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Fragile X Mental Retardation Protein in Learning-Related Synaptic Plasticity
Valentina Mercaldo,Giannina Descalzi,민쭈오 한국분자세포생물학회 2009 Molecules and cells Vol.28 No.6
Fragile X syndrome (FXS) is caused by a lack of the fragile X mental retardation protein (FMRP) due to silencing of the Fmr1 gene. As an RNA binding protein, FMRP is thought to contribute to synaptic plasticity by regulating plasticity-related protein synthesis and other signaling pathways. Previous studies have mostly focused on the roles of FMRP within the hippocampus - a key structure for spatial memory. However, recent studies indicate that FMRP may have a more general contribution to brain functions, in-cluding synaptic plasticity and modulation within the pre-frontal cortex. In this brief review, we will focus on recent studies reported in the prefrontal cortex, including the anterior cingulate cortex (ACC). We hypothesize that al-terations in ACC-related plasticity and synaptic modula-tion may contribute to various forms of cognitive deficits associated with FXS.
Kim, Susan S.,Descalzi, Giannina,Zhuo, Min Bentham Science Publishers Ltd 2010 CURRENT GENOMICS Vol.11 No.1
<P>Recent advances into the understanding of molecular mechanism of chronic pain have been largely developed through the use of genetic manipulations. This is in part due to the scarcity of selective pharmacological tools, which can be readily solved by creating knockout or transgenic mice. By identifying new genes that are of import, our efforts can then be aimed at studying relevant signaling pathways, and combination of pharmacological manipulations with genetic models can be used to further examine the specific mechanisms involved in chronic pain. In this review, we will examine the genetic models that are currently in use to study chronic pain in the anterior cingulate cortex: knockout mice; transgenic mice; and the strength of combining pharmacology with these genetic models.</P>
An Increase in Synaptic NMDA Receptors in the Insular Cortex Contributes to Neuropathic Pain
Qiu, Shuang,Chen, Tao,Koga, Kohei,Guo, Yan-yan,Xu, Hui,Song, Qian,Wang, Jie-jie,Descalzi, Giannina,Kaang, Bong-Kiun,Luo, Jian-hong,Zhuo, Min,Zhao, Ming-gao AAAS 2013 Science signaling Vol.6 No.275
<P><B>Stopping the Pain</B></P><P>Damage to the central or peripheral nervous system can trigger the development of neuropathic pain, which can manifest as painful sensations in response to stimuli that are not normally painful. Qiu <I>et al.</I> found that mice that had developed neuropathic pain after peripheral nerve injury showed changes in synaptic plasticity and increased abundance of synaptic NMDA receptors in the insular cortex, a region of the brain that is activated by acute and chronic pain. Using pharmacological inhibitors and transgenic mice, they mimicked these changes in vitro with insular cortical slices and thus identified the signaling pathway responsible. Mice injected with NMDA receptor inhibitors showed reduced behavioral signs of neuropathic pain after peripheral nerve injury. Thus, blocking NMDA receptor function in the insular cortex may prevent the development of neuropathic pain.</P>