PMID- 2458672
OWN - NLM
STAT- MEDLINE
DCOM- 19881027
LR  - 20200106
IS  - 0736-5748 (Print)
IS  - 0736-5748 (Linking)
VI  - 4
IP  - 1
DP  - 1986
TI  - Development of specificity and stereoselectivity of rat brain dopamine receptors.
PG  - 21-6
AB  - Prenatal exposure to the neuroleptic haloperidol has been reported to produce an 
      enduring decrement in the number of dopamine D2 receptors in rat striatum and a 
      persistent diminution of a dopamine dependent behavior, stereotypy. The ontogeny 
      of rat brain dopamine binding sites has been studied in terms of the kinetic 
      properties and phenotypic specificity in rat fetal brain through early postnatal 
      development. Sites showing some properties of the D2 binding site can be found 
      prior to gestational day (GD) 18, can be labeled with [3H]dopamine or 
      [3H]spiroperidol and can be displaced with dopaminergic agonists and antagonists. 
      Saturation kinetics for specific [3H]spiroperidol has previously been found to 
      occur on or about GD 18. It is of interest that the critical period for the 
      prenatal effect of haloperidol to reduce striatal D2 binding sites, GD's 15-18, 
      coincides with the period during which dopamine binding sites lack true 
      specificity, but can be labeled with dopaminergic ligands. In these experiments 
      the development of stereoselectivity of brain dopamine binding sites has been 
      examined. When rat mothers were given either the neuroleptic (+)-butaclamol or 
      its therapeutically inactive isomer (-)-butaclamol during the critical period 
      GD's 15-18, the number of [3H]spiroperidol binding sites in striata of offspring 
      was significantly reduced by both stereoisomers. This is in marked contrast to 
      the postnatal treatment effect by a neuroleptic in which upregulation of striatal 
      D2 binding sites occurs only by treatment with the therapeutically active isomer 
      (+)-butaclamol. In vitro studies of the direct effect of the stereoisomers of 
      butaclamol indicate that the recognition sites detected during fetal brain 
      development with [3H]spiroperidol do not distinguish between the isomers of 
      butaclamol.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Miller, J C
AU  - Miller JC
AD  - Millhauser Laboratories, Department of Psychiatry, New York University School of 
      Medicine, NY 10016.
FAU - Friedhoff, A J
AU  - Friedhoff AJ
LA  - eng
GR  - 14024/PHS HHS/United States
GR  - MH 08618/MH/NIMH 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  - United States
TA  - Int J Dev Neurosci
JT  - International journal of developmental neuroscience : the official journal of the 
      International Society for Developmental Neuroscience
JID - 8401784
RN  - 0 (Dibenzocycloheptenes)
RN  - 0 (Receptors, Dopamine)
RN  - 0 (Receptors, Dopamine D2)
RN  - 4X6E73CJ0Q (Spiperone)
RN  - A7A2802VNL (Butaclamol)
SB  - IM
MH  - Animals
MH  - Butaclamol/*pharmacology
MH  - Corpus Striatum/embryology/growth & development/*metabolism
MH  - Dibenzocycloheptenes/*pharmacology
MH  - Fetus/drug effects/*metabolism
MH  - Frontal Lobe/embryology/growth & development/metabolism
MH  - Gestational Age
MH  - Male
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Receptors, Dopamine/*metabolism/physiology
MH  - Receptors, Dopamine D2
MH  - Spiperone/*metabolism
MH  - Stereoisomerism
EDAT- 1986/01/01 00:00
MHDA- 1986/01/01 00:01
CRDT- 1986/01/01 00:00
PHST- 1986/01/01 00:00 [pubmed]
PHST- 1986/01/01 00:01 [medline]
PHST- 1986/01/01 00:00 [entrez]
AID - 0736-5748(86)90012-2 [pii]
AID - 10.1016/0736-5748(86)90012-2 [doi]
PST - ppublish
SO  - Int J Dev Neurosci. 1986;4(1):21-6. doi: 10.1016/0736-5748(86)90012-2.