibgs mice may be a 'protective factor'.
Slawecki
Craig J
CJ
Department of Neuropharmacology, The Scripps Research Institute, CVN-14, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. cslawecki@scripps.edu
Grahame
Nicholas J
NJ
Roth
Jennifer
J
Katner
Simon N
SN
Ehlers
C L
CL
D000161:Acoustic Stimulation; D000428:Alcohol Drinking / Q000503:physiopathology*; D000437:Alcoholism / Q000503:physiopathology; D000818:Animals; D001835:Body Weight; D002492:Central Nervous System Depressants / Q000008:administration & dosage* / Q000009:adverse effects*; D002540:Cerebral Cortex / Q000187:drug effects* / Q000503:physiopathology; D004195:Disease Models, Animal; D004569:Electroencephalography / Q000187:drug effects*; D000431:Ethanol / Q000008:administration & dosage* / Q000009:adverse effects*; D005071:Evoked Potentials / Q000187:drug effects*; D005625:Frontal Lobe / Q000187:drug effects; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D010296:Parietal Lobe / Q000187:drug effects; D010641:Phenotype; D012307:Risk Factors
D002492:Central Nervous System Depressants; D000431:Ethanol