KAIST 생명과학과동창회
  • News & Events
  • News


Astrocytes eat connections to maintain plasticity in adult brains


by The Korea Advanced Institute of Science and Technology (KAIST) 



    Astrocytes eat connections to maintain plasticity in adult brains

A 3-D image showing our synapse phagocytosis reporter in mouse hippocampus


Developing brains constantly sprout new neuronal connections called synapses as they learn and remember. Important connectionsthe ones that are repeatedly introduced, such as how to avoid dangerare nurtured and reinforced, while connections deemed unnecessary are pruned away. Adult brains undergo similar pruning, but it was unclear how or why synapses in the adult brain get eliminated.                      


Now, a team of KAIST researchers has found the mechanism underlying plasticity and, potentially, neurological disorders in adult brains. They published their findings on December 23 in Nature.


"Our findings have profound implications for our understanding of how neural circuits change during learning and memory, as well as in diseases," said paper author Won-Suk Chung, an assistant professor in the Department of Biological Sciences at KAIST. "Changes in synapse number have strong association with the prevalence of various neurological disorders, such as autism spectrum disorder, schizophrenia, frontotemporal dementia, and several forms of seizures."


Gray matter in the brain contains microglia and astrocytes, two complementary cells that, among other things, support neurons and synapses. Microglial are a frontline immunity defense, responsible for eating pathogens and dead cells, and astrocytes are star-shaped cells that help structure the brain and maintain homeostasis by helping to control signaling between neurons. According to Professor Chung, it is generally thought that microglial eat synapses as part of its clean-up effort in a process known as phagocytosis.


"Using novel tools, we show that, for the first time, it is astrocytes and not microglia that constantly eliminate excessive and unnecessary adult excitatory synaptic connections in response to neuronal activity," Professor Chung said. "Our paper challenges the general consensus in this field that microglia are the primary synapse phagocytes that control synapse numbers in the brain."


Professor Chung and his team developed a molecular sensor to detect synapse elimination by glial cells and quantified how often and by which type of cell synapses were eliminated. They also deployed it in a mouse model without MEGF10, the gene that allows astrocytes to eliminate synapses. Adult animals with this defective astrocytic phagocytosis had unusually increased excitatory synapse numbers in the hippocampus. Through a collaboration with Dr. Hyungju Park at KBRI, they showed that these increased excitatory synapses are functionally impaired, which cause defective learning and memory formation in MEGF10 deleted animals.


"Through this process, we show that, at least in the adult hippocampal CA1 region, astrocytes are the major player in eliminating synapses, and this astrocytic function is essential for controlling synapse number and plasticity," Chung said.


Professor Chung noted that researchers are only beginning to understand how synapse elimination affects maturation and homeostasis in the brain. In his group's preliminary data in other brain regions, it appears that each region has different rates of synaptic elimination by astrocytes. They suspect a variety of internal and external factors are influencing how astrocytes modulate each regional circuit, and plan to elucidate these variables.


"Our long-term goal is understanding how astrocyte-mediated synapse turnover affects the initiation and progression of various neurological disorders," Professor Chung said. "It is intriguing to postulate that modulating astrocytic phagocytosis to restore synaptic connectivity may be a novel strategy in treating various brain disorders."








List of Articles
번호 제목 글쓴이 날짜 조회 수
393 [정인경 교수님] 기저 질환이 없는 코로나19 환자의 중증 신규 유전적 위험 인자 규명 생명과학과 2022.09.29 37
392 [김은준 교수님] 자폐 진단․ 치료 골든타임, 동물실험으로 확인 생명과학과 2022.09.27 49
391 [송지준 교수님] 헌팅턴병 발병원인 제거를 위한 치료제 개발 방법 제시​ 생명과학과 2022.09.02 144
390 [조병관 교수님] 대량의 고농도 일산화탄소를 고부가가치 바이오케미칼로 전환하는 기술 개발 생명과학과 2022.07.15 163
389 [김대수 교수님] 액트노바, 카카오벤처스로부터 5억 규모 시드 투자 유치 "육안으로 진행되던 임상·비임상 분야 행동 실험 과정, 인공지능 영상처리 기술로 자동화" 생명과학과 2022.08.10 171
388 [김상규 교수님] 구글도 올라 탄 神으로 가는 길[과학을읽다] 생명과학과 2022.09.07 181
387 [이승희 교수님] 신경전달물질 소마토스타틴의 알츠하이머 독성 개선효과 발견​ 생명과학과 2022.07.25 192
386 [김은준 교수님] 대규모 한국인 자폐증 가족 유전체 연구를 통한 새로운 자폐 유전변이 최초 발견​ 생명과학과 2022.07.19 195
385 [전상용 교수님] 항암치료용 인공탄수화물 기반 나노의약 개발​ 생명과학과 2022.07.12 198
384 [김대수 교수님] “뇌는 무언가 실패하는 순간 발달...‘메타인지’로 창의성 키워야” [이노베이트코리아 2022] 생명과학과 2022.07.18 205
383 [메디포럼 정재언 대표] 메디포럼, 정재언 연구소장 신임 대표이사 선임…“임상 R&D 중심 경영 집중” 생명과학과 2022.03.14 212
382 [정원석 교수님] 카이스트, 노화된 뇌에서 생겨난 비정상적 별아교세포 ‘아프다(APDA)’발견 생명과학과 2022.08.08 215
381 [이승재 교수님] 건강한 장수를 유도하는 돌연변이 유전자 발굴 생명과학과 2021.11.24 245
380 [김세윤, 정원석, 손종우 교수님] 인공지능 기반 약물 가상 스크리닝 기술로 신규 항암 치료제 발굴 성공 생명과학과 2022.08.12 252
379 [루닛 서범석 대표] 바이오업계 유니콘 기대 루닛, 서범석 '치료 예측 AI' 고도화 박차 생명과학과 2022.04.27 265
378 [김찬혁, 정원석 교수님] 심각한 염증 부작용 없앤 새로운 알츠하이머병 치료제 개발​ 생명과학과 2022.08.22 267
377 [손종우 교수님] 서울의대동창회, 제25회 함춘학술상 수상자 선정 생명과학과 2022.03.08 269
376 [오병하 교수님] 오미크론에도 듣는 범용 항체, 국내에서 개발 생명과학과 2022.02.04 282
375 [한진희 교수님] 카이스트, 뉴런(신경 세포) 교체에 의한 기억저장 규명 생명과학과 2021.11.24 295
374 [최길주, 김상규 교수님] 카오스재단 2022 봄 카오스강연 ‘식물행성 (Plant Planet)’ 에서 강연(4/6) 생명과학과 2022.02.22 303
Board Pagination Prev 1 2 3 4 5 6 7 8 9 10 ... 20 Next
/ 20