PMID- 8098647
OWN - NLM
STAT- MEDLINE
DCOM- 19930621
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 608
IP  - 1
DP  - 1993 Apr 9
TI  - Prenatal cocaine administration stimulates fetal brain tyrosine hydroxylase 
      activity.
PG  - 129-37
AB  - Functional effects of prenatal cocaine exposure may be mediated in part by 
      changes in catecholaminergic development. The present study examined whether 
      cocaine administration influenced fetal brain activity of tyrosine hydroxylase 
      (TH), the rate-limiting enzyme in catecholamine biosynthesis. Subcutaneous (s.c.) 
      injection of pregnant rats with 40 mg/kg of cocaine HCl daily from gestational 
      day (GD) 8 to GD20 resulted in an 8.7% stimulation of fetal whole-brain TH 
      activity compared to controls. We then switched to a s.c. implantation procedure 
      involving Silastic capsules filled with 80 mg of cocaine base dissolved in 
      polyethylene glycol (PEG). Implantation of 2 such capsules on GD18 produced a 28% 
      increase in fetal TH activity measured only 3 days later on GD21. Subsequent 
      experiments demonstrated that GD14 implantation was equally effective in 
      stimulating fetal TH activity on GD17, but that the enzyme was unaffected in the 
      brains of the treated dams. When cocaine-containing capsules were implanted on 
      GD18, removed on GD21, and the females were allowed to deliver normally, 
      offspring TH activity was still elevated on postnatal day 10 but not later. 
      Finally, the presence of cocaine implants from GD18 to GD21 had no influence on 
      fetal brain neurotransmitter and metabolite concentrations, however, the treated 
      dams exhibited significant reductions in dopamine (DA) and the serotonin 
      metabolite, 5-hydroxyindoleacetic acid. We conclude that maternal cocaine 
      implants rapidly but transiently stimulate TH activity in the fetal brain, and 
      that such stimulation prevented the DA depletion observed in the dams.
FAU - Meyer, J S
AU  - Meyer JS
AD  - Department of Psychology, University of Massachusetts, Amherst 01003.
FAU - Dupont, S A
AU  - Dupont SA
LA  - eng
GR  - DA06495/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - I5Y540LHVR (Cocaine)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - 3,4-Dihydroxyphenylacetic Acid/metabolism
MH  - Animals
MH  - Brain/*drug effects/embryology/enzymology
MH  - Cocaine/*administration & dosage
MH  - Dopamine/metabolism
MH  - Embryonic and Fetal Development/drug effects
MH  - Female
MH  - Maternal-Fetal Exchange/*physiology
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Tyrosine 3-Monooxygenase/*drug effects
EDAT- 1993/04/09 00:00
MHDA- 1993/04/09 00:01
CRDT- 1993/04/09 00:00
PHST- 1993/04/09 00:00 [pubmed]
PHST- 1993/04/09 00:01 [medline]
PHST- 1993/04/09 00:00 [entrez]
AID - 0006-8993(93)90783-J [pii]
AID - 10.1016/0006-8993(93)90783-j [doi]
PST - ppublish
SO  - Brain Res. 1993 Apr 9;608(1):129-37. doi: 10.1016/0006-8993(93)90783-j.