PMID- 10531422
OWN - NLM
STAT- MEDLINE
DCOM- 19991119
LR  - 20191023
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 19
IP  - 21
DP  - 1999 Nov 1
TI  - A(2A) adenosine receptor deficiency attenuates brain injury induced by transient 
      focal ischemia in mice.
PG  - 9192-200
AB  - Extracellular adenosine critically modulates ischemic brain injury, at least in
      part through activation of the A(1) adenosine receptor. However, the role played 
      by the A(2A) receptor has been obscured by intrinsic limitations of A(2A)
      adenosinergic agents. To overcome these pharmacological limitations, we explored 
      the consequences of deleting the A(2A) adenosine receptor on brain damage after
      transient focal ischemia. Cerebral morphology, as well as vascular and
      physiological measures (before, during, and after ischemia) did not differ
      between A(2A) receptor knock-out and wild-type littermates. The volume of
      cerebral infarction, as well as the associated neurological deficit induced by
      transient filament occlusion of the middle cerebral artery, were significantly
      attenuated in A(2A) receptor knock-out mice. This neuroprotective phenotype of
      A(2A) receptor-deficient mice was observed in different genetic backgrounds,
      confirming A(2A) receptor disruption as its cause. Together with complimentary
      pharmacological studies, these data suggest that A(2A) receptors play a prominent
      role in the development of ischemic injury within brain and demonstrate the
      potential for anatomical and functional neuroprotection against stroke by A(2A)
      receptor antagonists.
FAU - Chen, J F
AU  - Chen JF
AD  - Molecular Neurobiology Laboratory, Department of Neurology, Massachusetts General
      Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
      chenjf@helix.mgh.harvard.edu
FAU - Huang, Z
AU  - Huang Z
FAU - Ma, J
AU  - Ma J
FAU - Zhu, J
AU  - Zhu J
FAU - Moratalla, R
AU  - Moratalla R
FAU - Standaert, D
AU  - Standaert D
FAU - Moskowitz, M A
AU  - Moskowitz MA
FAU - Fink, J S
AU  - Fink JS
FAU - Schwarzschild, M A
AU  - Schwarzschild MA
LA  - eng
GR  - 5P50 NS10828/NS/NINDS NIH HHS/United States
GR  - DA07496/DA/NIDA NIH HHS/United States
GR  - NS01729/NS/NINDS NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for
      Neuroscience
JID - 8102140
RN  - 0 (Receptor, Adenosine A2A)
RN  - 0 (Receptors, Purinergic P1)
SB  - IM
MH  - Aging/physiology
MH  - Animals
MH  - Blood Pressure
MH  - Body Temperature
MH  - Brain/anatomy & histology/physiology/*physiopathology
MH  - Brain Injury, Chronic/etiology/genetics/*physiopathology
MH  - Cerebral Cortex/blood supply
MH  - Cerebrovascular Circulation/*physiology
MH  - Genomic Library
MH  - Heart Rate
MH  - Hemodynamics/*physiology
MH  - Homozygote
MH  - Ischemic Attack, Transient/complications/genetics/*physiopathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - *Motor Activity
MH  - Receptor, Adenosine A2A
MH  - Receptors, Purinergic P1/*deficiency/genetics
MH  - Regional Blood Flow
PMC - PMC6782932
EDAT- 1999/10/26 00:00
MHDA- 1999/10/26 00:01
CRDT- 1999/10/26 00:00
PHST- 1999/10/26 00:00 [pubmed]
PHST- 1999/10/26 00:01 [medline]
PHST- 1999/10/26 00:00 [entrez]
PST - ppublish
SO  - J Neurosci. 1999 Nov 1;19(21):9192-200.