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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)