Alcohol and central neurotransmission

Ollat, H; Parvez, H.; Parvez, S.

doi:10.1016/0197-0186(88)90001-0

Cited by 96 publications

(14 citation statements)

References 149 publications

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“…This latter result excludes the possibility that the change in glutamate content was simply caused by alcohol sensitization after repeated exposures. This increase in glutamate would indicate a compensatory response by the amygdala to oppose the inhibitory effects of the acute ethanol dose of 2 g/kg, which stimulates GABAergic (Ollat et al 1988;Nevo and Hamon 1995) and inhibits glutamatergic (Nie et al 1994;Nevo and Hamon 1995) neurotransmissions. However, as demonstrated by the conditioned stimulus group (Fig.…”

Section: Discussionmentioning

confidence: 95%

Changes in the amygdala amino acid microdialysate after conditioning with a cue associated with ethanol

Quertemont¹,

Neuville²,

Witte³

1998

Psychopharmacology

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The excitatory amino acid neurotransmission within the amygdala has been implicated in learning associations between external stimuli and intrinsic reward values such that it may play a key role in conditioned drug effects. In the present studies, the responses of the excitatory amino acids, aspartate and glutamate together with the neuromodulatory sulphonated amino acid taurine, within the basolateral amygdala, to an odor cue repeatedly associated with acute ethanol injections (2g/kg, IP) have been investigated by a microdialysis technique combined with HPLC-EC analysis. After presentation of the ethanol-conditioned stimulus, a single IP saline injection induced an immediate and significant increase in the taurine microdialysate content which could be related to the neuromodulatory action of taurine. Furthermore, when the conditioned stimulus was combined with the ethanol injection (2g/kg, IP), significant increases in both taurine and glutamate microdialysate content were observed and indicated a learned compensatory response to counteract the acute effects of ethanol. These results demonstrate that changes in amygdala extracellular glutamate and taurine concentrations can be conditioned to ethanol-associated stimuli and are therefore probably implicated in the phenomenon of environmental-dependent tolerance to ethanol.

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Section: Discussionmentioning

confidence: 95%

Changes in the amygdala amino acid microdialysate after conditioning with a cue associated with ethanol

Quertemont¹,

Neuville²,

Witte³

1998

Psychopharmacology

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“…Three other studies reported less coffee consumption among PD cases than controls [18,25,26], although this was significant in only one [26]. Both ethanol [27,28] and caffeine [29][30][31] affect dopamine transmission and turnover in the basal ganglia and other brain regions.…”

Section: Discussionmentioning

confidence: 96%

Risk Factors for Parkinson’s Disease: The Leisure World Cohort Study

2001

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We conducted a case-control study nested within a prospective cohort study of 13,979 residents of Leisure World Laguna Hills, a retirement community in southern California, for etiologic clues for Parkinson’s disease (PD). Between 1981 (when first mailed a health survey) and 1998, we identified 395 PD cases from death certificates, hospital discharge diagnoses and a 1992 follow-up questionnaire. Six controls were individually matched on sex, birth date (±2 years), vital status and, if dead, death date (±1 year) to each case. Baseline characteristics of the 395 cases and 2,320 controls were analyzed as potential PD risk factors. The risk of PD was significantly reduced among smokers, hypertensives, coffee drinkers and alcohol consumers, and significantly increased among those with 3 or more children and with a high intake of total vitamin A and dietary vitamin C. The multivariate odds ratios (95% confidence intervals) were 0.42 (0.22–0.80) for current cigarette smokers of 1+ pack/day, 0.62 (0.48–0.80) for current users of hypertensive medication, 0.71 (0.52–0.95) for coffee drinkers of 2+ cups/day and 0.77 (0.58–1.03) for drinkers of 2+ alcoholic drinks/day. Risk increased with increasing number of children (1.25 for 1, 1.34 for 2 and 1.90 for 3+ children; p for trend = 0.0003). The increased risks among individuals in the highest third of total vitamin A intake and of dietary vitamin C intake were no longer statistically significant after adjusting for the other variables. These findings suggest several environmental factors that may be related to the development of PD and support a multifactorial etiology.

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“…Ethanol has been shown to alter the activity of various transmitters including GABA and monoamines (see Ollat et al, 1988, for a review). The levels and metabolism of GABA are affected by ethanol in several ways that may have a bearing on the clinical syndromes associated with alcohol abuse.…”

Section: Introductionmentioning

confidence: 99%

Increase in brain GABA-transaminase activity after chronic ethanol treatment in rats

Sherif

Wahlström

Oreland

1994

J. Neural Transmission

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The activity of gamma-aminobutyrate aminotransferase (GABA-T) was measured in the brains of rats treated both acutely and sub-chronically with ethanol. Previously, chronic treatment with ethanol for 90 weeks was found to increase the mean brain GABA-T activity by 20-45%. In the present study acute ethanol treatment (4 g/kg, i.p.) did not induce and change in the activity of brain GABA-T with the exception of a small increase in the cerebellum (8%) and, after repeated treatment with ethanol (4 g/kg/day, i.p.) for one and two weeks, no change in the activity of GABA-T was also found in any of the brain regions examined. Subchronic treatment with ethanol for 14 weeks, performed according to two different schedules involving a voluntary intake of ethanol in the drinking water, resulted in approximately a two-fold difference in ethanol intake. A mean increase of 50-85% in the activity of GABA-T was found in all the brain regions of rats with higher ethanol intake in comparison with the group of rats with lower ethanol intake. A bimodal distribution of brain GABA-T activity, however, was found in the ethanol-treated rats, with 60% of the rats having a two-fold increase and the remaining 40% having unchanged activities. The addition of pyridoxal phosphate to the incubation media increased the activity of brain mitochondria from ethanol-treated rats with high brain GABA-T, whereas there was a decrease in the activity in control rats and in ethanol-treated rats in which no increase in brain GABA-T had occurred. These results show firstly, that in a subpopulation of rats, subchronically treated with ethanol for 14 weeks, there was a two-fold increase in brain GABA-T activity, while in another subgroup no change occurred, and, secondly, that this increase in GABA-T activity was a consequence of a change in the response of the apoprotein to the addition of the cofactor pyridoxal phosphate.

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Alcohol and central neurotransmission

Cited by 96 publications

References 149 publications

Changes in the amygdala amino acid microdialysate after conditioning with a cue associated with ethanol

Changes in the amygdala amino acid microdialysate after conditioning with a cue associated with ethanol

Risk Factors for Parkinson’s Disease: The Leisure World Cohort Study

Increase in brain GABA-transaminase activity after chronic ethanol treatment in rats

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