Alcohol amplifies cingulate cortex signaling and facilitates immobilization-induced hyperalgesia in female rats.
Alcohol amplifies cingulate cortex signaling and facilitates immobilization-induced hyperalgesia in female rats.
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酒精放大了雌性大鼠的扣带皮质信号并促进了固定化诱导的痛觉过敏。
DOI:
10.1016/j.neulet.2021.136119
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发表时间:
2021-09-14
影响因子:
2.5
通讯作者:
Edwards S
中科院分区:
文献类型:
--
作者:
Cucinello-Ragland JA;Mitchell-Cleveland R;Bradley Trimble W;Urbina AP;Yeh AY;Edwards KN;Molina PE;Simon Peter L;Edwards S
Complex Regional Pain Syndrome (CRPS) is a musculoskeletal pain condition that often develops after limb injury and/or immobilization. Although the exact mechanisms underlying CRPS are unknown, the syndrome is associated with central and autonomic nervous system dysregulation and peripheral hyperalgesia symptoms. These symptoms also manifest in alcoholic neuropathy, suggesting that the two conditions may be pathophysiologically accretive. Interestingly, people assigned female at birth (AFAB) appear to be more sensitive to both CRPS and alcoholic neuropathy. To better understand the biobehavioral mechanisms underlying these conditions, we investigated a model of combined CRPS and alcoholic neuropathy in female rats. Animals were pair-fed either a Lieber-DeCarli alcohol liquid diet or a control diet for ten weeks. CRPS was modeled via unilateral hind limb cast immobilization for seven days, allowing for the other limb to serve as a within-subject control for hyperalgesia measures. To investigate the role of circulating ovarian hormones on pain-related behaviors, half of the animals underwent ovariectomy (OVX). Using the von Frey procedure to record mechanical paw withdrawal thresholds, we found that cast immobilization and chronic alcohol drinking separately and additively produced mechanical hyperalgesia observed 3 days after cast removal. We then examined neuroadaptations in AMPA GluR1 and NMDA NR1 glutamate channel subunits, extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) in bilateral motor and cingulate cortex across all groups. Consistent with increased pain-related behavior, chronic alcohol drinking increased GluR1, NR1, ERK, and CREB phosphorylation in the cingulate cortex. OVX did not alter any of the observed effects. Our results suggest accretive relationships between CRPS and alcoholic neuropathy symptoms and point to novel therapeutic targets for these conditions.
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影响因子:
1.5
作者:
Bass, Christopher;Yates, Gregory
通讯作者:
Yates, Gregory
DOI:
10.1111/acer.13252
发表时间:
2016-12
期刊:
Alcoholism, clinical and experimental research
影响因子:
--
作者:
Bergeson SE;Blanton H;Martinez JM;Curtis DC;Sherfey C;Seegmiller B;Marquardt PC;Groot JA;Allison CL;Bezboruah C;Guindon J
通讯作者:
Guindon J
影响因子:
14.5
作者:
Critchley, HD;Mathias, CJ;Dolan, RJ
通讯作者:
Dolan, RJ
影响因子:
2.6
作者:
de Mos, M.;Huygen, F. J. P. M.;Sturkenboom, M. C. J. M.
通讯作者:
Sturkenboom, M. C. J. M.
影响因子:
7.4
作者:
Beerthuizen, Annemerle;Stronks, Dirk L.;Huygen, Frank J. P. M.
通讯作者:
Huygen, Frank J. P. M.