Ethanol’s Action on Brain Biochemistry

Hoffman, Paula L.; Tabakoff, Boris

doi:10.1007/978-1-4757-9134-1_2

Cited by 36 publications

(8 citation statements)

References 213 publications

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“…5), J Neurochem , Vol 52, N o 6,1989 an interaction between ethanol and Ca2+ flux was apparently involved. Ethanol, in pharmacologically relevant concentrations, does alter Ca2+ mobilization (Hoffman and Tabakoff, 1985).…”

Section: Discussionmentioning

confidence: 99%

Effect of Acute Ethanol on Release of Endogenous Adenosine from Rat Cerebellar Synaptosomes

Clark

Dar

1989

Journal of Neurochemistry

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The effects of pharmacologically relevant concentrations of ethanol on the release of endogenous adenosine from rat cerebellar synaptosomes were investigated. Release was conducted for 5, 10, 30, or 60 s after which time the incubation medium (containing the released adenosine) was rapidly separated from the synaptosomal membranes by vacuum filtration. The adenosine content of the filtrate was measured by HPLC–fluorescence detection. Both basal and KCl‐stimulated adenosine release consisted of an initial rapid phase, for the first 10 s, that was followed by a relatively slower phase. Basal endogenous adenosine release was estimated as 199 ± 14 pmol/mg protein/5 s. Potassium (chloride) increased adenosine release from the basal level to 433 ± 83 pmol/mg protein/5 s. Ethanol caused a dose‐dependent increase of adenosine release. The interaction between dilazep and ethanol indicates that ethanol‐stimulated release does not involve the dilazep‐sensitive transport system. The results support previous findings that indicate that cerebellar adenosine is involved in the mediation of ethanol‐induced motor disturbances in the rat.

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Section: Discussionmentioning

confidence: 99%

Effect of Acute Ethanol on Release of Endogenous Adenosine from Rat Cerebellar Synaptosomes

Clark

Dar

1989

Journal of Neurochemistry

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“…In their discussion of the neuropsychology of alcoholism, Tarter and Edwards (1985, p. 220) concluded that' 'the investigations conducted to date do not reveal a disturbance in basic perceptual processes." Similar conclusions have been offered in discussions of alcohol and central nervous system function (e.g., Mitchell, 1985), pharmacology (e.g., Pohorecky & Brick, 1988;Ritchie, 1985), neuropathology (e.g., Freund, 1985), and brain biochemistry (e.g., Hoffman & Tabakoff, 1985). These reviews leave little reason to expect peripheral (precortical) visual processing to be impaired by moderate doses of alcohol.…”

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confidence: 61%

Alcohol impairs visual presence/absence detection more for females than for males

Avant

1990

Perception & Psychophysics

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Ninety subjects (45 males, 45 females) were given 0.0, 0.5, or 1.0 ml/kg body weight of 190-proofethanol and tested for chance-level presence/absence detection thresholds with energy-masked presentations of traffic signs and blank inputs. Alcohol produced higher blood alcohol concentration (BAC) levels, and higher detection threshold durations, for females than for males. These results indicate that alcohol influences precortical visual processing and that the influence is greater for females than for males. The higher bioavailability of alcohol in women is likely due to less gastric oxidation of ethanol in women than in men. Hills (1980) estimated that over 90% of the information input to the driver of an automobile is visual. The importance of understanding the effects of alcohol on vision should not be underestimated; however, the literature presents conflicting claims about the influence of alcohol on vision. Between 1940 and1984, at least eight literature reviews indicated that perception was minimally affected by alcohol (Carpenter, 1961;Grant, 1970;Jellinek & McFarland, 1940;Jones & Joscelyn, 1978;Marshall, 1941;Moskowitz, 1974;Voas, 1984;Wallgren & Barry, 1970). In their discussion of the neuropsychology of alcoholism, Tarter and Edwards (1985, p. 220) concluded that' 'the investigations conducted to date do not reveal a disturbance in basic perceptual processes." Similar conclusions have been offered in discussions of alcohol and central nervous system function (e.g., Mitchell, 1985), pharmacology (e.g., Pohorecky & Brick, 1988;Ritchie, 1985), neuropathology (e.g., Freund, 1985), and brain biochemistry (e.g., Hoffman & Tabakoff, 1985). These reviews leave little reason to expect peripheral (precortical) visual processing to be impaired by moderate doses of alcohol. Other studies suggest, however, that it may be premature to consider even retinal processes immune to the effects of alcohol. For example, alcohol has been reported to influence the action of certain neurotransmitters (e.g., Carmichael & Isreal, 1975;Kalant & Grose, 1967), the b-wave and c-wave of the electroretinogram (e.g., Ikeda, 1963;Skoog, 1974) 2851988), and recovery from the effects of glare and contrast sensitivity (e.g., Adams, 1978;Adams, Brown, & Flom, 1976).The visual masking procedure has not been used to examine the effects of alcohol on vision. Turvey (1973) has shown, however, that the procedure can distinguish between peripheral (precortical) and central (cortical) processing. To obtain masking in the peripheral visual system, the mask must be of greater energy than the target item, and the mask and target must be presented to the same eye. Such masking can function in both a forward and a backward direction. Central pattern masking can be obtained whether the target and mask inputs are to the same or to different eyes. It is governed by stimulus onset asynchrony between target and mask rather than by the energy relationship between the two. It functions primarily in a backward manner, and it requires some pattern similarity...

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“…Acute and chronic administration of ethanol in animals induces changes in the catecholaminergic, serotonergic, cholinergic. GABAergic and glutaminergic systems in the brain (Hoffman and Tabakoff, 1985;Engel and Liljequist, 1983;Hunt, 1985;Deitrich etal., 1989;Hoffman etal., 1990). Recently, the N-methyl-D-aspartate (NMDA) receptorgated ion channel has been reported to interact with ethanol in electrophysiological and biochemical experiments (Hoffman etal., 1989;Lovinger etal., 1989).…”

Section: Introductionmentioning

confidence: 98%

Cholinergic mechanisms in physical dependence on barbiturates, ethanol and benzodiazepines

Nordberg

Wahlström

1992

J. Neural Transmission

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The aim of this review is to summarize the effects of acute and chronic treatment with barbiturates, ethanol and benzodiazepines on cholinergic mechanisms in the brains of experimental animals. A single dose of each of these substances reduces the turnover of ACh in the brain. Long-term treatment has the opposite effect; complicated interactions including decreased content of ACh are induced. Barbiturates have been shown to bind stereospecifically to muscarinic and nicotinic receptors in the brain, but this has not been observed for ethanol or the benzodiazepines. The effects on the cholinergic system are affected by the length of treatment and choice of treatment regimen. No effect on cholinergic parameters, such as muscarinic receptors, in the brain is observed on withdrawal of ethanol or barbiturate treatment when the animals are still tolerant towards the substances. The increase in the number of muscarinic receptors observed in several brain regions on withdrawal is seen as a sign of cholinergic supersensitivity. The number of receptors returns to normal when abstinence convulsions have occurred. The assumption of a cholinergic influence is supported by the finding that atropine, given as a single dose on the day of withdrawal of barbital, can prevent the muscarinic receptor changes. Furthermore, long-term barbital or ethanol treatment can induce permanent persistent changes in the cholinergic system in the brain. Cognitive defects and a significant permanent reduction in the content of ACh can be measured in rats which have had long-term barbital treatment. Similarly, a reduced number of muscarinic receptors has been measured in different brain regions of chronic alcoholics. Accumulating data support the role of the cholinergic system in expressing symptoms of physical dependence on barbiturates, ethanol and benzodiazepines as well as in the permanent long-term effects observed after end of treatment.

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Ethanol’s Action on Brain Biochemistry

Cited by 36 publications

References 213 publications

Effect of Acute Ethanol on Release of Endogenous Adenosine from Rat Cerebellar Synaptosomes

Effect of Acute Ethanol on Release of Endogenous Adenosine from Rat Cerebellar Synaptosomes

Alcohol impairs visual presence/absence detection more for females than for males

Cholinergic mechanisms in physical dependence on barbiturates, ethanol and benzodiazepines

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