Central amygdala activation of extracellular signal-regulated kinase 1 and age-dependent changes in inflammatory pain sensitivity in mice.
Central amygdala activation of extracellular signal-regulated kinase 1 and age-dependent changes in inflammatory pain sensitivity in mice.
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DOI:
10.1016/j.neurobiolaging.2017.04.010
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发表时间:
2017-08
影响因子:
4.2
通讯作者:
Kolber BJ
中科院分区:
文献类型:
--
作者:
Sadler KE;Gartland NM;Cavanaugh JE;Kolber BJ
Aging populations are more sensitive to noxious stimuli as a result of altered somatosensory systems. In these experiments, we examined pain-like behaviors in young, middle-aged, and old mice during peripheral inflammation to determine if the same sensitivity exists in pre-clinical animal models. Immediately following injury, middle-aged and old mice exhibited more spontaneous pain-like behaviors than young mice, matching pain prevalence in clinical populations. Middle-aged and old mice also developed persistent mechanical hypersensitivity in the injured paw. Furthermore, old mice developed mechanical hypersensitivity in the non-injured paw suggesting age-dependent changes in central nociceptive systems. To address this end, pain-related protein expression was examined in the central nucleus of the amygdala (CeA), a limbic brain region that modulates somatic pain. Following injury, increased phosphorylation of extracellular-signal regulated kinase 1 (ERK1), a protein with known nociceptive functions, was observed in the right CeA of old mice and not middle-aged or young animals. These findings suggest that age-dependent changes in supraspinal nociceptive systems may account for increased pain-like behaviors in aging populations.