Effects of 250 mg% ethanol on monoamine and amino acid release from rat striatal slices

Murphy, J.M.; Cunningham, S. D.; McBride, William J.

doi:10.1016/0361-9230(85)90022-x

Cited by 27 publications

(6 citation statements)

References 21 publications

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“…[27] In the case of alcohol treatment, it was proved that the conversion level of DOPAC and HVA was elevated according to the concentration of alcohol in the blood. [28] And it was earlier reported that ethanol had no effect on endogenous release of DOPAC, HVA, or DA. However, ethanol did enhance the potassium stimulation, calcium-dependent release of glutamate and aspartate from the striatal region when compared with the normal brain.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological and Biochemical Interventions of Cigarette Smoke, Alcohol, and Sexual Mating Frequency on Idiopathic Rat Model of Parkinson's Disease

Ambhore¹,

Antony²,

Mali³

et al. 2012

Journal of Young Pharmacists

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Parkinson's Disease (PD) is a neurodegenerative disorder in the nigrostriatal pathway of animals and humans and is responsible for most of the movement disorders, including rigidity. The present study aimed to determine the effect of chronic cigarette smoke, alcohol intake, and frequent sexual mating on 1-Methyl-4-phenyl-1,2,3,6-tertahydro pyridine (MPTP)-induced rat model of PD. After treatment, the effect of these factors was determined by biochemical and molecular evaluation. Dopamine (DA) concentration, antioxidant enzymes, and mitochondrial activity decreased after treatment with cigarette smoke, alcohol, and frequent sexual mating when compared to the values in the control group. Excessive exposure of these factors may lead to neurodegeneration, dopaminergic toxicities, and, ultimately, clinical parkinsonism. Earlier literature from different publisher suggested that nicotine and cigarette smoke can protect the dopaminergic neurons in the substantia nigra against MPTP toxicity. In this study, we assessed the effect of the above three factors on an MPTP-treated rat model and concluded that they have a neurodegenerative effect and were found to be toxic to dopaminergic neurons in the substantia nigra. Further investigation is required to understand the exact etiology of clinical parkinsonism.

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Section: Discussionmentioning

confidence: 99%

Pharmacological and Biochemical Interventions of Cigarette Smoke, Alcohol, and Sexual Mating Frequency on Idiopathic Rat Model of Parkinson's Disease

Ambhore¹,

Antony²,

Mali³

et al. 2012

Journal of Young Pharmacists

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show abstract

“…The reason for these discrepancies remains unknown, but they may derive from differences in in vitro techniques. In calcium-replete medium, ethanol, at concentrations of 54-250 mM, has consistently failed to modify the KCl-induced release of endogenous DA from rat striatal slices in vitro (Holman and Snape, 1985;Murphy et al, 1985). In our preparation, which was shown to be calcium-dependent, we used a submaximal concentration of calcium.…”

Section: Discussionmentioning

confidence: 99%

Biochemical and behavioral evidence for an interaction between ethanol and calcium channel antagonists

Engel

Fahlke

Hulthe

et al. 1988

J. Neural Transmission

112

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In the present series of experiments we have studied the effects of the dihydropyridine calcium channel antagonist nifedipine on ethanol-induced changes in behavior and dopamine (DA) release and metabolism. The locomotor-stimulatory effect of low doses of ethanol (2.5 g/kg) was antagonized by nifedipine, whereas ethanol-induced sedation observed after higher doses (4.5 g/kg) was potentiated. Biochemical studies indicated that ethanol enhanced the metabolism and release of DA in the striatum and the DA-rich limbic regions measured by post mortem analyses of DA-metabolites by HPLC with electrochemical detection and by in vivo voltammetry in anaesthetized rats, respectively. Pretreatment with nifedipine antagonized the stimulatory effects of ethanol on the DA-system. Nifedipine reduced the preference for ethanol, estimated by the relative intake of ethanol (6% v/v) and water in a free-choice situation, suggesting an influence of nifedipine not only on the stimulatory but also on the positive reinforcing effects of ethanol. The present results suggest that the locomotor-stimulatory and positive reinforcing effects of ethanol as well as its enhancing effect on dopaminergic activity may involve an enhancement of calcium mediated mechanisms.

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“…Previous reports have suggested that ethanol either has no effect (12)(13)(14) or that it enhances the spontaneous release of DA (15,16) and inhibits the K + or electrically induced release of DA from rat striatal preparations (15,17). Previous reports have suggested that ethanol either has no effect (12)(13)(14) or that it enhances the spontaneous release of DA (15,16) and inhibits the K + or electrically induced release of DA from rat striatal preparations (15,17).…”

Section: Introductionmentioning

confidence: 99%

Effect of ethanol on [3H]Dopamine release in rat nucleus accumbens and striatal slices

1988

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Ethanol (10-200 mM) transiently increased tritium overflow from superfused rat nucleus accumbens slices previously incubated with [3H]dopamine (DA) and [14C]choline. The effect was greater in striatal tissue and did not appear to be a non-specific membrane effect since [14C]acetylcholine (ACh) release was not affected. Lack of antagonism by picrotoxin suggested that gamma-aminobutyric acid (GABA) receptors were not involved. Calcium was not a requirement and the DA uptake blocker, nomifensine, was without effect. Ethanol appeared to be causing [3H]DA release into the cytoplasm. K+ -stimulated release of [3H]DA and [14C]ACh from nucleus accumbens and striatal slices was not affected. Clonidine-mediated inhibition of the K+-evoked release of [3H]DA remained unaltered. Ethanol attenuated the isoproterenol-induced enhancement of [3H]DA release. Ethanol therefore appeared to interact with components of the DA terminal causing a transient increase in the release of neurotransmitter without impairing K+-evoked release but apparently interfering with the isoproterenol-induced effect.

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Effects of 250 mg% ethanol on monoamine and amino acid release from rat striatal slices

Cited by 27 publications

References 21 publications

Pharmacological and Biochemical Interventions of Cigarette Smoke, Alcohol, and Sexual Mating Frequency on Idiopathic Rat Model of Parkinson's Disease

Pharmacological and Biochemical Interventions of Cigarette Smoke, Alcohol, and Sexual Mating Frequency on Idiopathic Rat Model of Parkinson's Disease

Biochemical and behavioral evidence for an interaction between ethanol and calcium channel antagonists

Effect of ethanol on [3H]Dopamine release in rat nucleus accumbens and striatal slices

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