Myoung-Hwan Kim

IRSp53 is an adaptor protein that acts downstream of Rac and Cdc42 small GTPases and is implicated in the regulation of membrane deformation and actin filament assembly. In neurons, IRSp53 is an abundant postsynaptic protein and regulates actin-rich dendritic spines; however, its in vivo functions have not been explored. We characterized transgenic mice deficient of IRSp53 expression. Unexpectedly, IRSp53(-/-) neurons do not show significant changes in the density and ultrastructural morphologie

The clearance of Ca2+ from nerve terminals is critical for determining the build-up of residual Ca2+ after repetitive presynaptic activity. We found previously that K+-dependent Na+/Ca2+ exchangers (NCKXs) show polarized distributions in axon terminals of supraoptic magnocellular neurons and play a major role in Ca2+ clearance. The role of NCKXs in presynaptic terminals, however, has not been studied. We investigated the contribution of NCKX in conjunction with other Ca2+ clearance mechanisms at

Neurons are polarized into compartments such as the soma, dendrites, and axon terminals, each of which has highly specialized functions. To test whether Ca2+ is differently handled in different compartments of a neuron, we investigated Ca2+ clearance mechanisms in somata of supraoptic magnocellular neurosecretory cells (MNCs) and in their axon terminals located in neurohypophyses. Using patch-clamp and microfluorometry techniques, Ca2+ transients were evoked by depolarizing pulses. Endogenous Ca

Metabolic diseases affect various organs including the brain. Accumulation or depletion of substrates frequently leads to brain injury and dysfunction. Deficiency of aminopeptidase P1, a cytosolic proline‐specific peptidase encoded by the Xpnpep1 gene, causes an inborn error of metabolism (IEM) characterized by peptiduria in humans. We previously reported that knockout of aminopeptidase P1 in mice causes neurodevelopmental disorders and peptiduria. However, little is known about the pathophysiol

Anatomical connectivity and lesion-deficit studies have shown that the dorsal and ventral hippocampi contribute to cognitive and emotional processes, respectively. However, the role of the dorsal hippocampus (dHP) in emotional or stress-related behaviors remains unclear. Here, we showed that neuronal activity in the dHP affects stress-coping behaviors in mice via excitatory projections to the medial prefrontal cortex (mPFC). The antidepressant ketamine rapidly induced c-Fos expression in both th

이 글은 한국의 고등교육에서 최대의 쟁점으로 떠오른 대학 구조조정 문제를다룬다. 먼저 대학의 자율성과 공공성을 크게 훼손하고 있는 교육부의 총장 직선제 폐지 및 국공립대학 총장 임용 제청 거부 사태, 사학재단의 전횡과 비리의악화 등을 살펴본다. 또한 대학 구조조정을 위한 교육부의 대학평가 지표의 심각한 문제를 비판적으로 분석하고, ‘대학 평가 및 구조개혁에 관한 법률안’이고등교육의 질적 발전을 외면한 채 사학 소유주들의 학교법인 해산을 유도할재산 처분 특례에만 초점을 맞추고 있음을 파헤친다. 정부의 일방적인 구조조정 정책에 관한 대안으로서 주요 국립대학과 수도권의 일부 사립대학을 묶어신입생을 공동 선발하는 연합체제를 실현함으로써 한국의 대학입시 경쟁을 완화하는 동시에 이런 연합체제가 학문과 교육단위의 자율적인 혁신을 꾀하는 터전이 될 수 있도록 한다. 이 과정에서 관료주의의 억압과 간섭에서 벗어난 대학에 자율적이고 진정한 학문적 경쟁이 자리 잡아 내실 있는 구조조정이 실행될수 있으며

Abstract Inborn errors of metabolism (IEMs) are common causes of neurodevelopmental disorders, including microcephaly, hyperactivity, and intellectual disability. However, the synaptic mechanisms of and pharmacological interventions for the neurological complications of most IEMs are unclear. Here, we report that metabolic dysfunction perturbs neuronal NMDA receptor (NMDAR) homeostasis and that the restoration of NMDAR signaling ameliorates neurodevelopmental and cognitive deficits in IEM model