PMID- 17258238
OWN - NLM
STAT- MEDLINE
DCOM- 20070601
LR  - 20220223
IS  - 0028-3908 (Print)
IS  - 0028-3908 (Linking)
VI  - 52
IP  - 4
DP  - 2007 Mar
TI  - Neurosteroid estradiol rescues ischemia-induced deficit in the long-term 
      potentiation of rat hippocampal CA1 neurons.
PG  - 1124-38
AB  - Increasing evidence indicates that neurosteroid 17beta-Estradiol (E2), a type of 
      female sex hormone, has a neuroprotective effect against cerebral injury. 
      However, it remains unknown whether E2 can also protect the hippocampal CA1 
      neurons from functional deficits in synaptic transmission and plasticity caused 
      by ischemia. To address this issue, adult male Wistar rats were subjected to mild 
      global cerebral ischemia created by four-vessel occlusion (4VO) for 10min, and 
      the effects of E2 administration against the ischemic injury were investigated. 
      The electrophysiological properties of Schaffer collateral-CA1 synapses were 
      examined 7days after ischemia by applying a real-time optical recording technique 
      to the hippocampal slices stained with a voltage-sensitive dye (RH482). The 
      ischemic brain showed a decreased basal synaptic transmission and an impairment 
      of LTP induction, but no alteration in paired-pulse facilitation. The 
      administration of E2 (1mg/kg) 3h before ischemia was able to protect CA1 neurons 
      from these ischemia-induced synaptic dysfunctions. The estrogen receptor-alpha 
      (ERalpha) selective agonist, propyl pyrazole triol (PPT, 2mg/kg), exerted a 
      similar protective effect, but the estrogen receptor-beta (ERbeta) agonist, 
      diarylpropiolnitrile (DPN, 8mg/kg), failed to do so. A histological examination 
      revealed that the transient global cerebral ischemia markedly reduced the density 
      of pyramidal neurons in the CA1 region. The cell loss was significantly 
      attenuated by E2 and PPT but not by DPN, as observed in synaptic functions. These 
      findings suggest that E2 can protect neurons not only from cell death but also 
      from functional damages due to a relatively mild degree of transient cerebral 
      ischemia, and this effect is mediated by ERalpha, but not by ERbeta.
FAU - Dai, Xiaoniu
AU  - Dai X
AD  - Department of Physiology, Nagoya University Graduate School of Medicine, 65 
      Tsurumai, Nagoya 466-8550, Japan.
FAU - Chen, Ling
AU  - Chen L
FAU - Sokabe, Masahiro
AU  - Sokabe M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070125
PL  - England
TA  - Neuropharmacology
JT  - Neuropharmacology
JID - 0236217
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Phenols)
RN  - 0 (Pyrazoles)
RN  - 0T83Y6JZPF (4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol)
RN  - 4TI98Z838E (Estradiol)
SB  - IM
MH  - Animals
MH  - Dose-Response Relationship, Radiation
MH  - Drug Interactions
MH  - Electric Stimulation/methods
MH  - Estradiol/*administration & dosage/agonists
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Excitatory Postsynaptic Potentials/drug effects/radiation effects
MH  - Hippocampus/*pathology/physiopathology
MH  - In Vitro Techniques
MH  - Infarction, Middle Cerebral Artery/*pathology/physiopathology/*prevention & 
      control
MH  - Long-Term Potentiation/*drug effects
MH  - Male
MH  - Neurons/*drug effects
MH  - Phenols
MH  - Pyrazoles/pharmacology
MH  - Rats
MH  - Rats, Wistar
EDAT- 2007/01/30 09:00
MHDA- 2007/06/02 09:00
CRDT- 2007/01/30 09:00
PHST- 2006/08/19 00:00 [received]
PHST- 2006/11/28 00:00 [revised]
PHST- 2006/11/29 00:00 [accepted]
PHST- 2007/01/30 09:00 [pubmed]
PHST- 2007/06/02 09:00 [medline]
PHST- 2007/01/30 09:00 [entrez]
AID - S0028-3908(06)00409-6 [pii]
AID - 10.1016/j.neuropharm.2006.11.012 [doi]
PST - ppublish
SO  - Neuropharmacology. 2007 Mar;52(4):1124-38. doi: 10.1016/j.neuropharm.2006.11.012. 
      Epub 2007 Jan 25.