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Thread: Opiates/oids work as anti-psychotics? How?

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    Opiates/oids work as anti-psychotics? How? 
    #1
    Bluelighter Ho-Chi-Minh's Avatar
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    I just want to know how, if they do work as such, given the strong dopamine release...it just seems counter-intuitive
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    #2
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    consult pubmed
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    #3
    Med Sci Monit. 2012 Jul;17):HY23-6.
    Low dose morphine adjuvant therapy for enhanced efficacy of antipsychotic drug action: potential involvement of endogenous morphine in the pathophysiology of schizophrenia.
    Stefano GB, Králíčková M, Ptacek R, Kuzelova H, Esch T, Kream RM.
    Source
    Neuroscience Research Institute, State University of New York-College at Old Westbury, Old Westbury, NY 11568, USA. gstefano@sunynri.org
    Abstract
    Major thematic threads linking extensive preclinical and clinical efforts have established a working mechanistic scheme whereby atypical antipsychotic drugs ameliorate negative DSM IV diagnostic criteria by effecting relatively potent blockade of serotonin (5-HT)(2A) receptors coupled with weaker antagonism of dopamine D(2) receptors in frontal cortical areas. These contentions are more or less supported by in vitro binding experiments employing cloned receptors on cultured cells, although significant functional involvement of 5-HT(2C) receptors has also been proposed. It is interesting that a key statistical analysis indicates a major shift in usage back to typical antipsychotic agents for management of schizophrenia from 1995-2008, whereas off-label usage of atypical antipsychotic agents was markedly increased or expanded for bipolar affective disorder. Importantly, meta-analyses generally did not support efficacy differences between the other atypical antipsychotics compared with the older typical agents. A critical examination of putative functional linkages of morphine and its type-selective mu opioid receptor to higher order cortical regulation of cognitive processes may provide novel insights into human behavioral processes that are severely impaired in schizophrenia spectrum disorders.
    PMID: 22739740 [PubMed - indexed for MEDLINE]

    This one is particularly interesting, but not very effective at proving that it is an effective drug:

    Heroin Add & Rel Clin Probl 1999; 1 (1): 43-44 Letters to the Editor

    Methadone as a Mood Stabilizer
    Pier Paolo Pani, Alessandro Agus, Gian Luigi Gessa

    TO THE EDITOR: The positive effect of opioid agonists in psychotic disorders has
    repeatedly been hypothesized. Methadone has been noted as interfering positively with
    depressive affects and psychotic rage (3); buprenorphine has been considered for its
    antidepressant activity (2).
    We report a case in which methadone seems to have a role in the treatment of a
    bipolar mood disorder.
    Mr. A was admitted to a methadone maintenance treatment program (MMTP) at age
    26, after three years of heroin addiction. Upon intake he exhibited major depression
    (according with DSM-III-R), with anxiety, guilt and suicidal thinking, which subsided
    within 10 days of treatment with methadone (50 mg/day). The MMTP, lasting three
    years, was interrupted because of six months’ incarceration for old crimes. Mr. A was
    readmitted to a MMTP two months after release, relating his heroin-relapse to a new
    depressive episode begun while in prison. Major depression was again ascertained,
    subsiding only with methadone treatment (40 mg/day).
    After four years of heroin-free MMTP (morphinuria-results confirmed), Mr. A
    requested detoxification, as he had the chance to commute impending imprisonment for
    a therapeutic community programme. After a complete medical and psychiatric
    evaluation, detoxification was started and accomplished within 7 days of in-patient
    treatment with clonidine and benzodiazepines. At discharge, the patient started feeling
    extraordinarily well, attractive and successful. This status evolved rapidly into mania
    (according to DSM-IV), with euphoria, insomnia, delusions and hallucinations. Over
    the next two months the patient was repeatedly hospitalized and treated with neuroleptics
    and benzodiazepines. While euphoria, delusions and hallucinations subsided, restlessness,
    nervousness and insomnia increased. There were rapid mood shifts from dysphoria to
    depression, and suicidal thoughts appeared. Mr. A started stating that only methadone
    could give him relief. A mixed status was diagnosed (according to DSM-IV), and
    treatment started with lithium and carbamazepine (serum concentration were 0.70 mEq/
    L and 9.5 µg/mL, respectively), as well as clonazepam and clotiapine ( 6 and 80 mg/day,
    respectively). After one month without improvement, Mr. A came to the service,
    2
    “Bernard B. Brodie” Department of Neuroscience, University of Cagliari, Italy
    1
    SerT, AUSL 8, Cagliari, Italy44
    Heroin Addiction and Related Clinical Problems
    claiming heroin use in the preceding three days in order to be allowed to re-enter the
    MMTP. After toxicological urinalysis confirmation, he was re-accepted into the
    programme and medicated with methadone (30 mg/day). In a few days his mood
    improved, and anxiety, insomnia and dysphoria subsided. This improvement continued
    with the increase of the daily dose to 50 mg. Upon follow-up, two months later, his mood
    was stable and the urine samples were consistently morphine-free. The patient was still
    taking methadone (50 mg/day), clotiapine (40 mg/day), lithium and carbamazepine
    (serum concentrations were 0.65 mEq/L and 9.4 µg/mL, respectively).
    The improvement of depression and psychotic symptoms in patients on methadone
    has been previously reported (3), as has the existence of psychosis during methadone
    detoxification (1); thus methadone appears to share some characteristics of mood
    stabilizers like lithium or carbamazepine.
    Our case seems to confirm the mood-stabilizing effect of methadone. Our patient
    spent a total of seven years in methadone maintenance and only one year out of it, both
    polarities of mood disorder being concentrated within this short period of time and
    resolved rapidly on re-entering the MMTP. Thus methadone may have played some role
    in preventing mood disorder relapses.
    References
    1. Bodkin J.A., Zornberg G.L., Scott E.L., Cole J.O. (1995): Buprenorphine
    treatment of refractory depression. J Clin Psychopharmacol. 15 (1): 49-56.
    2. Levinson I., Rosenthal R. N. (1995): Methadone withdrawal psychosis. J Clin
    Psychiatry 56 (2): 73-76.
    3. McKenna G.J. (1982): Methadone and opiate drugs: Psychotropic effect and selfmedication. In Verebey K. Ed. Opioids in mental illness: theories, clinical
    observations, and treatment possibilities. The New York Academy of Science,
    New York.
    Received and Accepted January, 15, 1999
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    #4
    Damn! Hammilton beat me to it. Morphine has been known to block several 5HT receptors for quite some time.
    However, it also reduces noradrenergic signalling so it does help reduce "agitation" in some cases. But, it is a very poor drug as is. Sigma agonism might play a role too.

    Perhaps the reduction in D2 receptors seen in addicts is somewhat protective?
    http://www.ncbi.nlm.nih.gov/pubmed/22015315

    Here's a study on opioid receptors in the schizophrenic (monkey) brain:
    http://www.ncbi.nlm.nih.gov/pubmed/21810780
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    #5
    The delta-opioid receptor activates astrocytes and GIRK potassium channels. Clozapine's active metabolite N-desmethylclozapine (delta-opioid-receptor agonist) is not very effective as an antipsychotic, however, in contrast to its effectiveness against cognitive and negative symptoms.
    My personal assumption is that GABA-B-receptors as a second GIRK channel opener are the missing link.
    http://www.ncbi.nlm.nih.gov/pubmed/21753741
    I remember a thread here where it was said that the combination of opiates and baclofen is quite unrecreational.
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    #6
    Hmm... The norclozapine thing is interesting. Not really a drug I ever looked at, but I can certainly see the similarity to SNC-80
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    #7
    Quote Originally Posted by Ho-Chi-Minh View Post
    I just want to know how, if they do work as such, given the strong dopamine release...it just seems counter-intuitive
    Opiates increase prolactin. antipsychotics increase prolactin. Prolactin inhibits dopamine, and prolactin increase is a common effect of nearly 100% (maybe not abilify) of antipsychotics and contributes to the antipsychotic effect.

    In one of the studies using methadone IIRC the increase in prolactin was directly correlated with antipsychotic effects.
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    #8
    Bluelighter Ho-Chi-Minh's Avatar
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    what other drugs increase prolactin?
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    #9
    Quote Originally Posted by Ho-Chi-Minh View Post
    what other drugs increase prolactin?
    these things can possibly:

    1. PHYSIOLOGICAL
    Coitus
    Exercise
    Lactation
    Pregnancy
    Sleep
    Stress
    2. PHARMACOLOGICAL
    Anesthetics
    Anticonvulsant
    Antihistamines (H2)
    Antihypertensives
    Cholinergic agonist
    Drug-induced hypersecretion
    Catecholamine depletor
    Dopamine receptor blockers
    Dopamine synthesis inhibitor
    Estogens: oral contraceptives; oral contraceptive withdrawal
    Neuroleptics/antypsychotics
    Neuropeptides
    Opiates and opiate antagonists
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    #10
    In one of the studies using methadone IIRC the increase in prolactin was directly correlated with antipsychotic effects.
    I'm not disagreeing, however, sedation is probably directly correlated, too. Ramelteon poses a risk for causing hyperprolactinemia. So does minoxidil, but I don't see anyone using Rogaine as an antipsychotic (I'm joking here- there are very good unrelated reasons why minoxidil shouldn't be consumed!).

    However, I'm not aware of any evidence pointing toward Ramelteon having antipsychotic effects. I don't see any studies on this aspect of the drug at all, actually.

    I think whatever the reason is, it will prove to be more complicated than we're currently able to realize.
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    #11
    Bluelighter Jean-Paul's Avatar
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    oh hi, i know nothing about anything. my only contribution is say that i believe opiates to put into 'hibernation' a great many number of things anyone could be experiencing at the time.
    temporary hibernation, my friends
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    #12
    Bluelighter Slum Survivor's Avatar
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    my sub doctor had some patients who were on a trial for treatment of mental disease such as depression. maybe they would work as an anti psycotic too. i used to work in a group home, and i noticed that the patients who were on opiates (when they were anyways) were much more down to earth. some even were on a combo of benzo's and opiates together. they were usually the more psycotic patients. if they missed the meds it took a long time to get back to normal...
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    #13
    In rats, mammary tumors are prolactin driven and virtually all pet rats develop mammary tumors by 2 years of age. So, my question, do we see prolactin driven mammary or any other kinds of tumors in people? I believe human mammary tumors are estrogen primed as they are in the dog and cat but are there any prolactin driven tumors in people? Thanks
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    #14
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    fairly sure that if prolactin-driven tumors exist they are not common. never heard of opioid/dopamine (ant)agonist drugs causing breast cancer with any regularity!
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    #15
    Hyperprolactinemia does seem to slightly increase the risk of cancer:

    Seventy-three malignant tumors were identified in the hyperprolactinemia patients and 660 tumors in the comparison group (HR 1.31; 95% confidence interval (CI): 1.02-1.6, mainly attributed to an increased risk of upper gastrointestinal cancer in both males and females (HR 3.69; 95% CI: 1.70-8.03) and hematopoietic cancer in females (HR 3.51; 95% CI: 1.06-11.6). Twelve breast cancers occurred in the female patients, corresponding to an HR of 1.09 (95% CI: 0.60-1.99). Prostate cancer risk in hyperprolactinemia men was reduced (HR 0.40; 95% CI: 0.16-0.99).
    Quote Originally Posted by bben View Post
    Opiates increase prolactin. antipsychotics increase prolactin. Prolactin inhibits dopamine, and prolactin increase is a common effect of nearly 100% (maybe not abilify) of antipsychotics and contributes to the antipsychotic effect.
    Pretty sure it's the other way around, dopamine at D2 is the primary inhibitor of prolactin.
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