PMID- 8601820
OWN - NLM
STAT- MEDLINE
DCOM- 19960509
LR  - 20191101
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 16
IP  - 7
DP  - 1996 Apr 1
TI  - D1 dopamine receptor activation is necessary for the induction of sensitization 
      by amphetamine in the ventral tegmental area.
PG  - 2411-20
AB  - Repeated intermittent exposure to amphetamine produces long-term enhancements in 
      the ability of this drug to produce locomotion and increase extracellular 
      dopamine (DA) in the nucleus accumbens (NAcc). Three experiments were conducted 
      to evaluate the role played by D1 DA receptors in the production of these changes 
      in response to amphetamine. Rats were preexposed to amphetamine, alone or with a 
      DA receptor antagonist, and tested for sensitization 1-3 weeks after the last 
      drug injection. On the test for sensitization, locomotor (experiments 1 and 2) 
      and NAcc DA (experiment 3) responses of the animals to a systemic amphetamine 
      injection were assessed. In the first experiment, systemic injections of the D1 
      DA receptor antagonist SCH23390, but not other DA receptor antagonists with 
      greater affinity for D2 DA and 5-HT2 receptors, blocked the development of 
      locomotor sensitization produced by systemic injections of amphetamine. In the 
      second experiment, locomotor sensitization induced by infusion of amphetamine 
      into the ventral tegmental area (VTA) was blocked when these injections were 
      preceded by systemic injections of SCH23390. Finally, in experiment three, 
      co-injecting SCH23390, but not its inactive enantiomer, with amphetamine into the 
      VTA during preexposure prevented sensitization of the NAcc DA response to this 
      drug. These results indicate that while D2 DA receptor activation is not 
      necessary for the induction of locomotor sensitization to amphetamine, D1 DA 
      receptors located in the VTA play a critical role in the development of 
      sensitized locomotor and NAcc DA response to this drug.
FAU - Vezina, P
AU  - Vezina P
AD  - Department of Psychiatry, The University of Chicago, Illinois 60637, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Amphetamines)
RN  - 0 (Receptors, Dopamine D1)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Amphetamines/*pharmacology
MH  - Animals
MH  - Behavior, Animal/drug effects
MH  - Dendrites/metabolism/ultrastructure
MH  - Dopamine/metabolism
MH  - Locomotion/drug effects
MH  - Male
MH  - Microdialysis
MH  - Microinjections
MH  - Nucleus Accumbens/drug effects/ultrastructure
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Dopamine D1/antagonists & inhibitors/*physiology
MH  - Sensitivity and Specificity
MH  - Ventral Tegmental Area/*drug effects/ultrastructure
PMC - PMC6578541
EDAT- 1996/04/01 00:00
MHDA- 1996/04/01 00:01
PMCR- 1996/10/01
CRDT- 1996/04/01 00:00
PHST- 1996/04/01 00:00 [pubmed]
PHST- 1996/04/01 00:01 [medline]
PHST- 1996/04/01 00:00 [entrez]
PHST- 1996/10/01 00:00 [pmc-release]
AID - 10.1523/JNEUROSCI.16-07-02411.1996 [doi]
PST - ppublish
SO  - J Neurosci. 1996 Apr 1;16(7):2411-20. doi: 10.1523/JNEUROSCI.16-07-02411.1996.