Effects of Ethanol on Voltage-Dependent Calcium Channel Function

Leslie, Steven W.

doi:10.1007/978-3-642-78435-4_3

Cited by 3 publications

(3 citation statements)

References 70 publications

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“…Such receptors include serotonin (5-HT) (11,35) voltage gated calcium channels (17); receptors for the excitatory amino acid, glutamate (12,35); GABA neurotransmission (23,44); catecholamines such as norepinephrine and dopamine (39). Changes in each of these receptors are suspected in not only producing dependence on alcohol, but also in claiming responsibility for the withdrawal syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…L-type calcium channels are primarily found on dendrites and neuronal cell bodies in the brain (17). Activation of these channels mediate long lasting increases in cytosolic calcium that may be linked with second messenger functions of calcium in brain, which includes involvement in neurotransmitter release.…”

Section: Discussionmentioning

confidence: 99%

“…Activation of these channels mediate long lasting increases in cytosolic calcium that may be linked with second messenger functions of calcium in brain, which includes involvement in neurotransmitter release. Evidence further indicates that chronic ethanol administration may result in upregulation of these L-type calcium channels with increasing calcium influx and that the temporary maintenance of these changes are involved in the development of functional tolerance, dependence, and in the withdrawal syndrome (14,17,32). …”

Section: Discussionmentioning

confidence: 99%

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Alcohol usage and abrupt cessation modulate diurnal activity

Norrell

Reyes-Vasquez

Burau

et al. 2010

Brain Research Bulletin

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Alcohol has many effects throughout the body. The effect on circadian rhythms and the correlation of these effects to withdrawal effects of alcohol present interesting findings. By measuring 3 planes of activity of female Sprague-Dawley rats during alcohol usage and continuing study through the first two days following withdrawal of alcohol allow for the observation of a drastic modulation of the circadian pattern of activity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Alcohol usage and abrupt cessation modulate diurnal activity

Norrell

Reyes-Vasquez

Burau

et al. 2010

Brain Research Bulletin

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Ethanol suppresses neuronal Ca2+ currents by effects on intracellular signal transduction

Kerschbaum

Hermann

1997

Brain Research

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Effects of Prenatal Ethanol Exposure on Voltage‐Dependent Calcium Entry into Neonatal Whole Brain‐Dissociated Neurons

Lee

Spuhler-Phillips

Randall

et al. 1996

Alcoholism Clin & Exp Res

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The effect of prenatal ethanol exposure on voltage-dependent calcium entry into neonatal-dissociated neurons was studied. Dissociated whole brain cells were isolated from neonates of prenatally ethanol-treated (ET), pair-fed (PF) control, and ad libitum (AL) control groups and loaded with fura-2. Prenatal ethanol exposure resulted in a significant reduction of calcium entry into K(+)-depolarized cells, compared with AL and PF control treatments. Initially, in dissociated cells from AL control animals, it was found that nifedipine (1 microM), omega-agatoxin (100 nM), and omega-conotoxin (500 nM), to a much lesser extent, significantly inhibited the 45 mM KCl-stimulated calcium entry. To determine the inhibitory action of prenatal ethanol exposure on N-, P-, and L-type voltage-dependent calcium channels, treatment of neonatal-dissociated neurons with different combinations of omega-conotoxin, omega-agatoxin, and nifedipine, respectively, was compared in the prenatal ethanol and control treatment groups. The inhibition of K(+)-stimulated increase in calcium entry by prenatal ethanol exposure was significantly less in the presence or absence of single antagonist conditions (ET < AL and PF). There was no apparent interaction of ethanol exposure and antagonist condition. However, the reduced calcium entry after prenatal ethanol exposure was superseded by the stronger inhibition in dual and triple antagonist conditions. The magnitude of the calcium response inhibition by the antagonist combinations was similar among the ET, PF, and AL groups. Thus, these results suggest that prenatal ethanol exposure decreases voltage-dependent calcium entry into neonatal-dissociated neurons in a manner that does not seem to involve the selective inhibition of any individual N-, P-, or L-type calcium channel.

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Effects of Ethanol on Voltage-Dependent Calcium Channel Function

Cited by 3 publications

References 70 publications

Alcohol usage and abrupt cessation modulate diurnal activity

Alcohol usage and abrupt cessation modulate diurnal activity

Ethanol suppresses neuronal Ca2+ currents by effects on intracellular signal transduction

Effects of Prenatal Ethanol Exposure on Voltage‐Dependent Calcium Entry into Neonatal Whole Brain‐Dissociated Neurons

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