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Stanley M. Crain

Researcher at Albert Einstein College of Medicine

Publications -  131
Citations -  7155

Stanley M. Crain is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Opioid & Opioid receptor. The author has an hindex of 48, co-authored 131 publications receiving 7078 citations. Previous affiliations of Stanley M. Crain include Yeshiva University.

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A general role for adaptations in G-proteins and the cyclic AMP system in mediating the chronic actions of morphine and cocaine on neuronal function.

TL;DR: The findings that chronic morphine and cocaine produce similar adaptations in the NAc, a brain region important for the reinforcing actions of many types of abused substances, suggest further that common mechanisms may underlie psychological aspects of drug addiction mediated by this brain region.
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Opioids can evoke direct receptor-mediated excitatory effects on sensory neurons.

TL;DR: The evidence for mediation of direct excitatory effects by naloxone-reversible opioid receptors is reviewed and it is proposed that this dual modulatory mechanism may help to account for previously unexplained enhancement by opioids of transmitter release, paradoxical hyperalgesic and aversive effects of opioids, and some aspects of opioid tolerance and addiction.
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Antagonists of excitatory opioid receptor functions enhance morphine's analgesic potency and attenuate opioid tolerance/dependence liability.

TL;DR: Clinical treatment of pain can be significantly improved by administering morphine or other conventional opioid analgesics together with appropriately low doses of an excitatory opioid receptor antagonist, according to preclinical studies in vitro and in vivo.
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Ultra-low concentrations of naloxone selectively antagonize excitatory effects of morphine on sensory neurons, thereby increasing its antinociceptive potency and attenuating tolerance/dependence during chronic cotreatment.

TL;DR: Cotreatment of mice with morphine plus ultra-low-dose NTX does, in fact, enhance the antinociceptive potency of morphine in tail-flick assays and attenuate development of withdrawal symptoms in chronic, as well as acute, physical dependence assays.
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Dual opioid modulation of the action potential duration of mouse dorsal root ganglion neurons in culture

TL;DR: The data indicate that opioid-induced APD prolongation is not mediated by pertussis toxin-sensitive G proteins and suggest that elevation of cyclic AMP levels may enhance opioid excitatory responsiveness.