Isoquinoline Alkaloids as Possible Regulators of Alcohol Addiction

Blum, Kenneth; Hamilton, MurrayG; Meyer, EleanorK; Hirst, Maurice; Marshall, Alice

doi:10.1016/s0140-6736(77)92981-6

Cited by 12 publications

(5 citation statements)

References 11 publications

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“…These findings are discordant with the results from studies in mice where Blum et al (1977a) demonstrated an attenuation of ethanol induced narcosis by naloxone and also found a reduced incidence of withdrawal convulsions in mice given naloxone prior to and during the ethanol intoxication period (Blum et al 1976). The ethanol vapour technique used (Goldstein 1972) unfortunately involved administration of pyrazole in order to 'insure higher and stable blood ethanol concentrations; pyrazole is a neurotoxic substance (Goldstein 1976) and hence results obtained after administration of pyrazole are of doubtful value when investigating development of physical dependence in the CNS.…”

Section: Discussionsupporting

confidence: 71%

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Absence of an Effect of Naloxone on Ethanol Intoxication and Withdrawal Reactions

Hemmingsen

Sørensen

1980

Acta Pharmacologica et Toxicologica

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Experimental and clinical results suggest a relationship between the action of ethanol and opiates. Therefore, we have tested whether the specific morphine antagonist naloxone (2 mg/kg intraperitoneally every six hours) affects signs of severe ethanol intoxication or modifies the withdrawal syndrome following chronic ethanol intoxication in rats. Using a double blind technique, we did not find any difference between saline treated and naloxone treated animals with respect to level of intoxication and severity of withdrawal symptoms. We must therefore conclude that naloxone does not modify signs of severe ethanol intoxication or change the ethanol withdrawal syndrome in the rat. These findings do not rule out that there might be a biochemical link between actions of ethanol and opiates, but this link is probably not localized at the level of specific drug receptor interaction.

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Section: Discussionsupporting

confidence: 71%

“…Studies with the specific opiate antagonist naloxone have suggested that this substance may reduce symptoms of severe ethanol intoxication (Blum et a/. 1977a;Ssrensen & Mattisson 1978) and also that naloxone may inhibit the development of ethanol dependence, i.e.…”

mentioning

confidence: 99%

Absence of an Effect of Naloxone on Ethanol Intoxication and Withdrawal Reactions

Hemmingsen

Sørensen

1980

Acta Pharmacologica et Toxicologica

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“…Moreover, Gold et al (29) suggested the idea that endogenous peptides physiologically provided normal inhibitory tone at the locus coeruleus and during opiate withdrawal and that attenuation of this inhibitory mechanism, due to reduced endogenous peptides, leads to norepinephrine-induced hyperactivity. Other earlier work by Blum and associates revealed shared mechanisms between alcohol and opiate withdrawal (30)(31)(32)(33)(34)(35), potentially through the opiate-like effects of isoquinolines, which provided the basis for understanding the role of dopamine in acute opiate abstinence (36).…”

Section: Importance Of Preclinical Models Of Addictionmentioning

confidence: 97%

Neurogenetics of acute and chronic opiate opioid abstinence treating symptoms and the cause

et al. 2017

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This review begins with a comprehensive history of opioid dependence and treatment in the United States. The focus is an evidence-based treatment model for opioid/opiate dependent individuals. The role of reward genetic polymorphisms and the epigenetic modifications that lead to vulnerability to use and misuse of opiates/opioid to treat pain are reviewed. The neurochemical mechanisms of acute opiate withdrawal and opiate/opioid reward mechanisms are explored with a goal of identifying specific treatment targets. Alterations in functional brain connectivity based on neurobiological mechanisms in heroin dependence and abstinence are also reviewed. A new clinical model an alternative to merely blocking acute withdrawal symptoms as identified in the DSM -5 is proposed. Genetic diagnosis at the onset of detoxification, to determine risk stratification, and identify polymorphic gene targets for pharmaceutical and nutraceutical interventions, followed by the simultaneous initiation of Medication Assisted Therapy (MAT), to enable psychological extinction, and steady pro-dopaminergic therapy with the goal of developing "dopamine homeostasis" is recommended. The objective of these interventions is to prevent future relapse by treating all "Reward Deficiency Syndrome" (RDS) behaviors and eventually make an addiction-free life possible

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“…This work suggested that alcohol and opiate addiction might have common neurochemical mechanisms. Indeed at the time controversy stimulated research by neuroscientists that provided evidence that: ethanol intake augmented the salsolinol metabolite in the rat brain [ 16 , 17 ]; salsolinol induced an increase in ethanol intake [ 15 ]; salsolinol acts like an opiate agonist [ [18] , [19] , [20] ]; and salsolinol induced alcohol withdrawal tremors blocked by narcotic antagonism [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Neurological correlates of brain reward circuitry linked to opioid use disorder (OUD): Do homo sapiens acquire or have a reward deficiency syndrome?

Gold

Baron

Bowirrat

et al. 2020

Journal of the Neurological Sciences

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The extant literature confirms that an array of polymorphic genes related to- neurotransmitters and second messengers govern the net release of dopamine in the Nucleus Accumbens (NAc) in the mesolimbic region of the brain. They are linked predominantly to motivation, anti-stress, incentive salience (wanting), and wellbeing. Notably, in 2000 the Nobel Prize was awarded to Carlsson, Greengard, and Kandel for their work on the molecular and cellular function of dopaminergic activity at neurons. This historical psychopharmacological work involved neurotransmission of serotonin, endorphins, glutamate, and dopamine, and the seminal work of Blum, Gold, Volkow, Nestler, and others related to neurotransmitter function and related behaviors. Currently, Americans are facing their second and worst opioid epidemic, prescribed opioids, and easy access drive this epidemic of overdoses, and opioid use disorders (OUDs). Presently the clinical consensus is to treat OUD, as if it were an opioid deficiency syndrome, with long-term to life-long opioid substitution therapy. Opioid agonist administration is seen as necessary to replace missing opioids, treat OUD, and prevent overdoses, like insulin is used to treat diabetes. Treatment of OUD and addiction, in general, is similar to the endocrinopathy conceptualization in that it views opioid agonist MATs as an essential core to therapy. Is this approach logical? Other than as harm reduction, is using opioids to treat OUD therapeutic or harmful in the long term? This historical Trieste provides a molecular framework to understand the current underpinnings of endorphinergic/dopaminergic mechanisms related to opioid deficiency syndrome and generalized reward processing depletion. WC 249.

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Isoquinoline Alkaloids as Possible Regulators of Alcohol Addiction

Cited by 12 publications

References 11 publications

Absence of an Effect of Naloxone on Ethanol Intoxication and Withdrawal Reactions

Absence of an Effect of Naloxone on Ethanol Intoxication and Withdrawal Reactions

Neurogenetics of acute and chronic opiate opioid abstinence treating symptoms and the cause

Neurological correlates of brain reward circuitry linked to opioid use disorder (OUD): Do homo sapiens acquire or have a reward deficiency syndrome?

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