Alcohol is a drug; a cautionary note on its use as a drug solvent

Little, H.J.

doi:10.1007/s00213-003-1580-1

Cited by 4 publications

(3 citation statements)

References 10 publications

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“…Unless stated otherwise, all analyses were followed by Bonferroni-Dunn post hoc tests, and P < 0.05 was considered statistically significant. To allow comparisons with in vitro studies (Little, 2003), conversion constants are provided for blood alcohol levels and ACTH and corticosterone levels in the figure legends.…”

Section: Data Presentation and Statistical Analysesmentioning

confidence: 99%

Alcohol self‐administration acutely stimulates the hypothalamic‐pituitary‐adrenal axis, but alcohol dependence leads to a dampened neuroendocrine state

Richardson

Lee

O’Dell

et al. 2008

Eur J of Neuroscience

263

225

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Clinical studies link disruption of the neuroendocrine stress system with alcoholism, but remaining unknown is whether functional differences in the hypothalamic-pituitary-adrenal (HPA) axis precede alcohol abuse and dependence or result from chronic exposure to this drug. Using an operant self-administration animal model of alcohol dependence and serial blood sampling, we show that long-term exposure to alcohol causes significant impairment of HPA function in adult male Wistar rats. Acute alcohol (voluntary self-administration or experimenter-administered) stimulated the release of corticosterone and its upstream regulator, adrenocorticotropic hormone, but chronic exposure sufficient to produce dependence led to a dampened neuroendocrine state. HPA responses to alcohol were most robust in ‘low-responding’ non-dependent animals (averaging < 0.2 mg/kg/session), intermediate in non-dependent animals (averaging ~0.4 mg/kg/session), and most blunted in dependent animals (averaging ~1.0 mg/kg/session) following several weeks of daily 30-min self-administration sessions, suggesting that neuroendocrine tolerance can be initiated prior to dependence and relates to the amount of alcohol consumed. Decreased expression of corticotropin-releasing factor (CRF) mRNA expression in the paraventricular nucleus of the hypothalamus and reduced sensitivity of the pituitary to CRF may contribute to, but do not completely explain, neuroendocrine tolerance. The present results, combined with previous studies, suggest that multiple adaptations to stress regulatory systems may be brought about by excessive drinking, including a compromised hormonal response and a sensitized brain stress response that together contribute to dependence.

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Section: Data Presentation and Statistical Analysesmentioning

confidence: 99%

Alcohol self‐administration acutely stimulates the hypothalamic‐pituitary‐adrenal axis, but alcohol dependence leads to a dampened neuroendocrine state

Richardson

Lee

O’Dell

et al. 2008

Eur J of Neuroscience

263

225

View full text Add to dashboard Cite

show abstract

“…Even apart from potential interactions between alcohol and dihydropyridines, the levels of alcohol that result when it is used as solvent have been too often ignored, as alcohol has behavioral effects at considerably lower doses than is often thought (Little, 2004). It is crucial in behavioral studies to provide the doses or concentrations of alcohol given if it is used as a solvent.…”

Section: B Use Of Solventsmentioning

confidence: 99%

“…In this study, nimodipine was dissolved in 50% alcohol. The volume of injection is not stated, but calculations suggest the alcohol dose could be 0.1-1 g/kg alcohol, doses known to have behavioral effects (Little, 2004). Although the vehicle was stated not to have effects alone, and even if smaller amounts of alcohol were used, acute interactions with the nimodipine could still have occurred (see section III.…”

Section: L-type Calcium Channels and Opioidsmentioning

confidence: 99%