PMID- 22940080
OWN - NLM
STAT- MEDLINE
DCOM- 20121219
LR  - 20191210
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Linking)
VI  - 526
IP  - 2
DP  - 2012 Sep 27
TI  - Absence of SHATI/Nat8l reduces social interaction in mice.
PG  - 79-84
LID - 10.1016/j.neulet.2012.08.028 [doi]
AB  - We previously identified a novel molecule "Shati/Nat8l" from the nucleus 
      accumbens of mice. However, the physiological roles of the SHATI protein are not 
      clear. To investigate the effect of SHATI on the central nervous system and 
      behavior, we studied knockout mice of this protein. We carried out various 
      behavior tests using Shati-knockout mice. Shati-knockout mice did not differ from 
      wild type mice in learning and memory. In the open field test, Shati-knockout 
      mice did not differ from wild-type mice in time of stay in the outer, middle and 
      center areas. On the other hand, Shati-knockout mice showed increases in rearing 
      and grooming time in the open field test, and exploration time of novel objects. 
      These results suggested that knockout of the Shati gene may increase exploration 
      in specific circumstances. Interestingly, the Shati-knockout mice avoided social 
      interaction with unfamiliar mice out of their home cage, although there was no 
      difference in social interaction in their home cage compared with wild type mice. 
      Lack of the Shati gene increased brain-derived neurotrophic factor (BDNF) mRNA in 
      the prefrontal cortex and hippocampus, and decreased glial cell line-derived 
      neurotrophic factor (GDNF) mRNA in the striatum and hippocampus, and 
      lipopolysaccharides-induced TNF-alpha factor (LITAF) mRNA in the striatum. Since 
      these factors play important roles in behavior, alteration of expression of these 
      factors may be related to the induction of exploration and reduction of social 
      interaction in Shati-knockout mice.
CI  - Copyright (c) 2012 Elsevier Ireland Ltd. All rights reserved.
FAU - Furukawa-Hibi, Yoko
AU  - Furukawa-Hibi Y
AD  - Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University 
      Graduate School of Medicine, Nagoya 466-8560, Japan.
FAU - Nitta, Atsumi
AU  - Nitta A
FAU - Fukumitsu, Hidefumi
AU  - Fukumitsu H
FAU - Somiya, Hitomi
AU  - Somiya H
FAU - Toriumi, Kazuya
AU  - Toriumi K
FAU - Furukawa, Shoei
AU  - Furukawa S
FAU - Nabeshima, Toshitaka
AU  - Nabeshima T
FAU - Yamada, Kiyofumi
AU  - Yamada K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120823
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
RN  - 0 (Litaf protein, mouse)
RN  - 0 (Nuclear Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factors)
RN  - EC 2.3.1.- (Acetyltransferases)
RN  - EC 2.3.1.- (Shati protein, mouse)
SB  - IM
MH  - Acetyltransferases/*genetics
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/metabolism
MH  - DNA-Binding Proteins
MH  - Exploratory Behavior
MH  - Glial Cell Line-Derived Neurotrophic Factor/genetics/metabolism
MH  - Grooming
MH  - Hippocampus/metabolism
MH  - Maze Learning
MH  - Memory
MH  - Mice
MH  - Mice, Knockout
MH  - Nuclear Proteins/genetics/metabolism
MH  - Prefrontal Cortex/metabolism
MH  - RNA, Messenger/metabolism
MH  - Recognition, Psychology
MH  - *Social Behavior
MH  - Transcription Factors/genetics/metabolism
EDAT- 2012/09/04 06:00
MHDA- 2012/12/20 06:00
CRDT- 2012/09/04 06:00
PHST- 2012/01/04 00:00 [received]
PHST- 2012/08/02 00:00 [revised]
PHST- 2012/08/15 00:00 [accepted]
PHST- 2012/09/04 06:00 [entrez]
PHST- 2012/09/04 06:00 [pubmed]
PHST- 2012/12/20 06:00 [medline]
AID - S0304-3940(12)01094-4 [pii]
AID - 10.1016/j.neulet.2012.08.028 [doi]
PST - ppublish
SO  - Neurosci Lett. 2012 Sep 27;526(2):79-84. doi: 10.1016/j.neulet.2012.08.028. Epub 
      2012 Aug 23.