Qian Song

TL;DR: It is found that stimulation in the anterior cingulate cortex (ACC) potentiated spinal excitatory synaptic transmission and this modulation is independent of the RVM, and that such top-down facilitation may contribute to the process of chronic neuropathic pain.

TL;DR: It is shown that the mechanical hypersensitivity, ongoing pain, anxiodepressive consequences, and their recoveries do not necessarily exhibit temporal synchrony during chronic pain processing, and that the hyperactivity of the anterior cingulate cortex is essential for driving the emotional impact of neuropathic pain.

TL;DR: It is found that in a mouse model in which peripheral nerve injury leads to the development of neuropathic pain, the insular cortex showed changes in synaptic plasticity, which were associated with a long-term increase in the amount of synaptic N-methyl-d-aspartate receptors, but not that of extrasynaptic NMDARs.

TL;DR: The results suggest that the expression of AMPARs is enhanced in the insular cortex after nerve injury by a pathway involving AC1, AKAP79/150, and PKA, and such enhancement may at least in part contribute to behavioral sensitization together with other cortical regions, such as the anterior cingulate and the prefrontal cortices.

TL;DR: It is demonstrated that FMRP plays an important role in pre-LTP in the adult mouse ACC, and loss of this pre- LTP may explain some of the behavioral deficits in Fmr1 KO mice.