2017
DOI: 10.1177/1744806917704769
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Activation of spinal alpha-7 nicotinic acetylcholine receptor shortens the duration of remifentanil-induced postoperative hyperalgesia by upregulating KCC2 in the spinal dorsal horn in rats

Abstract: Background Accumulating evidence has shown that the signal from spinal brain-derived neurotrophic factor/tyrosine receptor kinase B-K-Cl cotransporter-2 plays a critical role in the process of pain hypersensitivity. The activation of alpha-7 nicotinic acetylcholine receptors could have an analgesic effect on remifentanil-induced postoperative hyperalgesia. Nevertheless, whether intrathecal administration of PNU-120596, an alpha-7 nicotinic acetylcholine receptors selective type II positive allosteric modulator… Show more

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Cited by 14 publications
(4 citation statements)
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“…Previously innocuous stimulation then evokes discharge patterns characteristic for nociceptive stimulation (Pitcher and Henry 2004 ; Sharif et al 2005 ). A synopsis of this data suggests that KCC2 may represent an important novel target for the development of analgesics (Gu et al 2017a , b ).…”
Section: Dorsal Horn and Nociceptionmentioning
confidence: 99%
“…Previously innocuous stimulation then evokes discharge patterns characteristic for nociceptive stimulation (Pitcher and Henry 2004 ; Sharif et al 2005 ). A synopsis of this data suggests that KCC2 may represent an important novel target for the development of analgesics (Gu et al 2017a , b ).…”
Section: Dorsal Horn and Nociceptionmentioning
confidence: 99%
“…Most of the trials (16 trials) conducted measurements for 2 days. Cui et al [ 33 ] conducted the shortest trial, which lasted 5 h, while Gu et al [ 37 ] conducted the longest trial, lasting 21 days. The most common remifentanil administration regimens were 0.04 mg/kg subcutaneous infusion for 30 min (9 trials) or 1.0 μg/kg/min intravenous infusion for 60 min (6 trials).…”
Section: Resultsmentioning
confidence: 99%
“…Antinociceptive actions mediated through GABA receptors on neurons were posed to be impaired and therefore to contribute further to LTP in hyperalgic signaling, enhancing perpetuation of OIH [ 93 , 94 ]. The impairment of GABA receptors in these conditions, while experimentally achieved through induction of inhibitory neuronal KCC2 channels [ 2 , 95 ], was not shown to be clinically applicable in acute OIH using acetazolamide, a pharmacological inhibitor of carbonic anhydrase in clinical use [ 67 , 96 ]. In an RCT involving patients under surgical analgesia using remifentanil, concomitantly revealing hyperalgic manifestations compatible with OIH, acetazolamide was unsuccessful in reverting these disturbances through the additional use of this substance [ 67 ], unlike other substances applied in similar conditions as mentioned in Table 2 .…”
Section: Resultsmentioning
confidence: 99%