Effect of chronic treatment with ethanol and withdrawal of ethanol on binding of [H]SCH23390 to D1 dopamine receptor in rat visual cortex and hippocampus. An autoradiographic study (original) (raw)
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Effects of chronic ethanol intake at a low dose on the rat brain dopaminergic system
Alcohol, 1993
Effects of chronic ethanol intake at a low dose on the rat brain dopaminergic system. ALCOHOL 10(1) 45-49, 1993.-The effects of 8-week ethanol treatment (3% v/v in drinking water) on the rat brain dopaminergic system were investigated. Chronic ethanol consumption induced a significant increase in the number of dopamine Dt receptor sites in the caudate putamen. Conversely, no significant changes were observed in D2 receptor density or affinity. Biochemical results were in agreement with behavioral data, as amphetamine-induced locomotor hyperactivity was significantly higher in ethanol-treated rats in comparison to controls. Moreover, grooming behavior in response to SKF 38393, a selective agonist of DI receptors was potentiated in ethanol-treated rats, whereas locomotor hyperactivity induced by LY 171555 (a selective agonist of D 2 receptors) was not affected by ethanol treatment. The results indicate that changes in dopamine receptors may occur in the central nervous system at levels of ethanol intake that do not induce tolerance or dependence.
Ethanol and dopaminergic systems
Pharmacology Biochemistry and Behavior, 1983
Chronic ethanol consumption produces derangements of cell membrane structure, perhaps by changing membrane lipid content. This impairment leads to modification of membrane-related processes. In fact, after chronic ethanol exposure, an increase in striatal adenylate-cyclase activity occurs. On the other hand, dopamine is unable to further potentiate the production of cyclic AMP. This finding demonstrates that the dopaminergic receptor associated with adenylate-cyclase activity is affected by chronic ethanol treatment. In particular, the affinity of the dopaminergic receptor labelled by 3H-Spiperone is enhanced. In addition, the receptor-adenylate cyclase coupling system is impaired after chronic in vivo exposure of animals to ethanol. Ethanol Striatal dopaminergic systems Dopamine receptors Adenylate cyclase Guanyl nucleotides
Dopamine Metabolism and Receptor Function After Acute and Chronic Ethanol
Journal of Neurochemistry, 1980
Abstract: Acute ethanol treatment in rats elicits a selective increase in dihydroxyphenylacetic acid (DOPAC) content in striatum. In contrast, striatal DOPAC concentration does not differ from normal values after chronic ethanol treatment. Chronic administration of ethanol however causes a selective increase of specific [3H]spiroperidol binding and met-enkephalin content in the striatum. Kinetic analysis of [3H]spiroperidol binding data shows that after chronic ethanol treatment there is a significant increase in the affinity constant rather than in the number of binding sites for the ligand. Our results support the hypothesis that dopaminergic mechanisms at both pre- and postsynaptic level may be involved in the mediation of some of the central effects observed after ethanol consumption.
Alcoholism: Clinical and Experimental Research, 2006
Background: Dopaminergic (DA) activity in the extended amygdala (EA) has been known to play a pivotal role in mediating drug and alcohol addiction. Alterations of DA activity within the EA after chronic exposure to alcohol or substances of abuse are considered a major mechanism for the development of alcoholism and addiction. To date, it is not clear how different patterns of chronic alcohol drinking affect DA receptor levels. Therefore, the current studies investigated the effects of chronic ethanol consumption, with or without deprivations, on D1 and D2 receptor densities within the EA.
Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology, 1996
Intraperitoneal injection 10 min before sacrifice of 1.5 g ethanol/kg weight produced an increase in rat striatal levels of homovanillic acid (HVA) (p < 0.05) but did not affect the striatal concentrations of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), serotonin (5HT) and 5-hydroxyindoleacetic acid (5-HIAA). A similar ethanol treatment led to decreases in 5-HT (p < 0.05) and 5-HIAA (p < 0.05) from cerebral cortex (prefrontal and anterior cingulate areas). The results point to several ethanol-linked alterations in central serotonergic and dopaminergic systems. COMP BIOCHEM PHYSIOL 113C, 399402, 1996.
Alcohol, 2011
Moderate ethanol exposure produces neuroadaptive changes in the mesocorticolimbic dopamine system in nondependent rats, and increases measures of dopamine neuronal activity in vitro and in vivo. Moreover, moderate ethanol drinking and moderate systemic exposure elevates extracellular dopamine levels in mesocorticolimbic projection regions. However, the neuroadaptive changes subsequent to moderate ethanol drinking on basal dopamine levels have not been investigated in the ventral tegmental area (VTA). In the current study, adult female alcohol-preferring (P) rats were divided into alcohol-naïve, alcohol drinking, and alcohol deprived groups. The alcohol drinking group had continuous access to water and ethanol (15%, v/v) for 8 weeks. The alcohol deprived group had 6 weeks of access followed by 2 weeks of ethanol deprivation, 2 weeks of ethanol re-exposure, followed again by 2 weeks of deprivation. The deprived rats demonstrated a robust alcohol deprivation effect upon ethanol reinstatement. The alcohol-naïve group had continuous access to water only. In the last week of the drinking protocol, all rats were implanted with unilateral microdialysis probes aimed at the posterior VTA and no-net-flux microdialysis was conducted to quantify extracellular dopamine levels and dopamine clearance. Results yielded significantly lower basal extracellular dopamine concentrations in the posterior VTA of the alcohol drinking group compared to the alcohol naive and alcohol deprived groups (3.8 ± 0.3 vs. 5.0 ± 0.5 [p < 0.02] and 4.8 ± 0.4 nM, [p < 0.05], respectively). Extraction fractions were significantly (p < 0.0002) different between the alcohol drinking and alcohol naive groups (72 ± 2 vs. 46 ± 4%, respectively) and not significantly different (p = 0.051) between alcohol deprived and alcohol naive groups (61 ± 6% for the alcohol deprived group). The data indicate that reductions in basal DA levels within the posterior VTA occur after moderate chronic ethanol intake in nondependent P rats. This reduction may result, in part, from increased DA uptake and may be important for the maintenance of ethanol drinking. These adaptations normalize with ethanol deprivation and may not contribute to the alcohol deprivation effect.
Alcoholism: Clinical and Experimental Research, 2012
Background: The need of an animal model of alcoholism becomes apparent when we consider the genetic diversity of the human populations, an example being dopamine D2 receptor (DRD2) expression levels. Research suggests that low DRD2 availability is associated with alcohol abuse, while higher DRD2 levels may be protective against alcoholism. This study aims to establish whether (i) the ethanol-consuming mouse is a suitable model of alcohol-induced brain atrophy and (ii) DRD2 protect the brain against alcohol toxicity. Methods: Adult Drd2+ ⁄ + and Drd2) ⁄) mice drank either water or 20% ethanol solution for 6 months. At the end of the treatment period, the mice underwent magnetic resonance (MR) imaging under anesthesia. MR images were registered to a common space, and regions of interest were manually segmented. Results: We found that chronic ethanol intake induced a decrease in the volume of the temporal and parietal cortices as well as the caudal thalamus in Drd2) ⁄) mice. Conclusions: The result suggests that (i) normal DRD2 expression has a protective role against alcohol-induced brain atrophy and (ii) in the absence of Drd2 expression, prolonged ethanol intake reproduces a distinct feature of human brain pathology in alcoholism, the atrophy of the temporal and parietal cortices.
Bidirectional changes in striatal D2-dopamine receptor density during chronic ethanol intake
Alcohol, 1992
changes in striatal D2-dopamine receptor density during chronic ethanol intake. ALCOHOL 9(2) 133-137, 1992.-Results of previous studies on the effects of ethanol consumption for a single fixed period on the properties of D2 dopamine receptors appear contradictory and inconclusive. In this study, we have examined the time course of the effects of dietary ethanol on the properties of striatal D2 dopamine receptor. Ethanol intake led to a significant decrease in the maximum number (B,,) after 1 (35% of control) and 2 weeks (48% of control), but not after 3 (93% of control) or 4 weeks (97% of control) of treatment. However, there was a significant increase in B, , , after 6 (118% of control) and 10 weeks (123% of control) of ethanol consumption. The affinity (K,) of the receptor, however, remained unaltered in all cases. In conclusion, these data show that the duration of ethanol exposure may be an important determinant regulating D2-dopamine receptor density.