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Title Acute stress and Synaptic plasticity Abstract Acute episodes of stress are crucial for survival whereas chronic stress is detrimental. Learning and memory are particularly susceptible to stress and the underlying mechani sms have been extensively studied with respect to chronic stress, which results in cog nitive deficits and neurodegeneration. In contrast, little is known about how acute str ess is able to enhance cognitive performance. We have therefore examined the effect s of acute stress and brief exposure to glucocorticoids on long-term potentiation (LTP) in the hippocampus, a well-established model system for investigating the synaptic bas is of learning and memory. Our study has uncovered a novel mechanism whereby ac ute stress can facilitate synaptic plasticity in the hippocampus. We find that hippoca mpal slices, either prepared from rats following 30 min restraint stress or directly exp osed to glucocorticoids (GCs), exhibits an NMDAR resistant form of LTP that is abs ent in controls and which results in a larger magnitude of LTP in the stressed group. The stressors activate PKA, increase the phosphorylation of Ser845 on GluA1 subunit of AMPAR and increase the surface expression of the GluA1 subunit. These subunit s likely form functional homomeric AMPARs that trigger the stressor-induced LTP (s LTP) since it is completely prevented by IEM-1460, an inhibitor of Ca2+-permeable A MPARs. Although NMDARs are not required for the induction of sLTP they are ess ential for the sensitisation of the plasticity state, during the exposure to GCs. Thus a cute stressors elicit an NMDAR-dependent form of metaplasticity that enhances LTP v ia the priming of a form of LTP that is independent of, but additive with, NMDARdependent LTP. 1. 인적사항 국 문 조지훈 영 문 Jihoon Jo 휴대전화 010-4470-5409 E-mail [email protected] 전 화 062-220-4419 성 명 우편번호 직 장 주 소 광주광역시 501-746 동구 백서로 160 FAX 전남대학교 의과대학 233 호 우편번호 자 택 주 소 503-775 광주광역시 남구 봉선 2 동 포스코 전 화 062-673-5409 더샵아파트 102 동 2101 호 2. 학력사항 연도 학 력 학위 부터 까지 대학교 전공명 지도교수 1992.03 1999.02 인하대학교 생물학 이창중 학사 1999.03 2001.02 인하대학교 신경과학 이창중 석사 2002.05 2006.04 신경과학 Kei Cho 박사 Univ. of Sheffield, U.K. 최종학위논문제목 Developmental change of the mechanism of long-term synaptic depression in the perirhinal cortex by visual experience 3. 경력 연도(부터-까지) 2006 2006 기관명 직위(직명) Univ. of Sheffield, U.K. Postdoctoral Research 비 고 Associate 2006 2010 Univ. of Bristol, U.K. Tenured Research Fellow 2011 2013 인하대학교 조교수 2013 현재 전남대학교 부교수 정년직 4. 대표적 논문 실적 구분 논문 Sensing change: The emerging role 논문 게재연도 (권, 쪽) (등록연도) DEVELOPMENTAL BIOLOGY disease (22, 530-535) prevented by manipulation of a signaling pathway involving 역할 Impact Factor SEMINARS IN CELL & of calcium sensors in neuronal Aß1-42 inhibition of LTP is 논문 게재지 2011 공동저자 6.646 2011 제 1 저자 15.531 2010 공동저자 7.271 2010 제 1 저자 15.531 2010 제 1 저자 32.401 2009 공동저자 2.587 Nature Neuroscience (14, 545-547) caspase-3, Akt and GSK-3ß Regulation of Synaptic Rac1 Activity, Long-Term Potentiation 논문 Maintenance, and Learning and Journal of Neuroscience (30, 14134- Memory by BCR and ABR Rac GTPase-Activating Proteins Muscarinic receptors induce LTD of 논문 NMDA receptor-mediated EPSCs via a mechanism involving 14144) Nature Neuroscience (13, 1216-1224) hippocalcin, AP2 and PSD-95 Caspase-3 activation via 논문 mitochondria is required for long- Cell term depression and AMPA receptor (141, 859-871) internalization 논문 Neuronal calcium sensors and Biochemical Society synaptic plasticity Transactions 비고 (37, 1359-1363) A novel mechanism of hippocampal 논문 Molecular LTD involving muscarinic receptortriggered interactions between AMPARs, GRIP and liprin-alpha Brain 2009 공동저자 4.20 2008 제 1 저자 14.736 2007 공동저자 14.736 2006 제 1 저자 15.531 (2, 18) Metabotropic glutamate receptor- 논문 mediated LTD involves two Neuron 2+ (60, 1095-1111) interacting Ca sensors,NCS1andPICK1 Synaptic Accumulation of PSD-95 논문 and Synaptic Function Regulated by Neuron Phosphorylation of Serine-295 of (56, 488-502) PSD-95 Experience-dependent modification 논문 of mechanisms depression of long-term Nature Neuroscience (9, 170-172)