Anti-Endorphin Effects of Methadone

Ms, Gold; Pottash, A.L.C.; Extein, Irl; Kleber, HerbertD.

doi:10.1016/s0140-6736(80)92125-x

Cited by 15 publications

(4 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… [ 60 ] Bromocriptine treatment for cocaine abuse: the dopamine (DA) depletion hypothesis Bromocriptine, a DA/antagonist, appears to have efficacy with acute and maintenance trials and may represent a test of the cocaine-dopamine hypothesis and new adjunctive treatment for cocaine abuse. [ 61 ] Anti-endorphin effects of methadone. Depression is common and may be induced by methadone.…”

Section: Theorems Relevant To Opioid Peptides and Reward Processing Dmentioning

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

View full text Add to dashboard Cite

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.

show abstract

Section: Theorems Relevant To Opioid Peptides and Reward Processing Dmentioning

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

View full text Add to dashboard Cite

show abstract

“…Often the popular media have seized on fragments of evidence supporting this attractive hypothesis as if they were a full demonstration. The fact that endogenous opiate levels are somewhat lower in human beings and animals that have been given exogenous opiates (Gold, Pottash, Extein, and Kleber, 1980;Herz, 1981) is far from proof of the hypothesis. Are these lower endogenous opiate levels long-lived?…”

Section: Induced Metabolic Change As the Cause Of Addictionmentioning

confidence: 99%

When experimental psychology is not empirical enough: The case of the "exposure orientation."

Alexander¹

1984

Canadian Psychology / Psychologie canadienne

View full text Add to dashboard Cite

Most psychologists accept the familiar view that exposure to opiate drugs engenders a powerful tendency toward subsequent addictive use. However, a review of historical, clinical, and experimental evidence shows that this view of addiction, which can be labelled the "exposure orientation," is not true. Therefore, psychology would appear to be helping to support a popular misconception. Experimental psychology, in particular, is not being fully empirical when it dwells on the meagre experimental basis for the exposure orientation and ignores the larger body of observable fact that discredits it. A fuller empiricism could re-assert psychology's authority to lead, rather than follow, popular culture.

show abstract

“…The National Institute of Drug Abuse Director Nora Volkow and other leading neuroscientists have consistently stated and presented supporting evidence that addiction in general, and OUD specifically, is a brain disorder [7][8][9][10][11]. Extended opioid use causes multiple important and seemingly irreversible changes to the brain, especially its dopamine [11] and opioid systems [12,13]. Opioid agonists like heroin, methadone, or fentanyl stimulate and overwhelm the dopamine and opioid systems.…”

Section: Introductionmentioning

confidence: 99%

Treatment resistant opioid use disorder (TROUD): Definition, rationale, and recommendations

Wolf

Gold

2020

Journal of the Neurological Sciences

View full text Add to dashboard Cite

Anti-Endorphin Effects of Methadone

Cited by 15 publications

References 18 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?

When experimental psychology is not empirical enough: The case of the "exposure orientation."

Treatment resistant opioid use disorder (TROUD): Definition, rationale, and recommendations

Contact Info

Product

Resources

About