Ming-Gang Liu

TL;DR: It is demonstrated that tail amputation causes LTD impairment within the ACC circuit and that this can be rescued by activation of mGluR1, a form of metaplasticity that involved the activation of protein kinase C.

TL;DR: In this article, a 64-channel recording system was designed to characterize the basic synaptic mechanisms for insular long-term potentiation (LTP), and an enduring form of late-phase LTP (L-LTP) could be reliably recorded for at least 3 h in different layers of IC slices after theta burst stimulation.

TL;DR: This study is the first report of the network properties of L-LTP in the anterior cingulate cortex in the ACC, and provides basic mechanisms for future treatment of cortex-related cognitive defects in fragile X patients.

TL;DR: It is shown for the first time that repetitive low‐frequency stimulation (LFS) can elicit frequency‐dependent LTD of glutamate receptor‐mediated excitatory synaptic transmission in both superficial and deep layers of the IC of adult mice, and the basic mechanisms of LTD in the IC are characterised at the network level.

TL;DR: It is found that tail amputation in adult mice produced a selective loss of low frequency stimulation-induced LTD in the IC, without affecting (RS)-3,5-dihydroxyphenylglycine (DHPG)-evoked LTD, and it is suggested that restoration of insular LTD may represent a novel therapeutic strategy against the synaptic dysfunctions underlying the pathophysiology of phantom pain.