Dopamine D1-like receptors are directly involved in the generation of reward-related signals
in the brain. In drug-naïve animals, selective stimulation of D1 receptors is sufficient to support acquisition and maintenance of self-administration
behavior (
1
). Blockade of D1 receptors strongly attenuates the rewarding effects of psychostimulant drugs such
as cocaine and amphetamine, and D1 receptor knockout mice fail to acquire cocaine self-administration behavior (
1
). D1 receptors are positively coupled to stimulatory G proteins and adenylate cyclase,
and can facilitate excitatory input to D1-expressing neurons in striatal reward regions. Drug-naïve rodents self-administer
direct optogenetic excitation of D1-containing striatal neurons, essentially bypassing D1 receptor effects (
2
). In contrast to D1 receptors, selective stimulation of D2-like receptors fails to engender primary rewarding effects in drug-naïve rodents,
but it can facilitate the conditioned rewarding effects of environmental stimuli associated
with prior drug self-administration (
1
,
3
).To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
April 16,
2014
Identification
Copyright
© 2014 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
ScienceDirect
Access this article on ScienceDirectLinked Article
- Diminished Role of Dopamine D1-Receptor Signaling with the Development of an Addicted Phenotype in RatsBiological PsychiatryVol. 76Issue 1
- PreviewAlthough considerable evidence implicates dopamine D1-receptor signaling in the nucleus accumbens in motivation for cocaine during early stages of addiction, less is known with regard to its role after the development of addiction. Here, we examined its role in the development of an addicted phenotype in intact male and female rats, and in female rats that were either resistant or vulnerable to developing this phenotype.
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