Local cerebral glucose utilization after relapse in ethanol drinking in alcohol-preferring (P) rats

Daniel G. Smith, Jennifer E. Learn, William J. McBride, Lawrence Lumeng, Ting Kai Li, James M. Murphy

Research output: Contribution to journalArticle

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Abstract

The [14C]-2-deoxyglucose ([14C]-2-DG) quantitative autoradiographic technique was used to determine rates of local cerebral glucose utilization (LCGU) in discrete brain regions of adult, male alcohol-preferring (P) rats after 2 weeks of ethanol deprivation (E-D), 3 and 14 days of ethanol-relapse drinking (E-R3; E-R14), and in P rats, which were chronically drinking ethanol (E-C) for 8 weeks during daily 3-h scheduled-access sessions to 15% (vol./vol.) ethanol and water, or were ethanol-naive (E-N). The hypothesis to be tested was that ethanol-relapse drinking is initiated to restore changes in functional activity back to their chronic ethanol-exposed state. The LCGU rates were measured 1 h before the scheduled-access session. Mean ethanol intake did not differ among the groups. The LCGU rates were decreased in 41 of 57 regions or subregions examined in E-C rats compared with findings for E-N rats, including subregions of the cerebral cortex, hippocampus, and structures in the mesocorticolimbic and nigrostriatal systems. After 2 weeks of deprivation, LCGU values tended to return toward control values (E-N) in most CNS regions and did not differ significantly from control values in 12 regions or subregions (e.g., parts of the limbic system, cerebral cortex). Compared with LCGU values that recovered toward control levels in the E-D group, ethanol-relapse drinking was associated with decreased LCGU values in (1) 4 of 10 limbic structures, (2) all 6 cerebral cortical regions, (3) 1 of 4 basal ganglia regions, (4) 2 of 7 hippocampus subregions, and (5) 1 of 6 thalamic nuclei. The present results indicate that ethanol-relapse drinking was associated with reduced LCGU rates in most CNS regions that recovered toward control values and suggested to us that ethanol-relapse drinking may be initiated to restore neuronal function to its prior chronic ethanol-exposure state.

Original languageEnglish
Pages (from-to)115-126
Number of pages12
JournalAlcohol
Volume27
Issue number2
DOIs
StatePublished - 2002

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Alcohol Drinking
Rats
Ethanol
utilization
alcohol
Alcohols
Glucose
Recurrence
deprivation
Values
Drinking
Cerebral Cortex
brain
Hippocampus
Group
water
Thalamic Nuclei
Limbic System
Level control

Keywords

  • Alcohol relapse
  • Alcohol-preferring (P) rats
  • Local cerebral glucose utilization

ASJC Scopus subject areas

  • Biochemistry
  • Medicine(all)
  • Behavioral Neuroscience
  • Neuroscience(all)
  • Toxicology
  • Health(social science)

Cite this

Smith, D. G., Learn, J. E., McBride, W. J., Lumeng, L., Li, T. K., & Murphy, J. M. (2002). Local cerebral glucose utilization after relapse in ethanol drinking in alcohol-preferring (P) rats. Alcohol, 27(2), 115-126. https://doi.org/10.1016/S0741-8329(02)00216-1

Local cerebral glucose utilization after relapse in ethanol drinking in alcohol-preferring (P) rats. / Smith, Daniel G.; Learn, Jennifer E.; McBride, William J.; Lumeng, Lawrence; Li, Ting Kai; Murphy, James M.

In: Alcohol, Vol. 27, No. 2, 2002, p. 115-126.

Research output: Contribution to journalArticle

Smith, DG, Learn, JE, McBride, WJ, Lumeng, L, Li, TK & Murphy, JM 2002, 'Local cerebral glucose utilization after relapse in ethanol drinking in alcohol-preferring (P) rats', Alcohol, vol. 27, no. 2, pp. 115-126. https://doi.org/10.1016/S0741-8329(02)00216-1
Smith, Daniel G. ; Learn, Jennifer E. ; McBride, William J. ; Lumeng, Lawrence ; Li, Ting Kai ; Murphy, James M. / Local cerebral glucose utilization after relapse in ethanol drinking in alcohol-preferring (P) rats. In: Alcohol. 2002 ; Vol. 27, No. 2. pp. 115-126.
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