Articles: hyperalgesia.
-
Intraoperative remifentanil anesthesia exaggerates postoperative pain sensitivity. Recent studies recapitulate the significance of protein kinase Mζ in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated pathologic pain. Kalirin-7, a Rho guanine nucleotide exchange factor, coordinates AMPA receptor trafficking and dendritic spine plasticity. This study examines whether protein kinase Mζ and Kalirin-7 contribute to remifentanil-induced postincisional hyperalgesia via AMPA receptor. ⋯ Spinal protein kinase Mζ regulation of GluA1-containing AMPA receptor trafficking and spine morphology via Kalirin-7 overexpression is a fundamental pathogenesis of remifentanil-induced hyperalgesia in rats.
-
The study aimed to investigate the physiology, psychophysics, pathology and their relationship in reversible nociceptive nerve degeneration, and the physiology of acute hyperalgesia. ⋯ These observations suggested the relationship between nociceptive nerve terminals and brain responses to thermal stimuli changed during different degree of skin denervation, and CHEP to low-intensity heat stimulus can reflect the physiology of hyperalgesia.
-
Journal of neurotrauma · Jul 2018
Traumatic Brain Injury Disrupts Pain Signaling in the Brainstem and Spinal Cord.
Chronic pain is a common consequence of traumatic brain injury (TBI) that can increase the suffering of a patient and pose a significant challenge to rehabilitative efforts. Unfortunately, the mechanisms linking TBI to pain are poorly understood, and specific treatments for TBI-related pain are still lacking. Our laboratory has shown that TBI causes pain sensitization in areas distant to the site of primary injury, and that changes in spinal gene expression may underlie this sensitization. ⋯ Here we expand our knowledge of pain after TBI in two ways: (1) by outlining the neuropathology in pain-related centers of the brain and spinal cord involved in DNIC using the rat lateral fluid percussion (LFP) model of TBI, and (2) by evaluating the effects of a potent histone acetyl transferase inhibitor, anacardic acid (AA), on LFP-induced pain behaviors and neuropathology when administered for several days after TBI. The results revealed that TBI induces transient mechanical allodynia and a chronic persistent loss of DNIC. Further, while short-term AA treatment can block acute nociceptive sensitization and some early neuropathological changes, this treatment neither prevented the loss of DNIC nor did it alter long-term neuropathological changes in the brain or spinal cord.
-
Physiology & behavior · Jul 2018
Anxiety- but not depressive-like behaviors are related to facial hyperalgesia in a model of trigeminal neuropathic pain in rats.
Trigeminal neuralgia (TN) is a painful condition characterized by excruciating facial pain, which has a serious impact on quality of life. Depression and anxiety have been commonly associated with TN, but clinical studies report that these comorbidities are frequently underdiagnosed and undertreated in TN patients. Herein it was investigated if rats submitted to the infraorbital nerve constriction (CION), a model of trigeminal neuropathic pain, would display anxiety- and depressive-like behaviors in addition to the facial sensory changes in different time points after the nerve injury. ⋯ The depressive-like behavior was assessed by measuring the time of immobility on the forced swim test (FST) and sucrose preference (SP) in rats previously tested for heat (day 5) and mechanical allodynia (days 15, 30 and 45) induced by CION. The evaluation of immobility time on FST and sucrose preference consumption revealed that both CION rats did not displayed depressive- and anhedonic-like behavior at any time point evaluated. Altogether, these results demonstrate that trigeminal neuropathic pain in rats leads to the development of anxiety-, but not depressive-like behavior, suggesting that the CION model represents a methodology that allows the study of drugs targeting both pain and anxiety.
-
Psychosocial factors such as anxiety, depression and catastrophizing, commonly associated with established chronic pain, also may be associated with an increased risk of chronic postsurgical pain (CPSP) when present preoperatively. We used a repeat social defeat (RSD) paradigm to induce psychosocial stress in rodents prior to incisional surgery of the paw. Mixed effects growth curve models were utilized to examine resolution of mechanical hypersensitivity in rats for four weeks following surgery. ⋯ Prior exposure to RSD significantly increased microglial activation and neuronal sensitization (pERK-IR) within the ipsilateral spinal cord. In conclusion, we found that chronic social stress alters the neurobiological response to surgical injury, resulting in slowed recovery. This model maybe useful for future interventional studies examining the mechanistic interactions between depression and risk of CPSP.