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Opiate

About: Opiate is a research topic. Over the lifetime, 4323 publications have been published within this topic receiving 177638 citations.


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Journal ArticleDOI
09 Mar 1973-Science
TL;DR: Tritiated naloxone, a powerful opiate antagonist, specifically binds to an opiate receptor of mammalian brain and guinea pig intestine that closely parallels their pharmacological potency.
Abstract: Tritiated naloxone, a powerful opiate antagonist, specifically binds to an opiate receptor of mammalian brain and guinea pig intestine. Competition for the opiate receptor by various opiates and their antagonists closely parallels their pharmacological potency. The opiate receptor is confined to nervous tissue.

2,319 citations

Journal ArticleDOI
TL;DR: The history of opiate withdrawal scales is reviewed and a template version of the COWS that can be copied and used clinically is appended.
Abstract: The clinical opiate withdrawal scale (COWS) is a clinician-administered, pen and paper instrument that rates eleven common opiate withdrawal signs or symptoms. The summed score of the eleven items can be used to assess a patient's level of opiate withdrawal and to make inferences about their level of physical dependence on opioids. With increasing use of opioids for treatment of pain and the availability of sublingual buprenorphine in the United States for treatment of opioid dependence, clinical assessment of opiate withdrawal intensity has received renewed interest. Buprenorphine, a partial opiate agonist at the mu receptor, can precipitate opiate withdrawal in patients with a high level of opioid dependence who are not experiencing opioid withdrawal. Since development of the first opiate withdrawal scale in the mid-1930s, many different opioid withdrawal scales have been used in clinical and research settings. This article reviews the history of opiate withdrawal scales and the context of their initial use. A template version of the COWS that can be copied and used clinically is appended. PDF formatted versions of the COWS are also available from the websites of the American Society of Addiction Medicine, the California Society of Addiction Medicine, the UCLA Integrated Substance Abuse Programs, and AlcoholMD.com.

798 citations

Journal ArticleDOI
09 Nov 1978-Nature
TL;DR: Single-cell recording and microiontophoretic techniques were used to establish the development of tolerance of LC cells to the depressant effects of morphine, naloxone-induced withdrawal activations of LC neuronal firing in morphine-dependent animals, and the ability of clonidine to suppress the withdrawal of LC neurones through a non-opiate receptor.
Abstract: NORADRENERGIC neurones of the locus coeruleus (LC; A6 of ref. 1) are inhibited by the systemic or local administration of adrenergic agonists2–5, opiates6,7 and enkephalins8,9. The adrenergic receptors of the LC, which are of the presynaptic or α2 type5, seem to mediate inhibitory responses to recurrent LC collaterals10 and adrenaline inputs from the lower brain stem4,11. In addition to adrenergic receptors, there are opiate receptors located in the LC12,13 which presumably mediate the actions of endogenous opiate-like substances (enkephalins and β-endorphin) located in nerve terminals within the LC14–16. Recently, clonidine, which is the most powerful of the α2 agonists known to inhibit the firing of LC neurones3,5, has been reported to suppress the symptoms of opiate withdrawal in humans17. On this basis, the latter authors suggested that the opiate-withdrawal syndrome may be due in part to increased noradrenergic neuronal activity in areas such as the LC which are regulated by both α2 adrenoceptors and opiate receptors. In this connection, it is interesting that the drug piperoxane, which blocks α2 adrenoceptors and accelerates the firing of LC neurones4,5 produces many of the symptoms (such as anxiety and hypertension) seen in opiate withdrawal18. In the present study, single-cell recording and microiontophoretic techniques were used to establish the development of tolerance of LC cells to the depressant effects of morphine, naloxone-induced withdrawal activations of LC neuronal firing in morphine-dependent animals, and the ability of clonidine to suppress the withdrawal of LC neurones through a non-opiate receptor.

795 citations

Journal ArticleDOI
05 Nov 1976-Science
TL;DR: The endogenous morphinomimetic brain peptides Met5-enkephalin and alpha-, beta-, and gamma-endorphins have been evaluated in rats after intracerebrospinal fluid injection and their potent and divergent responses to naturally occurring subtances suggest that alterations in their homeostatic regulation could have etiological significance in mental illness.
Abstract: The endogenous morphinomimetic brain peptides Met5-enkephalin and alpha-, beta-, and gamma-endorphins have been evaluated in rats after intracerebrospinal fluid injection. beta-Endorphin produces marked, prolonged muscular rigidity and immobility similar to a catatonic state, counteracted by the opiate antagonist naloxone; this effect occurs at molar doses 1/100 to 1/400 that at which the other peptides or morphine block the response to painful stimuli. All peptides evoked dose-related, naloxone-reversible, wet-dog shakes in rats that had not been exposed to drugs. beta-Endorphin produced hypothermia, whereas gamma-endorphin produced hyperthermia. Such potent and divergent responses to naturally occurring subtances suggest that alterations in their homeostatic regulation could have etiological significance in mental illness.

792 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202336
202289
202133
202058
201931
201834