Dopamine D5 receptor immunolocalization in rat and monkey brain

Ciliax, Brian J.; Nash, Norman R.; Heilman, Craig J.; Sunahara, Roger K.; Hartney, Anne; Tiberi, Mario; Rye, David B.; Caron, Marc G.; Niznik, Hyman B.; Levey, Aĺlan I.

doi:10.1002/1098-2396(200008)37:2<125::aid-syn7>3.0.co;2-7

Cited by 194 publications

(105 citation statements)

References 59 publications

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“…Anatomical evidence suggests that any postsynaptic effect of mixed D 1 /D 5 agents in midbrain DA cells is likely mediated via DA D 5 receptors. D 5 receptors are present on cell bodies in the VTA and substantia nigra (Ciliax et al, 2000;Khan et al, 2000), and they localize postsynaptically on tyrosine hydroxylase-positive neurons (Kahn et al, 2000). In contrast, no 4 synaptic vesicle-enriched (LP2) fractions from saline (S) or 30 min after intraperitoneal injection of cocaine (C; 15 mg/kg), resolved by SDS-PAGE (50 g per lane).…”

Section: Discussionmentioning

confidence: 69%

“…DA neurons in the midbrain have been shown to express DA D 5 receptors (Ciliax et al, 2000;Khan et al, 2000), suggesting that cocaine-induced increase in extracellular DA results in stimulation of postsynaptic DA D 5 receptors. Presently, there are no pharmacological agents available to distinguish D 1 receptors from D 5 receptors.…”

Section: Effects Of Dopamine Reuptake Inhibitors Agonists and Antagmentioning

confidence: 99%

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

et al. 2006

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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.

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Section: Discussionmentioning

confidence: 69%

Section: Effects Of Dopamine Reuptake Inhibitors Agonists and Antagmentioning

confidence: 99%

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

et al. 2006

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“…These rarely occurring SSCs in nonpyramidal neurons were never seen in association with DARs [see Khan et al (2001) for D 2 R, Muly et al (1998) for D 1 R]. In addition, both the D 5 R protein and D 5 R mRNA are localized predominantly in pyramidal neurons (Bergson et al, 1995a;Ariano et al, 1997;Ciliax et al, 2000). Therefore, in the following sections, we describe the subcellular expression patterns of DAR subtypes in the pyramidal perisomatic region.…”

Section: Resultsmentioning

confidence: 99%

Microdomains for Dopamine Volume Neurotransmission in Primate Prefrontal Cortex

Paspalas¹

2004

Journal of Neuroscience

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The explicit yet enigmatic involvement of dopamine in cortical physiology is in part volumetric (beyond the synapse), as is apparently the action of neuroleptics targeting dopamine receptors. The notion that nonsynaptic neuronal membranes would translate extracellular dopamine into receptor-specific spatiotemporal downstream signaling, similar to the chemical synapse, is intriguing. Here, we report that dopamine D 5 (but not D 1 or D 2 ) receptors in the perisomatic plasma membrane of prefrontal cortical neurons form discrete and exclusively extrasynaptic microdomains with inositol 1,4,5-trisphosphate-gated calcium stores of subsurface cisterns and mitochondria. These findings introduce a novel dopaminoceptive substratum in the brain and a unique D 5 receptor-specific signaling paradigm.

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“…The density of D 1 receptors is considerably higher than D 2 receptors throughout the cortex with differential distribution in the rat mPFC (Vincent et al, 1995), and low levels of D 2 receptors have been detected in the hippocampus (Meador-Woodruff et al, 1989;Levey et al, 1993). The majority of dopamine receptors in the hippocampus are from the D 1 -like subfamily of receptors (Dawson et al, 1986), with a high density of the D 5 receptor (Ciliax et al, 2000). Furthermore, it has been reported that administration of SKF-38393 increased hippocampal acetylcholine (ACh) release in young and aged rats (Hersi et al, 1995), which improved performance in the Morris water maze, thus suggesting a mechanism for the cognitive enhancing effects of SKF-38393.…”

Section: Discussionmentioning

confidence: 99%

D1-like receptor activation improves PCP-induced cognitive deficits in animal models: Implications for mechanisms of improved cognitive function in schizophrenia

McLean

Idris

Woolley

et al. 2009

European Neuropsychopharmacology

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Phencyclidine (PCP) produces cognitive deficits of relevance to schizophrenia in animal models. The aim was to investigate the efficacy of the D 1 -like receptor agonist, SKF-38393, to improve PCP-induced deficits in the novel object recognition (NOR) and operant reversal learning (RL) tasks. Rats received either sub-chronic PCP (2 mg/kg) or vehicle for 7 days, followed by a 7-day washout. Rats were either tested in NOR or the RL tasks. In NOR vehicle rats successfully discriminated between novel and familiar objects, an effect abolished in PCP-treated rats. SKF-

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Dopamine D5 receptor immunolocalization in rat and monkey brain

Cited by 194 publications

References 59 publications

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

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

Microdomains for Dopamine Volume Neurotransmission in Primate Prefrontal Cortex

D1-like receptor activation improves PCP-induced cognitive deficits in animal models: Implications for mechanisms of improved cognitive function in schizophrenia

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Dopamine D5 receptor immunolocalization in rat and monkey brain

Cited by 194 publications

References 59 publications

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

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

Microdomains for Dopamine Volume Neurotransmission in Primate Prefrontal Cortex

D1-like receptor activation improves PCP-induced cognitive deficits in animal models: Implications for mechanisms of improved cognitive function in schizophrenia

Contact Info

Product

Resources

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

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