Analgesic effects of 3-carboxysalsolinol alone and in combination with morphine

Marshall, Alice; Hirst, Maurice; Blum, Kenneth

doi:10.1007/bf01944172

Cited by 33 publications

(2 citation statements)

References 10 publications

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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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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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“…By comparison, the attenuation of alcohol drinking was associated with opioid receptor antagonists (Marshall, Hirst, & Blum, 1977), binding of a tetrahydroisoquinolin (THIQ) to opiate receptors in the brain (Blum, Eubanks, Wallace, Schwertner, & Morgan, 1976; Myers, 1989), and marked differences in enkephalin values in animals genetically predisposed to the ingestion of alcohol (Blum, Elston, DeLallo, Briggs, & Wallace, 1983). Finally, Myers (Myers, 1989) proposed that the dopaminergic reward pathways that traverse the meso-limbicforebrain systems of the brain constitute an “integrative anatomical substrate for the adduct-opioid cascade of neuronal events which promote and sustain the aberrant drinking of alcohol.”…”

Section: Introductionmentioning

confidence: 99%

Hypothesizing Darkness Induced Alcohol Intake Linked to Dopaminergic Regulation of Brain Function

Blum¹,

Oscar‐Berman²,

Badgaiyan³

et al. 2014

PSYCH

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Understanding the role of neurotransmission in the prefrontal cortex and mesolimbic brain regions has become the subject of intensive neuroscience research worldwide. In the 1970s, our group provided evidence that rats exposed to darkness significantly augmented their alcohol intake. At that time, we proposed that melatonin was the culprit. At around the same time, our laboratory, amongst a few others, proposed that dopamine-adducts with acetaldehyde to induce alcohol intake both in rodents and in humans. While the work in these areas has declined considerably over the years, more recent scientifically sound studies continue to show the importance of these earlier controversial ideas involving alcohol abuse and alcoholism. A review of the literature has provided impetus to systematically access the newer genetic and molecular neurobiological findings relevant to the physiological and psychological motives for high alcohol consumption in animals and humans alike. Thus, we hypothesize that darkness-induced alcohol intake is linked not only to serotonergic-melatonin mechanisms, but also to dopaminergic regulation of brain mesolimbic pathways involving neuronal expression switching in response to long photoperiods affecting gene expression.

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Gibt es biochemische Verknüpfungen zwischen den Wirkungen von Alkohol und Opiaten? Tetrahydroisochinoline und alternative Möglichkeiten

Urwyler¹

1985

Suchtproblematik

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Analgesic effects of 3-carboxysalsolinol alone and in combination with morphine

Cited by 33 publications

References 10 publications

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

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

Hypothesizing Darkness Induced Alcohol Intake Linked to Dopaminergic Regulation of Brain Function

Gibt es biochemische Verknüpfungen zwischen den Wirkungen von Alkohol und Opiaten? Tetrahydroisochinoline und alternative Möglichkeiten

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