The distribution of a dopamine D2 receptor mRNA in rat brain

Weiner, David M.; Brann, Mark R.

doi:10.1016/0014-5793(89)80960-3

Cited by 114 publications

(70 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similar to results previously reported in the rat brain, all fIve of the dopamine receptors appear to be expressed in this region of the human brain. Further, the expression of these genes appears somewhat simi lar in the human to that seen in the rat, especially the minimal distribution of 0 1 receptor mRNA in the hip pocampus relative to the mRNAs encoding the other four receptors (Mansour et al 1991;Meador-Woodruff et al 1991;Fremeau et al 1991;Mengod et al 1991;Weiner et al 1991). These data are in reasonable agree ment, but not complete agreement, with previous bind ing results.…”

Section: Discussionsupporting

confidence: 79%

“…Although the determination of both mRNA and binding sites in some ways provide complemen tary information, the determination of dopamine recep tor mRNA distributions allows the identifIcation of specific dopaminoceptive cells. The consensus of a number of studies is that the only region that expresses all fIve of these receptor mRNAs is the hippocam pal formation; 02, 03, 04, and Os are all expressed throughout the hippocampal formation of the rat, pri marily in the pyramidal cell layer of the hippocampus and in the granular cell layer of the dentate gyrus (Tiberi et al 1991;Meador-Woodruff et al 1989Sokoloff et al 1992;O'Malley et al 1992;Najlerahim et al 1989;Weiner and Brann 1989;Mengod et al 1989;Bouthe net et al 1991;Landwehrmeyer et al 1993). 0 1 recep tor mRNA was found to be more limited in its distribu tion, being located predominantly in the ventral portion of the dentate gyrus (Mansour et al 1991;Meador Woodruff et al 1991;Fremeau et al 1991;Mengod et al 1991;Weiner et al 1991).…”

Section: Discussionmentioning

confidence: 99%

“…1991). These two receptors share similar pharmacological profIles, although they have distinct anatomical distributions (Mansour et al 1991;Meador Woodruff et al 1991Fremeau et al 1991;Men god et al 1991;Weiner et al 1991;Tiberi et al 1991).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Dopamine Receptor Gene Expression in the Human Medial Temporal Lobe

Meador‐Woodruff

Grandy

Tol

et al. 1994

Neuropsychopharmacol

150

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Dopamine Receptor Gene Expression in the Human Medial Temporal Lobe

Meador‐Woodruff

Grandy

Tol

et al. 1994

Neuropsychopharmacol

150

View full text Add to dashboard Cite

“…Presently, there are no pharmacological agents available to distinguish D 1 receptors from D 5 receptors. However, neither D 1 receptor mRNA nor protein has been found in DA cell bodies (Weiner et al, 1991;Yung et al, 1995) Interestingly, the effect on NMDAR EPSCs induced by SKF81297 developed during the drug application and did not require a period of washout (Fig. 2 B).…”

Section: Effects Of Dopamine Reuptake Inhibitors Agonists and Antagmentioning

confidence: 95%

Cocaine Enhances NMDA Receptor-Mediated Currents in Ventral Tegmental Area Cells via Dopamine D₅Receptor-Dependent Redistribution of NMDA Receptors

et al. 2006

View full text Add to dashboard Cite

Cocaine-induced plasticity of glutamatergic synaptic transmission in the ventral tegmental area (VTA) plays an important role in brain adaptations that promote addictive behaviors. However, the mechanisms responsible for triggering these synaptic changes are unknown. Here, we examined the effects of acute cocaine application on glutamatergic synaptic transmission in rat midbrain slices. Cocaine caused a delayed increase in NMDA receptor (NMDAR)-mediated synaptic currents in putative VTA dopamine (DA) cells. This effect was mimicked by a specific DA reuptake inhibitor and by a DA D 1 /D 5 receptor agonist. The effect of cocaine was blocked by a DA D 1 /D 5 receptor antagonist as well as by inhibitors of the cAMP/cAMP-dependent protein kinase A (PKA) pathway. Furthermore, biochemical analysis showed an increase in the immunoreactivity of the NMDAR subunits NR1 and NR2B and their redistribution to the synaptic membranes in VTA neurons. Accordingly, NMDAR-mediated EPSC decay time kinetics were significantly slower after cocaine, suggesting an increased number of NR2B-containing NMDARs. Finally, pharmacological analysis indicates that NR2B subunits might be incorporated in triheteromeric NR1/NR2A/NR2B complexes rather than in "pure" NR1/NR2B NMDA receptors. Together, our data suggest that acute cocaine increases NMDAR function in the VTA via activation of the cAMP/PKA pathway mediated by a DA D 5 -like receptor, leading to the insertion of NR2B-containing NMDARs in the membrane. These results provide a potential mechanism by which acute cocaine promotes synaptic plasticity of VTA neurons, which could ultimately lead to the development of addictive behaviors.

show abstract

“…Particularly unclear is the extent to which D 1 receptors within the striatum versus extrastriatal D 1 receptors contribute to this phenomenon. Although virtually all striatal cholinergic interneurons express D 2 receptor mRNA in high abundance, only a fraction of these cells are reported to express low levels of D 1 receptor mRNA (Le Moine et al, 1990Moine et al, , 1991Weiner et al, 1991). Studies of ACh release using in vitro striatal slice preparations are primarily negative or equivocal, generally reporting no detectable D 1 receptor-mediated modulation of ACh output in this situation (Scatton, 1982;Consolo et al, 1987;Dolezal et al, 1992;Tedford et al, 1992).…”

Section: Dopamine D 1 Receptor; In Vivo Microdialysismentioning

confidence: 99%

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Abercrombie

Deboer

1997

J. Neurosci.

View full text Add to dashboard Cite

Dopamine release can regulate striatal acetylcholine efflux in vivo through at least two receptor mechanisms: (1) direct inhibition by dopamine D 2 receptors on the cholinergic neurons, and (2) excitation initiated by dopamine D 1 receptors. The neuroanatomical locus of the latter population of D 1 receptors and the pathway(s) involved in the expression of their influence are controversial issues. We have tested the hypothesis that D 1 receptors in substantia nigra pars reticulata are involved in the excitatory component of dopaminergic actions on striatal acetylcholine output. In vivo microdialysis was used in awake rats. Infusion of the selective D 1 receptor agonist R(ϩ)-1-Phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol (SKF 38393) hydrochloride into pars reticulata of substantia nigra elicited a significant increase in striatal acetylcholine efflux. Likewise, D-amphetamine applied into pars reticulata of substantia nigra by reverse dialysis produced an elevation in acetylcholine output measured at a second microdialysis probe in the striatum. Application of D-amphetamine in the striatum by reverse dialysis elicited a decrease in striatal acetylcholine efflux that could be reversed subsequently by local application of Damphetamine in substantia nigra pars reticulata. A 2 mg/kg intraperitoneal dose of D-amphetamine, which has no net effect on striatal acetylcholine output under control conditions, elicited a significant decrease in acetylcholine efflux when the D 1 receptor antagonist R(ϩ)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SCH 23390) hydrochloride was applied simultaneously via a second microdialysis probe in substantia nigra pars reticulata. Thus, an excitatory D 1 -mediated influence on striatal acetylcholine output is initiated in substantia nigra pars reticulata, and this influence contributes to the effects of indirect dopaminergic agonists such as D-amphetamine on striatal acetylcholine efflux. These results indicate an important role of somatodendritic dopamine release, in addition to nerve terminal dopamine release, in the regulation of activity in basal ganglia circuits.

show abstract

The distribution of a dopamine D2 receptor mRNA in rat brain

Cited by 114 publications

References 31 publications

Dopamine Receptor Gene Expression in the Human Medial Temporal Lobe

Dopamine Receptor Gene Expression in the Human Medial Temporal Lobe

Cocaine Enhances NMDA Receptor-Mediated Currents in Ventral Tegmental Area Cells via Dopamine D₅Receptor-Dependent Redistribution of NMDA Receptors

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Contact Info

Product

Resources

About

The distribution of a dopamine D2 receptor mRNA in rat brain

Cited by 114 publications

References 31 publications

Dopamine Receptor Gene Expression in the Human Medial Temporal Lobe

Dopamine Receptor Gene Expression in the Human Medial Temporal Lobe

Cocaine Enhances NMDA Receptor-Mediated Currents in Ventral Tegmental Area Cells via Dopamine D5Receptor-Dependent Redistribution of NMDA Receptors

Substantia Nigra D1Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Contact Info

Product

Resources

About

Cocaine Enhances NMDA Receptor-Mediated Currents in Ventral Tegmental Area Cells via Dopamine D₅Receptor-Dependent Redistribution of NMDA Receptors

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism