Role of Sigma Receptor and Neurosteroids in Pain Sensation

2011 ◽  
Vol 31 (2) ◽  
pp. 123
Author(s):  
Jang-Hern Lee
2015 ◽  
Vol 53 (2) ◽  
pp. 1329-1342 ◽  
Author(s):  
Lu Yang ◽  
Honghong Yao ◽  
Xufeng Chen ◽  
Yu Cai ◽  
Shannon Callen ◽  
...  

Mediscope ◽  
2020 ◽  
Vol 7 (1) ◽  
pp. 51-57
Author(s):  
Sayema Ainan

Management of chronic pain is one of the most important reason to which medications are given. Traditional medicines which have been used to relieve pain are having a number of limitations. Therefore, novel therapies for pain treatment are essential. Our nervous system can process any kind of injurious stimuli, which is known as nociception. The mechanism of nociception involves a complex interaction of peripheral and central nervous system structures. Brain or cerebral cortex has its own controlling mechanism for pain perception. Trigeminal nerve is the fifth cranial nerve and it receives pain sensation from oro- and craniofacial region and sends the information up to cortex. Recent investigations demonstrate another important role of cortical neurons in addition to pain perception, that is, corticotrigeminal (cortex to trigeminal) pathway excites neurons in the trigeminal nerve that leads to decrease in the pain response induced by noxious stimuli. Thus, as this mechanism can be induced at early stage of nociception, it may reduce the pain sensation. So, the corticotrigeminal pathway could be a new potential target for pain therapies. This short review revisits the concepts how stimulation of primary somatosensory cortex can be transmitted via corticotrigeminal tract which aim for the inhibitory neurons in spinal trigeminal nucleus caudalis (SpVc) and thus potentially generate a feedforward inhibition, explaining the pain modulatory role of the corticotrigeminal pathway. Mediscope Vol. 7, No. 1: Jan 2020, Page 51-57


2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Guo-Qiang Wang ◽  
Cheng Cen ◽  
Chong Li ◽  
Shuai Cao ◽  
Ning Wang ◽  
...  

Abstract The medial prefrontal cortex (mPFC) is implicated in processing sensory-discriminative and affective pain. Nonetheless, the underlying mechanisms are poorly understood. Here we demonstrate a role for excitatory neurons in the prelimbic cortex (PL), a sub-region of mPFC, in the regulation of pain sensation and anxiety-like behaviours. Using a chronic inflammatory pain model, we show that lesion of the PL contralateral but not ipsilateral to the inflamed paw attenuates hyperalgesia and anxiety-like behaviours in rats. Optogenetic activation of contralateral PL excitatory neurons exerts analgesic and anxiolytic effects in mice subjected to chronic pain, whereas inhibition is anxiogenic in naive mice. The intrinsic excitability of contralateral PL excitatory neurons is decreased in chronic pain rats; knocking down cyclin-dependent kinase 5 reverses this deactivation and alleviates behavioural impairments. Together, our findings provide novel insights into the role of PL excitatory neurons in the regulation of sensory and affective pain.


Author(s):  
Istvan Nagy

The landmark paper discussed in this chapter, published by Davis et al. in 2000, describes the role of the capsaicin receptor, which is called transient receptor potential cation channel subfamily vanilloid member 1 (TRPV1), in inflammatory thermal hyperalgesia. Capsaicin, the pungent agent found in hot peppers, has been linked to pain for centuries because it induces a burning pain sensation which, after prolonged application of the agent, turns into analgesia. Because of this, capsaicin has been used to relieve pain, most likely since prehistoric times. The elucidation of the role of TRPV1 in nociceptive processing was heralded as the starting point for the development of agents which would revolutionize pain management. Unfortunately, that promise is yet to be realized and apparently we need a more detailed understanding of the role of TRPV1 in physiological and pathological processes in order to fulfil the analgesic potential of drugs acting on this receptor.


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