Research Papers: Pathology:
Altered expression of neuropeptide Y receptors caused by focal cortical dysplasia in human intractable epilepsy
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Lin Li1,2,3,*, Jiahui Deng1,2,3,*, Changqing Liu1,*, Hanjiang Luo4, Yuguang Guan1, Jian Zhou1, Xueling Qi1, Tianfu Li2,3, Zhiqing David Xu3,4,5 and Guo-Ming Luan1,2,3
1 Department of Functional Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, P.R. China
2 Beijing Key Laboratory in Epilepsy, Beijing, P.R. China
3 Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing, P.R. China
4 Beijing Key Laboratory of Neural Regeneration and Repair, Department of Neurobiology, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, P.R. China
5 Department of Neuroscience, Karolinska Institute, Stockholm, Sweden
* These authors have contributed equally to this work
Guo-Ming Luan, email:
Keywords: focal cortical dysplasia, neuropeptide Y Y1 receptor, neuropeptide Y Y2 receptor, neuropeptide Y Y5 receptor, Pathology section
Received: September 08, 2015 Accepted: January 29, 2016 Published: March 02, 2016
Focal cortical dysplasia (FCD) is a common cause of pharmacologically-intractable epilepsy, however, the precise mechanisms underlying the epileptogenicity of FCD remains to be determined. Neuropeptide Y (NPY), an endogenous anticonvulsant in the central nervous system, plays an important role in the regulation of neuronal excitability. Increased expression of NPY and its receptors has been identified in the hippocampus of patients with mesial temporal lobe epilepsy, presumed to act as an endogenous anticonvulsant mechanism. Therefore, we investigated whether expression changes in NPY receptors occurs in patients with FCD. We specifically investigated the expression of seizure-related NPY receptor subtypes Y1, Y2, and Y5 in patients with FCD versus autopsy controls. We found that Y1R and Y2R were up-regulated at the mRNA and protein levels in the temporal and frontal lobes in FCD lesions. By contrast, there was no significant change in either receptor detected in parietal lesions. Notably, overexpression of Y5R was consistently observed in all FCD lesions. Our results demonstrate the altered expression of Y1R, Y2R and Y5R occurs in FCD lesions within the temporal, frontal and parietal lobe. Abnormal NPY receptor subtype expression may be associated with the onset and progression of epileptic activity and may act as a therapeutic candidate for the treatment of refractory epilepsy caused by FCD.
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