Mol Pain
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While the PKCγ neurons in spinal dorsal horn play an indispensable part in neuropathic allodynia, the exact effect of PKCγ neurons of brain regions in neuropathic pain remains elusive. Mounting research studies have depicted that the anterior cingulate cortex (ACC) is closely linked with pain perception and behavior, the present study was designed to investigate the contribution of PKCγ neurons in ACC to neuropathic allodynia and pain-related emotion in newly developed Prkcg-P2A-Tdtomato mice. ⋯ We conclude that the PKCγ neurons in ACC are closely linked with neuropathic allodynia and pain-related emotional behaviors.
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Chronic neuropathic pain is a debilitating ordeal for patients worldwide and pharmacological treatment efficacy is still limited. As many pharmacological interventions for neuropathic pain often fail, insights into the underlying mechanism and role of identified receptors is of utmost importance. An important target for improving treatment of neuropathic pain is the descending serotonergic system as these projections modulate nociceptive signaling in the dorsal horn. ⋯ Analgesia due to neuromodulatory intervention like SCS restores the inhibitory function of the descending serotonergic system and involves 5-HT2, 5-HT3 and 5-HT4 receptors. The results of this systematic review provide insights and suggestions for further pharmacological and or neuromodulatory treatment of neuropathic pain based on targeting selected serotonergic receptors related to descending modulation of nociceptive signaling in spinal dorsal horn. With the novel developed SCS paradigms, the descending serotonergic system will be an important target for mechanism-based stimulation induced analgesia.
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Central post-stroke pain (CPSP) is a type of neuropathic pain caused by dysfunction in the spinothalamocortical pathway. However, no animal studies have examined comorbid anxiety and depression symptoms. Whether the typical pharmacological treatments for CPSP, which include antidepressants, selective serotonin reuptake inhibitors (SSRIs), and anticonvulsants, can treat comorbid anxiety and depression symptoms in addition to pain remains unclear? The present study ablated the ventrobasal complex of the thalamus (VBC) to cause various CPSP symptoms. The effects of the tricyclic antidepressants amitriptyline and imipramine, the SSRI fluoxetine, and the anticonvulsant carbamazepine on pain, anxiety, and depression were examined. ⋯ In summary, antidepressants and SSRIs but not anticonvulsants can effectively ameliorate pain and comorbid anxiety and depression in CPSP. The present findings, including discrepancies in the effects observed following treatment with anticonvulsants, antidepressants, and SSRIs in this CPSP animal model, can be applied in the clinical setting to guide the pharmacological treatment of CPSP symptoms.