期刊
BIOLOGICAL PSYCHIATRY
卷 79, 期 9, 页码 716-726出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2015.07.005
关键词
Computational models; Gamma oscillations; Inhibition; NMDA hypofunction; Parvalbumin; Schizophrenia
资金
- National Institute of Mental Health [T32MH020002, MH091407, MH094670]
- National Eye Institute [K99 EY025026]
- Swartz Foundation
- Howard Hughes Medical institute
N-methyl-D-aspartate receptor (NMDAR) hypofunction in parvalbumin-expressing (PV+) inhibitory neurons (INs) may contribute to symptoms in patients with schizophrenia (SZ). This hypothesis was inspired by studies in humans involving NMDAR antagonists that trigger SZ symptoms. Animal models of SZ using neuropharmacology and genetic knockouts have successfully replicated some of the key observations in human subjects involving alteration of gamma band oscillations (GBO) observed in electroencephalography and magnetoencephalography signals. However, it remains to be seen if NMDAR hypofunction in PV+ neurons is fundamental to the phenotype observed in these models. In this review, we discuss some of the key computational models of GBO and their predictions in the context of NMDAR hypofunction in INs. While PV+ INs have been the main focus of SZ studies in animal models, we also discuss the implications of NMDAR hypofunction in other types of INs using computational models for GBO modulation in the visual cortex.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据