Blocking N-Methyl-D-aspartic Acid (NMDA) Receptor Inhibits Heat-Sensitization Response of Moxibustion in Stroke Rats

Our previous studies demonstrated that effects of moxibustion heavily relied on heat-sensitization response, a specific sensation induced by moxibustion in the ill body. On the sensation, long-term potentiation (LTP) of prelimbic cortex was attributed to heat-sensitization responses. The N-methyl-D-aspartic acid (NMDA) receptor plays a key role in LTP induction; however, little is known about the role of NMDA receptor in heat-sensitization response. The present study investigated the role of NMDA receptor in heat-sensitization response, specifically, NMDA receptor was inhibited by competitive glutamatergic antagonist, (±)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP), observing the frequency of heat-sensitization response in moxibustion treatment and evaluating the conducive outcomes to cerebral infarct rats for rehabilitation. Heat-sensitization response in cerebral infarct rats was regularly measured for all the samples when exposed to moxibustion. Intraperitoneal injection of CPP was conducted, and soon afterwards, a significant drop of heat-sensitization response in all the samples was measured. Moreover, moxibustion efficiency on rehabilitation was unfavourably affected in cerebral infarct rats when compared to vehicle injection control. This indicated that NMDA receptor antagonist made a negative impact on induction of heat-sensitization response and consequently affected cerebral infarct rats to rehabilitate under moxibustion treatment. It also suggested that activating NMDA receptor played a positive part in ischemic stroke rehabilitation, and regulating its activity could be a feasible way to increase heat-sensitization response, improving the effect of moxibustion.

Understanding Acupoint Sensitization: A Narrative Review on Phenomena, Potential Mechanism, and Clinical Application

As part of traditional Chinese medicine, acupoints are considered a dynamic functional area, which can reflect the internal condition of the body. When the body is suffering from disease or injury, corresponding acupoints are believed to be activated and manifest in several sensitized forms, including expansion of the receptive field, pain sensitization, and heat sensitization. Such phenomena are believed to gradually disappear concomitantly with recovery from the disease. Acupoint states are therefore changeable according to health status, a phenomenon known as acupoint sensitization. This review aims to provide an overview of acupoint sensitization based on existing research results and determine priorities for future research. Systematic literature retrieval was conducted in Medline, Embase, Cochrane Library, CINAHL, and AMED from inception to 18 July 2018. Current evidence from research findings to date indicate that acupoint sensitization is based on neurogenic inflammation and that stimulation of sensitized acupoints presents a potential trend of generating a better clinical effect when compared with stimulation of unsensitized points.

Long-Term Potentiation of Prelimbic Cortex Ascribed to Heat-Sensitization Responses of Moxibustion

Heat-sensitization responses occurred in certain patients while exposed to suspended moxibustion. The response often indicated that the efficacy of moxibustion to those with it tended to triumph over those without. However, its mechanism remains to be explained. Our previous fMRI and EEG studies confirmed the changes of activities in cerebral certain regions accompanied with heat-sensitization responses, especially in prefrontal cortex. Therefore, we hypothesize that neurological system is involved in moxibustion-induced heat-sensitization responses. In the present study, phosphorylation of Cofilin representing long-term potentiation in synapse of prelimbic cortex of medial prefrontal cortex in stroke rats over suspended moxibustion was assessed, and the size of phosphorylated Cofilin positive spine in synapse was also measured. The result showed that heat-sensitization responses were observed to augment cerebral ischemic stroke-induced phosphorylation of Cofilin in prelimbic cortex of rats and increase the numbers of large synapses. This indicated that long-term potentiation of prelimbic cortex was attributed to heat-sensitization responses that were certain neurological responses of medial prefrontal cortex to suspended moxibustion.