PMID- 8836580
OWN - NLM
STAT- MEDLINE
DCOM- 19961220
LR  - 20071114
IS  - 0165-3806 (Print)
IS  - 0165-3806 (Linking)
VI  - 94
IP  - 2
DP  - 1996 Jul 20
TI  - A1-adenosine receptor gene expression in fetal rat brain.
PG  - 205-23
AB  - Adenosine influences neurotransmitter release, neuronal excitability, and firing 
      rate, through A1-adenosine receptors (A1-R). Caffeine and related methylxanthines 
      are adenosine receptor antagonists. Exposure of developing rodents to caffeine is 
      associated with subtle, long-term changes in neurochemistry and behavior. The 
      developmental appearance of A1-R gene expression was examined in rats by in situ 
      hybridization. On gestational day (GD) 10, A1-R mRNA was expressed at very high 
      levels in placental mesometrium. Expression of A1-R mRNA in brain was first 
      detected on GD 14. Hybridization was restricted to portions of neuroepithelium, 
      caudate-putamen, piriform cortex, hypoglossal nucleus, and ventral horn of spinal 
      cord. Neuroepithelial A1-R mRNA increased in intensity and distribution at 
      subsequent ages, reaching a maximum on GD 20 (the latest age studied). 
      Hybridization signal was detected, with regional variation in intensity, 
      throughout much of the brain by GD 16, with additional increases in extent and 
      intensity through GD 20. Generally, a caudal > rostral gradient of hybridization 
      intensity was apparent. The distribution on GD 20 resembled the widespread yet 
      heterogeneous pattern observed in the adult, with high levels of A1-R gene 
      expression in cortex, hippocampus, thalamus, cerebellum, pontine nuclei, 
      brainstem motor nuclei, and spinal cord. Northern blot analysis confirmed the 
      age-related increase in abundance of A1-R transcripts (ca. 3.5 and 5.5 kb). The 
      early and widespread expression of A1-R mRNA, coupled with previous reports of 
      prenatal A1-R binding, suggests that adenosine and adenosine antagonists, 
      including caffeine, may influence neuronal differentiation, migration or 
      synaptogenesis, thus producing long-lasting effects on brain and behavior.
FAU - Weaver, D R
AU  - Weaver DR
AD  - Laboratory of Developmental Chronobiology, Massachusetts General Hospital, Boston 
      02114, USA. weaver@helix.mgh.harvard.edu
LA  - eng
GR  - HD 29470/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res Dev Brain Res
JT  - Brain research. Developmental brain research
JID - 8908639
RN  - 0 (Receptors, Purinergic P1)
SB  - IM
MH  - Animals
MH  - Blotting, Northern
MH  - Brain/embryology/*metabolism
MH  - Embryonic and Fetal Development/physiology
MH  - Gene Expression Regulation, Developmental/*physiology
MH  - Gestational Age
MH  - In Situ Hybridization
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Purinergic P1/*genetics
EDAT- 1996/07/20 00:00
MHDA- 1996/07/20 00:01
CRDT- 1996/07/20 00:00
PHST- 1996/07/20 00:00 [pubmed]
PHST- 1996/07/20 00:01 [medline]
PHST- 1996/07/20 00:00 [entrez]
AID - 0165380696000491 [pii]
PST - ppublish
SO  - Brain Res Dev Brain Res. 1996 Jul 20;94(2):205-23.