PMID- 23503673
OWN - NLM
STAT- MEDLINE
DCOM- 20131029
LR  - 20131121
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 31
IP  - 5
DP  - 2013 May
TI  - Dexmedetomidine ameliorates intracerebral hemorrhage-induced memory impairment by 
      inhibiting apoptosis and enhancing brain-derived neurotrophic factor expression 
      in the rat hippocampus.
PG  - 1047-56
LID - 10.3892/ijmm.2013.1301 [doi]
AB  - Intracerebral hemorrhage (ICH) is a severe type of stroke causing neurological 
      dysfunction with a high mortality rate. Dexmedetomidine is an agonist for 
      alpha2‑adrenoreceptors with sedative, anxiolytic, analgesic and anesthetic effects. 
      In the present study, we investigated the effects of dexmedetomidine on 
      short‑term and spatial learning memory, as well as its effects on apoptosis 
      following the induction of ICH in rats. A rat model of IHC was created by an 
      injection of collagenase into the hippocampus using a stereotaxic instrument. 
      Dexmedetomidine was administered intraperitoneally daily for 14 consecutive days, 
      commencing 1 day after the induction of ICH. The step‑down avoidance test for 
      short‑term memory and the radial 8‑arm maze test for spatial learning memory were 
      conducted. Terminal deoxynucleotidyl transferase‑mediated dUTP nick end-labeling 
      (TUNEL) assay, immunohistochemistry for caspase‑3, and western blot analysis for 
      Bcl‑2, Bax, Bid and caspase-3 expression were performed for the detection of 
      apoptosis in the hippocampus. Western blot analysis for the brain‑derived 
      neurotrophic factor (BDNF) and tyrosine kinase B (TrkB) was also performed for 
      the detection of cell survival in the hippocampus. The induction of ICH 
      deteriorated short‑term and spatial learning memory, increased apoptosis and 
      suppressed BDNF and TrkB expression in the hippocampus. Treatment with 
      dexmedetomidine ameliorated the ICH‑induced impairment of short‑term and spatial 
      learning memory by suppressing apoptosis and enhancing BDNF and TrkB expression. 
      In the normal rats, dexmedetomidine exerted no significant effects on memory 
      function and apoptosis. The present results suggest the possibility that 
      dexmedetomidine may be used as a therapeutic agent for the conservation of memory 
      function in stroke patients.
FAU - Hwang, Lakkyong
AU  - Hwang L
AD  - Department of Physiology, College of Medicine, Kyung Hee University, Seoul 
      130-701, Republic of Korea.
FAU - Choi, In-Young
AU  - Choi IY
FAU - Kim, Sung-Eun
AU  - Kim SE
FAU - Ko, Il-Gyu
AU  - Ko IG
FAU - Shin, Mal-Soon
AU  - Shin MS
FAU - Kim, Chang-Ju
AU  - Kim CJ
FAU - Kim, Sang-Hoon
AU  - Kim SH
FAU - Jin, Jun-Jang
AU  - Jin JJ
FAU - Chung, Jun-Young
AU  - Chung JY
FAU - Yi, Jae-Woo
AU  - Yi JW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130313
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (BH3 Interacting Domain Death Agonist Protein)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (bcl-2-Associated X Protein)
RN  - 67VB76HONO (Dexmedetomidine)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Animals
MH  - *Apoptosis/drug effects
MH  - Avoidance Learning/drug effects
MH  - BH3 Interacting Domain Death Agonist Protein/metabolism
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - CA1 Region, Hippocampal/drug effects/enzymology/*pathology/physiopathology
MH  - Caspase 3/metabolism
MH  - Cerebral Hemorrhage/complications/*drug therapy/*pathology/physiopathology
MH  - DNA Fragmentation/drug effects
MH  - Dexmedetomidine/pharmacology/*therapeutic use
MH  - In Situ Nick-End Labeling
MH  - Maze Learning
MH  - Memory Disorders/drug therapy/*etiology/pathology/physiopathology
MH  - Memory, Short-Term/drug effects
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/metabolism
MH  - bcl-2-Associated X Protein/metabolism
EDAT- 2013/03/19 06:00
MHDA- 2013/10/30 06:00
CRDT- 2013/03/19 06:00
PHST- 2013/01/27 00:00 [received]
PHST- 2013/03/08 00:00 [accepted]
PHST- 2013/03/19 06:00 [entrez]
PHST- 2013/03/19 06:00 [pubmed]
PHST- 2013/10/30 06:00 [medline]
AID - 10.3892/ijmm.2013.1301 [doi]
PST - ppublish
SO  - Int J Mol Med. 2013 May;31(5):1047-56. doi: 10.3892/ijmm.2013.1301. Epub 2013 Mar 
      13.