Neonatal and Pediatric Medicine
Open Access

GPR56: Its Regulation in GABAergic Neurons and Possible Involvement in Neuro Developmental Disorders

Ayako Y Murayama^1,2 and Hideyuki Okano^1,2*

¹Department of Physiology, Keio University School of Medicine, Tokyo, Japan

²Laboratory for Marmoset Neural Architecture, Center for Brain Science, RIKEN, Wako, Japan

Received Date: Mar 16, 2021 / Accepted Date: Mar 30, 2021 / Published Date: Apr 06, 2021

Citation: Okano H, Murayama AY (2021) GPR56: Its Regulation in GABAergic Neurons and Possible Involvement in Neuro Developmental Disorders. Neonat Pediatr Med 7:209.

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Copyright: ©  2021 Murayama AY, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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One-third of patients with epilepsy have intractable seizures that cannot be controlled with any currently available antiepileptic drugs . It has been well known that there are patients afflicted with epilepsy with mutations in some G protein-coupled receptors (GPCRs). Patients with the 15-bp deletion within the upstream region of non-cording exon 1m of human G protein-coupled receptors 56 (GPR56) gene exhibit cortical malformation and develop young-onset epilepsy. In our recent report , to understanding the mechanism underlying the etiological role of this 15-bp deletion , we examined the function of a cis-regulatory element containing this 15-bp in the control of expression pattern of GPR56 using marmoset as a nonhuman primate animal model. We showed that the cis-regulatory element drives expression of GPR56 preferentially in GABAergic neurons in developing brain and suggest that pathogenic mechanisms of epilepsy in patients with a 15-bp deletion may be explained in part by the developmental abnormality or dysfunction of GABAergic neurons.

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