PMID- 8192685
OWN - NLM
STAT- MEDLINE
DCOM- 19940623
LR  - 20071114
IS  - 0067-8694 (Print)
IS  - 0067-8694 (Linking)
VI  - 59
DP  - 1993
TI  - Animal models of alcoholism: genetic strategies and neurochemical mechanisms.
PG  - 173-91
AB  - Evidence from human studies indicates that response to alcohol consumption and 
      the probability of developing alcoholism have a heritable basis. The involvement 
      of several genes encourages the application of classical genetics to elucidate 
      the genetic basis of alcohol abuse. Quantitative genetics can provide evidence 
      for modes of inheritance and estimates of gene number. Therefore, inbred strains 
      and selective breeding programmes have been used to demonstrate a genetic basis 
      for the physiological and behavioural effects of ethanol in rodents. 
      Neurochemical studies have shown that ethanol has effects on membrane fluidity, 
      and on membrane receptors, ion channels and enzymes (Fig. 1). Comparison of these 
      in animal lines selected for a particular response (or lack of response) to 
      ethanol has disclosed differences in membrane composition (notably in 
      polysialogangliosides), and in the functioning of NaK-ATPase, Na+ channels and 
      gamma-aminobutyric acid (GABAA) receptors. Not all of these effects were observed 
      at relevant ethanol concentrations, but differences in the properties of GABAA 
      receptors between lines are the most compelling. Thus classical genetic 
      strategies, while labour intensive with respect to the generation and maintenance 
      of animal lines, have proven useful in dissecting the molecular, cellular and 
      behavioural effects of alcohol and their genetic variability.
FAU - Collins, A C
AU  - Collins AC
AD  - Institute for Behavioral Genetics, University of Colorado, Boulder 80309.
FAU - Wehner, J M
AU  - Wehner JM
FAU - Wilson, W R
AU  - Wilson WR
LA  - eng
GR  - AA-03527/AA/NIAAA NIH HHS/United States
GR  - AA-06391/AA/NIAAA NIH HHS/United States
GR  - AA-07567/AA/NIAAA NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - England
TA  - Biochem Soc Symp
JT  - Biochemical Society symposium
JID - 7506896
SB  - IM
MH  - Alcoholism/*genetics/*metabolism
MH  - Animals
MH  - Brain Chemistry/*physiology
MH  - Disease Models, Animal
RF  - 91
EDAT- 1993/01/01 00:00
MHDA- 1993/01/01 00:01
CRDT- 1993/01/01 00:00
PHST- 1993/01/01 00:00 [pubmed]
PHST- 1993/01/01 00:01 [medline]
PHST- 1993/01/01 00:00 [entrez]
PST - ppublish
SO  - Biochem Soc Symp. 1993;59:173-91.