Neurotransmitter and Neuromodulatory Mechanisms Involved in Alcohol Abuse and Alcoholism.

Nevo, Igal; Hamon, M.

doi:10.1097/00000374-200408002-00203

Cited by 42 publications

(57 citation statements)

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“…Low CSF HVA may have more to do with psychopathology related to alcoholism as opposed to mood disorder biology. Our finding is consistent with studies that suggest that dopaminergic mechanisms play a part in the biology of alcohol use disorders, including mechanisms of alcohol dependence and withdrawal (Diana et al, 1993;Weiss et al, 1996;Weiss and Koob, 1991;Koob, 1992;Noble, 1996;Wiesbeck et al, 2000;Fromme and D'Amico, 1999;Nevo and Hamon, 1995;Roos and Silfverskiöld, 1973;Kato et al, 1979;Goldman et al, 1992;Takahashi et al, 1974;Major et al, 1977;Fujimoto et al, 1983;Roy et al, 1991a;Virkkunen et al, 1996;Fils-Aime et al, 1996;Petrakis et al, 1999;Samson et al, 1990;Valenzuela and Harris, 1997;Robinson and Berridge, 1993;VavrousekJakuba et al, 1992;Quarfordt et al, 1991;Modell et al, 1993;Grace, 2000).…”

Section: Biological Findingssupporting

confidence: 90%

“…Brain dopaminergic, serotonergic, and noradrenergic systems have been implicated in biological mechanisms of both depression and alcoholism (for reviews, see Nemeroff et al, 1997;Fromme and D'Amico, 1999;Geracioti, 1997;Koob, 1992;Kapur and Mann, 1992;Nevo and Hamon, 1995;Oquendo and Mann, 2000;Valenzuela and Harris, 1997;Schatzberg et al, 2002). The cerebrospinal fluid (CSF) concentrations of the dopamine, serotonin, and to a lesser degree norepinephrine metabolites, homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG), respectively, are presumed to reflect the turnover of parent neurotransmitters in the central nervous system (Moir et al, 1970;Bowers, 1972;Stanley et al, 1985;Sharma et al, 1994;Reuster et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Lower CSF Homovanillic Acid Levels in Depressed Patients with a History of Alcoholism

Sher

Oquendo

et al. 2003

Neuropsychopharmacol

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Major depression and alcoholism are often comorbid, resulting in more impairment and more suicidal behavior compared with either diagnosis alone. This study compared clinical features and cerebrospinal fluid (CSF) monoamine metabolites in depressed subjects with and without a history of alcoholism and healthy volunteers. We hypothesized that depressed subjects with a history of alcoholism would be more aggressive, impulsive, and suicidal than depressed subjects without a history of alcoholism, and would have lower CSF monoamine metabolite levels. We compared 63 subjects with a current major depressive episode (MDE) and a history of alcoholism, 72 subjects with a current MDE but without a history of alcoholism, and 22 healthy volunteers. Participants with a history of alcoholism were in remission for at least 6 months. All subjects were free from prescribed medications known to affect brain serotonin, dopamine, or norepinephrine systems for a minimum of 14 days. Depressive symptoms, lifetime aggression, impulsivity, Axis II disorders, and suicidal behavior were assessed. CSF was sampled and homovanillic acid (HVA), 5-hydroxyindolacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) were assayed by high-performance lipid chromatography with electrochemical detection. Depressed subjects with a history of alcoholism did not differ from depressed subjects without a history of alcoholism in current severity of depressive symptoms, or in past suicidal behavior. Depressed subjects with a history of alcoholism had lower CSF HVA levels, and higher lifetime aggression and current suicide ideation scale scores and were more likely to be tobacco smokers compared with depressed subjects without a history of alcoholism. Low HVA was present after adjustment for sex, aggression and depression scores, cigarette smoking, antisocial and borderline personality disorders, psychomotor retardation, and delusions. Controls had CSF HVA levels intermediate between the two depressed groups. We found no group difference in CSF 5-HIAA and MHPG levels. In individuals with current MDE, those with a history of comorbid alcoholism had lower CSF HVA levels compared with those without a history of alcoholism. Low CSF HVA suggests that impaired dopaminergic activity is associated with a history of alcoholism in persons with current MDE.

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Section: Biological Findingssupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Lower CSF Homovanillic Acid Levels in Depressed Patients with a History of Alcoholism

Sher

Oquendo

et al. 2003

Neuropsychopharmacol

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“…Evidence exists that alcohol addicts display a decreased level of 5-HT receptors, whereas pharmacological agents activating the serotonin system can effectively reduce ethanol consumption [137].…”

Section: -Htmentioning

confidence: 99%

Serotonin as a Modulator of Glutamate- and GABA-Mediated Neurotransmission: Implications in Physiological Functions and in Pathology

Ciranna

2006

257

170

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Abstract:The neurotransmitter serotonin (5-HT), widely distributed in the central nervous system (CNS), is involved in a large variety of physiological functions. In several brain regions 5-HT is diffusely released by volume transmission and behaves as a neuromodulator rather than as a "classical" neurotransmitter. In some cases 5-HT is co-localized in the same nerve terminal with other neurotransmitters and reciprocal interactions take place. This review will focus on the modulatory action of 5-HT on the effects of glutamate and -amino-butyric acid (GABA), which are the principal neurotransmitters mediating respectively excitatory and inhibitory signals in the CNS. Examples of interaction at preand/or post-synaptic levels will be illustrated, as well as the receptors involved and their mechanisms of action. Finally, the physiological meaning of neuromodulatory effects of 5-HT will be briefly discussed with respect to pathologies deriving from malfunctioning of serotonin system.

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“…Acute or chronic ethanol ingestion has been shown to induce significant changes in neurotransmitter systems (1)(2)(3). Among these, dopamine (DA) and 5-hydroxytryptamine (5-HT) have received special attention because of their putative role in the motivational effects of ethanol (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic ethanol treatment on monoamine levels in rat hippocampus and striatum

Vasconcelos

Cavalcante

Aguiar

et al. 2004

Braz J Med Biol Res

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We studied the effects of ethanol on concentrations of noradrenaline (NE), dopamine (DA) and serotonin (5-HT) and their metabolites in rat hippocampus and striatum. Ethanol (2 or 4 g/kg, po, from a 20% aqueous solution) was administered daily to male Wistar rats (4-13 per group) for 30 days and animals were sacrificed 30 min or 48 h after the last administration. Monoamines were measured by HPLC and considered significant at P < 0.05. A 47% increase in 5-HT levels was observed in the hippocampus with 4 g/kg ethanol in the 30-min protocol. Ethanol (2 and 4 g/kg) decreased DA (2114.5 ± 126.4 and 1785.1 ± 234.2 ng/g wet tissue, respectively) and 3,4-dihydroxyphenylacetic acid (DOPAC, 1477.6 ± 132.1 and 1218.8 ± 271.7 ng/g wet tissue, respectively) levels, while the higher dose also decreased NE (159.8 ± 13.5), 5-HT (228.0 ± 46.8) and 5-hydroxy-3-indoleacetic acid (5-HIAA, 304.4 ± 37.2 ng/g wet tissue), in the striatum after a 48-h withdrawal as compared to controls (DA: 3063.9 ± 321.3; DOPAC: 2379.6 ± 256.0; NE: 292.8 ± 50.2; 5-HT: 412.4 ± 36.2; 5-HIAA: 703.9 ± 61.4 ng/g wet tissue). In the 30-min protocol, ethanol (2 or 4 g/kg) decreased striatal NE (66 and 70%) and DA (50 and 36%) levels. On the other hand, increases were seen in 5-HIAA (146 and 153%) and 5-HT (59 and 86%) levels. Ethanol (2 g/kg, po) increased the homovanillic acid (HVA)/DA ratio (129%) in the striatum in the 30-min protocol, while at the higher dose it increased the HVA/DA ratio in the 48-h protocol (61%). These results indicate alterations in monoamines, mainly in the striatum, after chronic ethanol, which are influenced by dose and by the length of time after the last drug administration.

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Neurotransmitter and Neuromodulatory Mechanisms Involved in Alcohol Abuse and Alcoholism.

Cited by 42 publications

References 0 publications

Lower CSF Homovanillic Acid Levels in Depressed Patients with a History of Alcoholism

Lower CSF Homovanillic Acid Levels in Depressed Patients with a History of Alcoholism

Serotonin as a Modulator of Glutamate- and GABA-Mediated Neurotransmission: Implications in Physiological Functions and in Pathology

Effects of chronic ethanol treatment on monoamine levels in rat hippocampus and striatum

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