PMID- 19164851
OWN - NLM
STAT- MEDLINE
DCOM- 20090414
LR  - 20200319
IS  - 0922-6028 (Print)
IS  - 0922-6028 (Linking)
VI  - 27
IP  - 1
DP  - 2009
TI  - Different postischemic protein expression of the GABA(A) receptor alpha2 subunit 
      and the plasticity-associated protein MAP1B after treatment with BDNF versus 
      G-CSF in the rat brain.
PG  - 27-39
LID - 10.3233/RNN-2009-0459 [doi]
AB  - PURPOSE: Recent data indicate that both brain-derived neurotrophic factor (BDNF) 
      and granulocyte-colony stimulating factor (G-CSF) exert substantial 
      neuroregenerative effects and improve functional outcome after ischemic stroke. 
      In the present study, we checked for potential differences in the postischemic 
      modulation of various excitatory and inhibitory neurotransmitter receptors as 
      well as various marker molecules for structural plasticity by BDNF versus G-CSF. 
      METHODS: Adult male Wistar rats were subjected to photothrombotic ischemia and 
      subsequently treated with NaCl, BDNF or G-CSF, respectively. After 6 weeks, 
      postischemic protein expression of the NR1, GluR1 and alpha2 subunit of the NMDA, 
      AMPA and GABA(A) receptor, respectively, was semiquantitatively determined ipsi- 
      and contralateral to the ischemic lesion. Structural plasticity was further 
      analyzed immunohistochemically using antibodies against MAP1B, MAP2 and 
      synaptophysin. RESULTS: Only BNDF caused a significantly reduced postischemic 
      protein expression of the GABA(A) receptor alpha2 subunit and the NR1 subunit of 
      the NMDA receptor in the hippocampus. Furthermore, BDNF compared to G-CSF 
      increased MAP1B protein expression in the periischemic regenerative region. 
      CONCLUSIONS: Although both BDNF and G-CSF have been shown to improve postischemic 
      functional outcome to a similar extent, exogenous administration results in 
      different underlying structural reorganization processes suggesting specific 
      modulations of plasticity-associated events by these trophic factors.
FAU - Muller, Harald D
AU  - Muller HD
AD  - Division of Neuropathology, Bezirkskrankenhaus Gunzburg, Gunzburg, Germany.
FAU - Neder, Angelika
AU  - Neder A
FAU - Sommer, Clemens
AU  - Sommer C
FAU - Schabitz, Wolf-Rudiger
AU  - Schabitz WR
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - Netherlands
TA  - Restor Neurol Neurosci
JT  - Restorative neurology and neuroscience
JID - 9005499
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Gabra2 protein, rat)
RN  - 0 (MAP2 protein, rat)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Receptors, GABA-A)
RN  - 0 (Synaptophysin)
RN  - 0 (microtubule-associated protein 1B)
RN  - 143011-72-7 (Granulocyte Colony-Stimulating Factor)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Brain/*drug effects/metabolism
MH  - Brain-Derived Neurotrophic Factor/*pharmacology/therapeutic use
MH  - Disease Models, Animal
MH  - Functional Laterality
MH  - Gene Expression Regulation/*drug effects
MH  - Granulocyte Colony-Stimulating Factor/*pharmacology/therapeutic use
MH  - Intracranial Thrombosis/complications
MH  - Male
MH  - Microtubule-Associated Proteins/*metabolism
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, GABA-A/*metabolism
MH  - Stroke/drug therapy/etiology/*pathology/physiopathology
MH  - Synaptophysin/metabolism
EDAT- 2009/01/24 09:00
MHDA- 2009/04/15 09:00
CRDT- 2009/01/24 09:00
PHST- 2009/01/24 09:00 [entrez]
PHST- 2009/01/24 09:00 [pubmed]
PHST- 2009/04/15 09:00 [medline]
AID - 01544415727L23G5 [pii]
AID - 10.3233/RNN-2009-0459 [doi]
PST - ppublish
SO  - Restor Neurol Neurosci. 2009;27(1):27-39. doi: 10.3233/RNN-2009-0459.