Altered brain sensitivity to ethanol in mice after MPTP treatment

Yanai, Joseph; Shaanani, Ram; Pick, Chaim G.

doi:10.1016/0741-8329(94)00066-2

Cited by 9 publications

(5 citation statements)

References 20 publications

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“…On the other hand, the activation of the DAergic nigrostriatal pathway has been proposed to be implicated in the mechanisms underlying brain sensitivity to ethanol and represent a key element in addictive processes (Yanai et al 1995). The number and activity of postsynaptic DAergic receptors, as well as other neurotransmitters and/or neuromodulators, including opioid peptides, may be relevant in ethanol sensitivity (Yanai et al 1988;Crabbe et al 1990;Yanai et al 1995). Several studies support this view.…”

Section: Discussionmentioning

confidence: 91%

“…For instance, ethanol and opiates increase the firing rate of DAergic neurons in the SNc (which contains the somata of these neurons) (Iwatsubo and Clouet 1977;Mereu et al 1984) and stimulate DA release and metabolism in the striatum (Fadda et al 1980;Widdowson and Holman 1992). On the other hand, the activation of the DAergic nigrostriatal pathway has been proposed to be implicated in the mechanisms underlying brain sensitivity to ethanol and represent a key element in addictive processes (Yanai et al 1995). The number and activity of postsynaptic DAergic receptors, as well as other neurotransmitters and/or neuromodulators, including opioid peptides, may be relevant in ethanol sensitivity (Yanai et al 1988;Crabbe et al 1990;Yanai et al 1995).…”

Section: Discussionmentioning

confidence: 98%

“…Ethanol and barbiturate sensitivity has been studied in animal models by the response to druginduced narcosis. Several studies have shown that brain resistance to ethanol-and barbiturate-induced narcosis is of shorter duration in drug-treated animals than in their corresponding controls (Yanai et al 1988(Yanai et al , 1995. This response, measured as a reduction in drug-induced sleep time, has been interpreted as a decreased sensitivity (increased resistance) of the brain to the narcotic effects of ethanol and barbiturates.…”

Section: Introductionmentioning

confidence: 96%

“…This response, measured as a reduction in drug-induced sleep time, has been interpreted as a decreased sensitivity (increased resistance) of the brain to the narcotic effects of ethanol and barbiturates. The number and activity of postsynaptic DAergic receptors in the nigrostriatal pathway have been suggested to be relevant in drug sensitivity (Yanai et al 1988(Yanai et al , 1995. Studies in animals reveal that an increased number of striatal DAergic receptors is associated with an enhanced brain resistance to ethanol.…”

Section: Introductionmentioning

confidence: 97%

“…Ethanol has been shown to increase the firing rate of DAergic neurons in the substantia nigra pars compacta (SNc) (Mereu et al 1984) and to stimulate the release and metabolism of DA in the caudateputamen (CP) (Fadda et al 1980;Widdowson and Holman 1992). The DAergic activity in the nigrostriatal pathway has been suggested to play a major role in brain sensitivity to ethanol and to represent an important component in addictive behavior (Yanai et al 1995), although this pathway has not been implicated in ethanol reward circuits. A decreased sensitivity of the brain to a drug has been considered as a diminished response to the functional effects of that drug.…”

Section: Introductionmentioning

confidence: 99%

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Ethanol-induced Changes in Proenkephalin mRNA Expression in the Rat Nigrostriatal Pathway

2008

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Endogenous opioid systems have been suggested to play a key role in ethanol reinforcement mechanisms and alcohol-drinking behavior. Ethanol induces differential alterations in opioid peptide expression in brain areas of the reward circuits, which may be linked to the reinforcing effects of ethanol. In addition, ethanol-induced alterations in opioidergic nigrostriatal transmission could be involved in brain sensitivity to ethanol and play a role in addictive processes. The aim of this work was to study the effects of acute ethanol administration on proenkephalin (proenk) mRNA expression in the rat substantia nigra and caudate-putamen (CP) for up to 24 h post treatment. Male Wistar rats received ethanol (2.5 g/kg) or distilled water by intragastric administration, and proenk mRNA expression was studied by in situ hybridization and densitometry. Ethanol transiently increased proenk mRNA expression in the CP 1 h after drug administration. Proenk mRNA levels remained elevated 2 h post treatment in the anterior-medial and medial-posterior regions of the CP. In contrast, ethanol decreased proenk mRNA expression in the substantia nigra pars compacta and pars reticulata 2 h after drug exposure. Alterations in enkephalin expression in the substantia nigra and CP in response to ethanol exposure could be involved in the mechanisms underlying brain sensitivity to the drug.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Ethanol-induced Changes in Proenkephalin mRNA Expression in the Rat Nigrostriatal Pathway

2008

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Acute Ethanol Administration Differentially Alters Enkephalinase and Aminopeptidase N Activity and mRNA Levels in Regions of the Nigrostriatal Pathway

et al. 2012

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Opioid peptides play a key role in ethanol reinforcement and may also represent important determinants in brain sensitivity to ethanol through modulation of nigrostriatal dopaminergic activity. Regulation of opioid levels by peptidase-degrading enzymes could be relevant in ethanol's actions. The aim of this work was to study the acute ethanol (2.5 g/kg) effects on the activity and mRNA expression of enkephalinase (NEP) and aminopeptidase N (APN) in the rat substantia nigra (SN) and the anterior-medial (amCP) and medial-posterior (mpCP) regions of the caudate-putamen (CP). Enzymatic activities were measured by fluorometric assays and mRNA expression by reverse transcriptase polymerase chain reaction. Acute ethanol administration differentially altered peptidase activities and mRNA expression with different kinetics. Ethanol increased and decreased NEP mRNA levels in the SN and amCP, respectively, but produced biphasic effects in the mpCP. APN mRNA levels were increased by ethanol in all brain regions. Ethanol induced a transient and long-lasting increase in NEP (mpCP) and APN (amCP) activities, respectively. Peptidase activities were not changed by ethanol in the SN. Our results indicate that striatal NEP and APN are important ethanol targets. Ethanol-induced changes in these neuropeptidases in the CP could contribute to the mechanisms involved in brain sensitivity to ethanol.

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