The anterior cingulate cortex (ACC) is a well-known brain area that is associated with pain perception. Previous studies reported that the ACC has a specific role in the emotional processing of
pain.
Chronic pain is characterized by long-term potentiation that is induced in
pain pathways and contributes to
hyperalgesia caused by
peripheral nerve injury. The
mammalian target of rapamycin (mTOR) signaling, which is involved in synaptic
protein synthesis, could be a key factor controlling long-term potentiation in
neuropathic pain conditions. Until now, there have been no reports that studied the role of mTOR signaling in the ACC involved in
neuropathic pain. Therefore, this study was conducted to determine the relationship of mTOR signaling in the ACC and
neuropathic pain. Male Sprague-Dawley rats were subjected to
cannula implantation and nerve injury under
pentobarbital anesthesia. Microinjection with
rapamycin into the ACC was conducted under
isoflurane anesthesia on postoperative day (POD) 7. A behavioral test was performed to evaluate
mechanical allodynia, and optical imaging was conducted to observe the neuronal responses of the ACC to peripheral stimulation. Inhibition of mTOR by
rapamycin reduced
mechanical allodynia, down-regulated mTOR signaling in the ACC, and diminished the expressions of synaptic
proteins which are involved in excitatory signaling, thereby reducing
neuropathic pain-induced synaptic plasticity. These results suggest that inhibiting mTOR activity by
rapamycin in the ACC could serve as a new strategy for treating or managing
neuropathic pain before it develops into
chronic pain.