2017
DOI: 10.1038/nm.4281
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Blocking microglial pannexin-1 channels alleviates morphine withdrawal in rodents

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Cited by 131 publications
(111 citation statements)
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References 33 publications
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“…In line with preclinical findings that broad-spectrum glial inhibitors are effective at alleviating symptoms of opioid withdrawal, there are ongoing clinical trials testing the effectiveness of minocycline, a tetracycline antibiotic with reported inhibitory effects on glial cell activity, in a human cohort of opioid-dependent patients. Similarly, the clinically available nonselective Panx1 channel blocker probenecid, currently in use as an anti-gout medication, was found to be effective at alleviating opioid withdrawal in rodents [24]. Furthermore, a recent study by Corder et al reported that adverse effects of opioid use may be peripherally mediated [27].…”
Section: Targeting Novel Mechanisms: Translating Old and New Drugsmentioning
confidence: 95%
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“…In line with preclinical findings that broad-spectrum glial inhibitors are effective at alleviating symptoms of opioid withdrawal, there are ongoing clinical trials testing the effectiveness of minocycline, a tetracycline antibiotic with reported inhibitory effects on glial cell activity, in a human cohort of opioid-dependent patients. Similarly, the clinically available nonselective Panx1 channel blocker probenecid, currently in use as an anti-gout medication, was found to be effective at alleviating opioid withdrawal in rodents [24]. Furthermore, a recent study by Corder et al reported that adverse effects of opioid use may be peripherally mediated [27].…”
Section: Targeting Novel Mechanisms: Translating Old and New Drugsmentioning
confidence: 95%
“…These initial findings sparked a series of related research, further revealing the role of glial cells in opioid withdrawal. Blockade or modulation of proteins expressed on microglia within the PAG [22], nucleus accumbens [23] and spinal cord [24] alleviates the physical symptoms of morphine withdrawal. At the cellular level, blockade of glial function with fluoroacetate significantly reduced long-term potentiation within the spinal dorsal horn following high-frequency stimulation [25], demonstrating a cellular correlate to the influence of glial cell activity over neuronal function.…”
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confidence: 99%
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“…The only human gene mutation reported to date encodes a non-functional PANX1 variant that does not inhibit the function of wild type PANX1; it was found in a patient (homozygous for this allele) with disorders in several organs [49]. Investigations of pannexin-null mice have also implicated pannexins in contributing to protection from ischemic stroke injury [4,21], modulation of neuronal excitability and learning [43,44], bone development [27], narcotic withdrawal [14], and sleep-wake cycle regulation and behavior [29]. …”
Section: Pannexinsmentioning
confidence: 99%
“…Although some investigators have referred to MIH in association with morphine tolerance or withdrawal, it is now well accepted that they are sustained by distinct biological processes. For example, in contrast to MIH, tolerance was associated with platelet-derived growth factor receptor-β receptor signaling 7 and a recent report identifies microglial pannexin-1 overexpression as a distinct substrate for withdrawal to morphine 8 .…”
Section: Introductionmentioning
confidence: 99%