PMID- 25057210
OWN - NLM
STAT- MEDLINE
DCOM- 20140922
LR  - 20211021
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 34
IP  - 30
DP  - 2014 Jul 23
TI  - SCAMP5 plays a critical role in synaptic vesicle endocytosis during high neuronal 
      activity.
PG  - 10085-95
LID - 10.1523/JNEUROSCI.2156-14.2014 [doi]
AB  - Secretory carrier membrane protein 5 (SCAMP5), a recently identified candidate 
      gene for autism, is brain specific and highly abundant in synaptic vesicles 
      (SVs), but its function is currently unknown. Here, we found that knockdown (KD) 
      of endogenous SCAMP5 by SCAMP5-specific shRNAs in cultured rat hippocampal 
      neurons resulted in a reduction in total vesicle pool size as well as in 
      recycling pool size, but the recycling/resting pool ratio was significantly 
      increased. SCAMP5 KD slowed endocytosis after stimulation, but impaired it 
      severely during strong stimulation. We also found that KD dramatically lowered 
      the threshold of activity at which SV endocytosis became unable to compensate for 
      the ongoing exocytosis occurring during a stimulus. Reintroducing shRNA-resistant 
      SCAMP5 reversed these endocytic defects. Therefore, our results suggest that 
      SCAMP5 functions during high neuronal activity when a heavy load is imposed on 
      endocytosis. Our data also raise the possibility that the reduction in expression 
      of SCAMP5 in autistic patients may be related to the synaptic dysfunction 
      observed in autism.
CI  - Copyright (c) 2014 the authors 0270-6474/14/3410085-11$15.00/0.
FAU - Zhao, Haiyan
AU  - Zhao H
AD  - Department of Physiology and Biomedical Sciences, Biomembrane Plasticity Research 
      Center.
FAU - Kim, Yoonju
AU  - Kim Y
AD  - Department of Physiology and Biomedical Sciences, Biomembrane Plasticity Research 
      Center, Neuroscience Research Institute, Medical Research Center, and.
FAU - Park, Joohyun
AU  - Park J
AD  - Department of Physiology and Biomedical Sciences, Biomembrane Plasticity Research 
      Center, Neuroscience Research Institute, Medical Research Center, and.
FAU - Park, Daehun
AU  - Park D
AD  - Department of Physiology and Biomedical Sciences, Biomembrane Plasticity Research 
      Center.
FAU - Lee, Sang-Eun
AU  - Lee SE
AD  - Department of Physiology and Biomedical Sciences, Biomembrane Plasticity Research 
      Center.
FAU - Chang, Iree
AU  - Chang I
AD  - Department of Physiology and Biomedical Sciences.
FAU - Chang, Sunghoe
AU  - Chang S
AD  - Department of Physiology and Biomedical Sciences, Biomembrane Plasticity Research 
      Center, Neuroscience Research Institute, Medical Research Center, and Bio-Max 
      Institute, Seoul National University College of Medicine, Seoul, South Korea 
      110-799 sunghoe@snu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Carrier Proteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (SCAMP5 protein, human)
SB  - IM
MH  - Animals
MH  - Carrier Proteins/genetics/*physiology
MH  - Endocytosis/genetics/*physiology
MH  - Female
MH  - Gene Knockdown Techniques
MH  - HEK293 Cells
MH  - Hippocampus/cytology/physiology
MH  - Humans
MH  - Male
MH  - Membrane Proteins/genetics/*physiology
MH  - Neurons/*physiology
MH  - Primary Cell Culture
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Synaptic Vesicles/genetics/*physiology
PMC - PMC6608302
OTO - NOTNLM
OT  - SCAMP5
OT  - neuronal activity
OT  - recycling pool
OT  - resting pool
OT  - synaptic vesicle endocytosis
EDAT- 2014/07/25 06:00
MHDA- 2014/09/23 06:00
PMCR- 2015/01/23
CRDT- 2014/07/25 06:00
PHST- 2014/07/25 06:00 [entrez]
PHST- 2014/07/25 06:00 [pubmed]
PHST- 2014/09/23 06:00 [medline]
PHST- 2015/01/23 00:00 [pmc-release]
AID - 34/30/10085 [pii]
AID - 2156-14 [pii]
AID - 10.1523/JNEUROSCI.2156-14.2014 [doi]
PST - ppublish
SO  - J Neurosci. 2014 Jul 23;34(30):10085-95. doi: 10.1523/JNEUROSCI.2156-14.2014.