Postsynaptic potentiation of corticospinal projecting neurons

RV was used for retrograde monosynaptic labeling.

The viruses used in this article are in the table below

RV	SAD-DG-mcherry

Tao Chen, Kohei Koga, Giannina Descalzi, Shuang Qiu, Jian Wang, Le-Shi Zhang, Zhi-Jian Zhang, Xiao-Bin He, Xin Qin, Fu-Qiang Xu, JiHu, Feng Wei, Richard L Huganir, Yun-Qing Li and Min Zhuo
Pub Date: 2014-06-03, DOI: 10.1186/1744-8069-10-33, Email: [email protected]

Long-term potentiation (LTP) is the key cellular mechanism for physiological learning and pathological chronic pain. In the anterior cingulate cortex (ACC), postsynaptic recruitment or modification of AMPA receptor (AMPAR) GluA1 contribute to the expression of LTP. Here we report that pyramidal cells in the deep layers of the ACC send direct descending projecting terminals to the dorsal horn of the spinal cord (lamina I-III). After peripheral nerve injury, these projection cells are activated, and postsynaptic excitatory responses of these descending projecting neurons were significantly enhanced. Newly recruited AMPARs contribute to the potentiated synaptic transmission of cingulate neurons. PKA-dependent phosphorylation of GluA1 is important, since enhanced synaptic transmission was abolished in GluA1 phosphorylation site serine-845 mutant mice. Our findings provide strong evidence that peripheral nerve injury induce long-term enhancement of cortical-spinal projecting cells in the ACC. Direct top-down projection system provides rapid and profound modulation of spinal sensory transmission, including painful information. Inhibiting cortical top-down descending facilitation may serve as a novel target for treating neuropathic pain.

Figure 1. A model for the role of cingulate-spinal projection pathways in pain regulation and their synaptic plasticity after nerve injury.

In the present study, the authors employ integrative experimental approaches to show that long-term plastic changes taking place in these spinal cord projecting neurons in the deep layers of the ACC after nerve injury. The potentiated corticospinal projection will play direct and potent effects in pain regulation.

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