Microdialysis for the determination of acetaldehyde and ethanol concentrations in the striatum of freely moving rats

Jamal, Mostofa; Ameno, Kiyoshi; Kumihashi, Mitsuru; Ameno, Setsuko; Kubota, Takako; Wang, Weihuan; Ijiri, Iwao

doi:10.1016/j.jchromb.2003.09.015

Cited by 39 publications

(26 citation statements)

References 21 publications

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“…Nevertheless, increases in acetaldehydemetabolizing enzymes in the brain have been reported after previous ethanol exposure in rats, suggesting that acetaldehyde is present in the brain after consumption of ethanol (Amit et al, 1977;Amir, 1978). Moreover, recent studies have demonstrated the consistent detection of acetaldehyde in the brain after peripheral ethanol administration (Ward et al, 1997;Jamal et al, 2003). Some of the acetaldehyde present in the brain can be the result of acetaldehyde molecules that are produced peripherally and then reach the brain, although it is difficult for acetaldehyde to cross the blood-brain barrier because of the metabolic barrier presented by large concentrations of ALDH (Hunt, 1996;Quertemont and Tambour, 2004).…”

Section: Role Of Ethanol Metabolismmentioning

confidence: 99%

Motor Stimulant Effects of Ethanol Injected into the Substantia Nigra Pars Reticulata: Importance of Catalase-Mediated Metabolism and the Role of Acetaldehyde

Arizzi-LaFrance

Correa

Aragón

et al. 2005

Neuropsychopharmacol

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A series of experiments was conducted to investigate the locomotor effects of local injections of ethanol and the ethanol metabolite, acetaldehyde, into substantia nigra pars reticulata (SNr). Infusions of ethanol into SNr resulted in a dose-related increase in locomotor activity, with maximal effects at a dose of 1.4 mmol. Ethanol injected into a control site dorsal to substantia nigra failed to stimulate locomotion, and another inactive site was identified in brainstem areas posterior to substantia nigra. The locomotor effects of intranigral ethanol (1.4 mmol) were reduced by coadministration of 10 mg/kg sodium azide, a catalase inhibitor that acts to reduce the metabolism of ethanol into acetaldehyde in the brain. SNr infusions of acetaldehyde, which is the first metabolite of ethanol, also increased locomotion. Taken together, these results indicate that SNr is one of the sites at which ethanol and acetaldehyde may be acting to induce locomotor activity. These results are consistent with the hypothesis that acetaldehyde is a centrally active metabolite of ethanol, and provide further support for the idea that catalase activity is a critical step in the regulation of ethanol-induced motor activity. These studies have implications for understanding the brain mechanisms involved in mediating the ascending limb of the biphasic dose-response curve for the effect of ethanol on locomotor activity.

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Section: Role Of Ethanol Metabolismmentioning

confidence: 99%

Motor Stimulant Effects of Ethanol Injected into the Substantia Nigra Pars Reticulata: Importance of Catalase-Mediated Metabolism and the Role of Acetaldehyde

Arizzi-LaFrance

Correa

Aragón

et al. 2005

Neuropsychopharmacol

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“…11 There is growing evidence indicating that the in vivo formation of certain TIQs may be related to alcohol addiction. 12,13 The chirality of TIQs neurotoxicity has been receiving increasing research attention. Many chiral TIQ molecules have been shown to exhibit enantioselective neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Chiral CE Separation of Dopamine-Derived Neurotoxins

et al. 2005

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An enantiomeric separation of dopamine-derived neurotoxins by capillary electrophoresis has been developed. Tetrahydroisoquinoline (TIQ), dopamine (DA), (R/S)-1-benzyl-TIQ (BTIQ), (R/S)-6,7-dihydroxy-1-methyl-TIQ (salsolinol, Sal), and (R/S)-6,7-dihydroxy-1, 2-dimethyl-TIQ (N-methyl-salsolinol, NMSal) were studied as model compounds. The CE running buffer (50 mM phosphate buffer at pH 3.0) contained 1.5 M urea and 12 mM β-CD as a chiral selector. During separation, the (R)-enantiomers formed more stable inclusion complexes with β-CD, and thus had a longer migration time than their optical antipodes. It was noticed that the recovery rates of these TIQ derivatives were very poor (< 15%) during protein precipitation, a procedure widely used for cleaning up biological samples. The recovery was significantly improved by pre-mixing the sample with a surfactant (e.g., sodium hexanesulfonate or Triton X-100) to reduce the co-precipitation. The present method in combination with electrospray ionization tandem mass spectrometry (ESI-MS/MS) was applied to study samples obtained from in vitro incubation of two catecholamines, dopamine and epinine, with aldehydes forming neurotoxins including (S)-and (R)-NMSal enantiomers. The later is known to induce Parkinsonism in rats.

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“…The main effects of ethanol consumption are visible not only in the gastrointestinal tract or the circulatory system, but also on the central nervous system (CNS) where it causes significant relapses, substantially influencing the balance between excitatory and inhibitory phenomena in the brain, principally enhancing the action of GABA (the major inhibitory neurotransmitter), and consequently generating disinhibition, ataxia and sedation 1 . It has been largely demonstrated that acute and subchronic exposure to ethanol may have important repercussions on the brain, enhancing the dopamine neurotransmission in the mesolimbic system, producing an intensification of the dopaminergic neurons in VTA [2][3][4] and increasing dopamine levels in the nucleus accumbens 5 , thus playing an important role in the 'reward' system in the development of alcohol abuse and addiction [6][7][8] .…”

Section: Introductionmentioning

confidence: 99%