Effects of Acute and Chronic Alcohol Administration on Brain Membrane Transport Systems

Ay, Sun; Rn, Seaman; Cc, Middleton

doi:10.1007/978-1-4899-5181-6_9

Cited by 14 publications

(3 citation statements)

References 19 publications

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“…However, a simple working model would be that activation of presynaptic α2adrenoreceptors leading to a decrease locus coeruleus firing would exacerbate the central depressant effects of ethanol. It should be noted in this context that while some studies have suggested that ethanol might act as a NET blocker (Lin et al, 1997(Lin et al, , 1993 (but see Haughey et al, 2005;Sun et al, 1977), the present data do not directly speak to the issue of ethanol's potential actions at NET, but rather the interaction between NET inactivating compounds and ethanol. Another important caveat is that the depressant effects of ethanol itself are likely the result of actions on multiple sites that includes norepinephrine but also other systems, notably g-amino-butyric-acid (GABA) (Boehm et al, 2006).…”

Section: Discussioncontrasting

confidence: 59%

“…By removing norepinephrine from the extracellular space, the NE transporter (NET) provides a major mechanism for the regulation of synaptic levels of norepinephrine (Pacholczyk et al, 1991). In vivo voltametric studies have demonstrated that ethanol can inhibit clearance of norepinephrine in rat brain (Lin et al, 1997(Lin et al, , 1993, although data on ethanol effects on norepinephrine reuptake in synaptosomal preparations have been equivocal (Haughey et al, 2005;Sun et al, 1977). Recent studies demonstrate that genetic and pharmacological alterations in NET affect ethanol's depressant effects.…”

Section: Introductionmentioning

confidence: 99%

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Desipramine potentiation of the acute depressant effects of ethanol: Modulation by α2-adrenoreceptors and stress

et al. 2008

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Ethanol exerts effects on the brain noradrenergic system, and these are thought to contribute to the sedative/hypnotic (depressant) effects of ethanol. Recent studies suggest that the norepinephrine transporter (NET) plays an important role in modulating ethanol's depressant effects. The aim of the present study was to further characterize this role. Transporter blockers with varying affinity for NET versus the serotonin transporter (desipramine>fluoxetine>citalopram) were tested for their ability to alter ethanol's depressant effects, and for comparison, hypothermic effects. Effects of desipramine on another depressant, pentobarbital, were examined. Desipramine potentiation of ethanol's depressant effects was assessed following depletion of brain norepinephrine via N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSP-4) treatment, or depletion of brain 5-HT via para-chlorophenylalanine methyl ester hydrochloride (PCPA) treatment. The effects of co-administration of either the selective alpha2-adrenoreceptor agonist (dexmedetomidine) or the selective alpha2-adrenoreceptor antagonist (atipamezole) on desipramine's effect on ethanol's depressant effects were examined. Given the close link between stress, ethanol and norepinephrine, desipramine potentiation of ethanol's depressant effects was tested following repeated forced swim stress. Results showed that desipramine, but not SERT-selective doses of citalopram or fluoxetine, strongly potentiated the depressant (not hypothermic) effects of ethanol. These effects were mimicked by dexmedetomidine and blocked by atipamezole, but not by depletion of either norepinephrine or 5-HT. Desipramine potentiation of ethanol's depressant effects was abolished following repeated stress. Present findings further support a major role for NET and the alpha2-adrenoreceptor in modulating the depressant effects of ethanol, with possible implications for understanding the role of noradrenergic dysfunction in stress-related alcoholism.

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Section: Discussioncontrasting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Desipramine potentiation of the acute depressant effects of ethanol: Modulation by α2-adrenoreceptors and stress

et al. 2008

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“…Another trend was that grade 2 values were a little higher than grade 3 valueseven though statistical significance was seen only in the inorganic phosphate concentrations at admission. Calcium plays an important role in the neuronal membrane function, and alcohol influences the membrane function in many ways (26), just as alcohol influences the brain calcium membrane transport systems (10). Many animal studies and in vitro experiments have been carried out within this area, but unrealistically high alcohol concentrations have been used to produce significant changes (26).…”

Section: Discussionmentioning

confidence: 99%

Delirium tremens and related clinical states: changes in calcium and inorganic phosphate concentrations in plasma and cerebrospinal fluid

Kramp

Hemmingsen

1984

Acta Psychiatr Scand

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Calcium and inorganic phosphate were measured in blood and cerebrospinal fluid (CSF) in 11 patients during impending delirium tremens (grade 2) and in nine patients with fully developed delirium tremens (grade 3). The initial sampling of blood and CSF was performed at admission before treatment was initiated. The blood sampling was repeated daily until recovery and at this time a second lumbar puncture was also performed. In grade 3 patients the plasma calcium concentration showed a transient increase after admission; in grade 2 patients the plasma calcium concentration was also somewhat elevated. The changes in plasma calcium concentration after admission correlated significantly with the changes in blood alcohol concentration. In grade 3 patients the CSF calcium concentration decreased between admission and recovery, this possibly relating to an increased cerebral binding capacity in the post intoxication period. No statistically significant changes were seen in either of the diagnostic categories as far as plasma inorganic phosphate concentrations are concerned. CSF inorganic phosphate concentration decreased in a fashion correlated with CSF alcohol concentration and, finally, CSF inorganic phosphate at admission was somewhat lower in grade 3 patients as compared to grade 2, this possibly reflecting a more severe disturbance of cerebral metabolism in grade 3 patients. Essentially, grade 3 patients had lower CSF concentrations of both calcium and inorganic phosphate as compared to grade 2 patients and thus there may exist real differences in the metabolism of these two ions when a severe withdrawal reaction (grade 2) is compared to fully developed delirium tremens (grade 3).

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Biochemical and Biophysical Approaches in the Study of Ethanol-Membrane Interaction

Sun¹

1979

Biochemistry and Pharmacology of Ethanol

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Effects of Acute and Chronic Alcohol Administration on Brain Membrane Transport Systems

Cited by 14 publications

References 19 publications

Desipramine potentiation of the acute depressant effects of ethanol: Modulation by α2-adrenoreceptors and stress

Desipramine potentiation of the acute depressant effects of ethanol: Modulation by α2-adrenoreceptors and stress

Delirium tremens and related clinical states: changes in calcium and inorganic phosphate concentrations in plasma and cerebrospinal fluid

Biochemical and Biophysical Approaches in the Study of Ethanol-Membrane Interaction

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