ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Dopamine D1/D5 receptor modulates state-dependent switching of soma-dendritic Ca2+ potentials via differential protein kinase A and C activation in rat prefrontal cortical neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 77 citations in OpenAlex.
- Article
- Illusions, Delusions, and Your Backwards Bayesian Brain: A Biased Visual Perspective.Brain, behavior and evolution · 2020Review
- A Schizophrenia-Related Deletion Leads to KCNQ2-Dependent Abnormal Dopaminergic Modulation of Prefrontal Cortical Interneuron Activity.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Methamphetamine blunts Ca(2+) currents and excitatory synaptic transmission through D1/5 receptor-mediated mechanisms in the mouse medial prefrontal cortex.Addiction biology · 2016Article
- Dopamine modulation of transient receptor potential vanilloid type 1 (TRPV1) receptor in dorsal root ganglia neurons.The Journal of physiology · 2016Article
- Article
- Differential regulation of CaV1.2 channels by cAMP-dependent protein kinase bound to A-kinase anchoring proteins 15 and 79/150.The Journal of general physiology · 2014Article
- Article
- Review
- Rapid dopaminergic and GABAergic modulation of calcium and voltage transients in dendrites of prefrontal cortex pyramidal neurons.The Journal of physiology · 2012Article
- D1 receptor modulation of action potential firing in a subpopulation of layer 5 pyramidal neurons in the prefrontal cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Synaptic activity unmasks dopamine D2 receptor modulation of a specific class of layer V pyramidal neurons in prefrontal cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Predictive features of persistent activity emergence in regular spiking and intrinsic bursting model neurons.PLoS computational biology · 2012Article
- Dopamine receptor signaling and current and future antipsychotic drugs.Handbook of experimental pharmacology · 2012Review
- Pharmacology of signaling induced by dopamine D(1)-like receptor activation.Pharmacology & therapeutics · 2010Review
- Gene expression changes in the medial prefrontal cortex and nucleus accumbens following abstinence from cocaine self-administration.BMC neuroscience · 2010Article
- Dopamine modulates an mGluR5-mediated depolarization underlying prefrontal persistent activity.Nature neuroscience · 2009Article
- Carbon nanotubes might improve neuronal performance by favouring electrical shortcuts.Nature nanotechnology · 2009Article
- The neuropsychopharmacology of fronto-executive function: monoaminergic modulation.Annual review of neuroscience · 2009Review
- The role of the striatum in aversive learning and aversive prediction errors.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2008Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To determine the nature of dopamine modulation of dendritic Ca2+ signaling in layers V-VI prefrontal cortex (PFC) neurons, whole-cell Ca2+ potentials were evoked after blockade of Na+ and K+ channels. Soma-dendritic Ca2+ spikes evoked by suprathreshold depolarizing pulses, which could be terminated by superimposed brief intrasomatic hyperpolarizing pulses, are blocked by the L-type Ca2+ channel antagonist nimodipine (1 microM). The D1/D5 receptor agonist dihydrexidine (DHX) (0.01-10 microM; 5 min) or R-(+)SKF81291 (10 microM) induced a prolonged (>30 min) dose-dependent peak suppression of these Ca2+ spikes. This effect was dependent on [Ca2+]i- and protein kinase C (PKC)-dependent mechanisms because [Ca2+]i chelation by BAPTA or inhibition of PKC by bisindolymaleimide (BiM1), but not inhibition of [Ca2+]i release with heparin or Xestospongin C, prevented the D1-mediated suppression of Ca2+ spikes. Depolarizing pulses subthreshold to activating a Ca2+ spike evoked a nimodipine-sensitive Ca2+ "hump" potential. D1/D5 stimulation induced an N-[2-((o-bromocinamyl)amino)ethyl]-5-isoquinolinesulfonamide (H-89)- or internal PKA inhibitory peptide[5-24]-sensitive (PKA-dependent) transient (approximately 7 min) potentiation of the hump potential to full Ca2+ spike firing. Furthermore, application of DHX in the presence of the PKC inhibitor BiM1 or internal PKC inhibitory peptide[19-36] resulted in persistent firing of full Ca2+ spike bursts, suggesting that a D1/D5-PKA mechanism switches subthreshold Ca2+ hump potential to fire full Ca2+ spikes, which are eventually turned off by a D1/D5-Ca2+-dependent PKC mechanism. This depolarizing state-dependent, D1/D5-activated, bi-directional switching of soma-dendritic L-type Ca2+ channels via PKA-dependent potentiation and PKC-dependent suppression may provide spatiotemporal regulation of synaptic integration and plasticity in PFC.
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