PMID- 18547240
OWN - NLM
STAT- MEDLINE
DCOM- 20080820
LR  - 20211028
IS  - 1460-9568 (Electronic)
IS  - 0953-816X (Print)
IS  - 0953-816X (Linking)
VI  - 27
IP  - 10
DP  - 2008 May
TI  - Brain-derived neurotropic factor and neurogenesis in the adult rat dentate gyrus: 
      interactions with corticosterone.
PG  - 2493-500
LID - 10.1111/j.1460-9568.2008.06250.x [doi]
AB  - Flattening the diurnal corticosterone rhythm prevented the stimulating action of 
      L-NAME (a nitric oxide synthase, NOS, inhibitor) on progenitor cell proliferation 
      in the dentate gyrus in Lister-Hooded adult male rats. The increased expression 
      of brain-derived neurotrophic factor (BDNF) and trkB mRNA in the dentate gyrus 
      which otherwise occurred after L-NAME was also prevented by clamping the 
      corticoid rhythm in adrenalectomized rats, but was restored by daily additional 
      injections of corticosterone (which replicates the diurnal rhythm). Unilateral 
      infusions of BDNF into the lateral ventricle increased proliferation in the 
      dentate gyrus on the side of the infusion, but this was not observed following 
      implantation of subcutaneous corticosterone, which flattened the diurnal 
      corticosterone rhythm. 5HT1A mRNA in the dentate gyrus was increased on both 
      sides of the brain by unilateral BDNF infusions, but this was also prevented by 
      subcutaneous corticosterone pellets. These results show that the diurnal rhythm 
      of corticosterone regulates the stimulating action of NOS inhibitors on BDNF as 
      well as on neurogenesis in the dentate gyrus, and that BDNF becomes ineffective 
      on both proliferation rates and 5HT1A expression in the absence of a rhythm in 
      corticosterone. This, together with our previous findings, suggests that 
      corticoid rhythms permit both serotonin and NO access to BDNF, and the latter to 
      regulate progenitor cell activity.
FAU - Pinnock, Scarlett B
AU  - Pinnock SB
AD  - Department of Physiology, Development and Neuroscience, and Cambridge Centre for 
      Brain Repair, University of Cambridge, Cambridge, UK.
FAU - Herbert, Joe
AU  - Herbert J
LA  - eng
GR  - 080048/WT_/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 112692-38-3 (Receptor, Serotonin, 5-HT1A)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 333DO1RDJY (Serotonin)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type I)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism/pharmacology
MH  - Cell Differentiation/drug effects/*physiology
MH  - Cell Proliferation/drug effects
MH  - Circadian Rhythm/drug effects/physiology
MH  - Corticosterone/*metabolism/pharmacology
MH  - Dentate Gyrus/cytology/drug effects/*metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Injections, Intraventricular
MH  - Male
MH  - NG-Nitroarginine Methyl Ester/pharmacology
MH  - Neurons/drug effects/*metabolism
MH  - Nitric Oxide/metabolism
MH  - Nitric Oxide Synthase Type I/antagonists & inhibitors/metabolism
MH  - Periodicity
MH  - RNA, Messenger/drug effects/metabolism
MH  - Rats
MH  - Receptor, Serotonin, 5-HT1A/genetics
MH  - Receptor, trkB/genetics
MH  - Serotonin/metabolism
MH  - Stem Cells/drug effects/*metabolism
PMC - PMC2662436
MID - UKMS4081
OID - NLM: UKMS4081
EDAT- 2008/06/13 09:00
MHDA- 2008/08/21 09:00
PMCR- 2009/03/30
CRDT- 2008/06/13 09:00
PHST- 2008/06/13 09:00 [pubmed]
PHST- 2008/08/21 09:00 [medline]
PHST- 2008/06/13 09:00 [entrez]
PHST- 2009/03/30 00:00 [pmc-release]
AID - EJN6250 [pii]
AID - 10.1111/j.1460-9568.2008.06250.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 2008 May;27(10):2493-500. doi: 10.1111/j.1460-9568.2008.06250.x.