Dopamine Control of Gene Expression in Basal Ganglia Nuclei: Striatal and Nonstriatal Mechanisms

Mf, Chesselet; Delfs, Jill M.; MacKenzie, Larami

doi:10.1016/s1054-3589(08)60838-8

Cited by 5 publications

(6 citation statements)

References 6 publications

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“…On one hand, D 2 receptor activation is known to increase striatal calcineurin and MAP kinase activity via Ca 2ϩdependent mechanisms (Nishi et al, 1997;Yan et al, 1999). On the other hand, blockade of D 2 receptors or diminished D 2 receptor tone is known to increase striatal immediate early gene (IEG) and peptide expression (Chesselet et al, 1998). D 2 receptor activation also is necessary for certain forms of striatal use-dependent synaptic plasticity (Calabresi et al, 1992).…”

Section: Discussion D 2 Receptors In Striatal Medium Spiny Neurons Acmentioning

confidence: 99%

“…First, dopamine-depleting lesions increase striatal expression of enkephalin, a peptide released by medium spiny neurons expressing D 2 receptors (Gerfen, 1992). Second, neuroleptic blockade of D 2 receptors increases striatal expression of immediate early genes and glutamic acid decarboxylase (Chesselet et al, 1998). These changes are taken as evidence of D 2 receptor-mediated suppression of neural activity and gene transcription.…”

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confidence: 99%

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D₂Dopamine Receptors in Striatal Medium Spiny Neurons Reduce L-Type Ca²⁺Currents and Excitability via a Novel PLCβ1–IP₃–Calcineurin-Signaling Cascade

Tkatch²,

et al. 2000

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In spite of the recognition that striatal D(2) receptors are critical determinants in a variety of psychomotor disorders, the cellular mechanisms by which these receptors shape neuronal activity have remained a mystery. The studies presented here reveal that D(2) receptor stimulation in enkephalin-expressing medium spiny neurons suppresses transmembrane Ca(2+) currents through L-type Ca(2+) channels, resulting in diminished excitability. This modulation is mediated by G(beta)(gamma) activation of phospholipase C, mobilization of intracellular Ca(2+) stores, and activation of the calcium-dependent phosphatase calcineurin. In addition to providing a unifying mechanism to explain the apparently divergent effects of D(2) receptors in striatal medium spiny neurons, this novel signaling linkage provides a foundation for understanding how this pivotal receptor shapes striatal excitability and gene expression.

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Section: Discussion D 2 Receptors In Striatal Medium Spiny Neurons Acmentioning

confidence: 99%

mentioning

confidence: 99%

D₂Dopamine Receptors in Striatal Medium Spiny Neurons Reduce L-Type Ca²⁺Currents and Excitability via a Novel PLCβ1–IP₃–Calcineurin-Signaling Cascade

Tkatch²,

et al. 2000

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“…Post-synaptic NMDA receptors modulate D 2 -like antagonist-induced H3 phospho-acetylation in striatal neurons Previous studies demonstrated that blockade of D 2 -like receptors in striatal neurons induces gene expression through synergistic interaction of cAMP-PKA signaling and glutamatergic input emanating from the cerebral cortex and subcortical areas (Boegman and Vincent 1996;Konradi et al 1996;Chesselet et al 1998;de Souza and Meredith 1999;Hussain et al 2001). It is thought that glutamatergic signaling activates NMDA receptors that, in turn, regulate voltageoperated Ca 2+ channels (Rajadhyaksha et al 1999).…”

Section: Blockade Of D 2 -Like Receptors Induces Global H3 Phospho-acmentioning

confidence: 99%

Dopamine D₂‐like antagonists induce chromatin remodeling in striatal neurons through cyclic AMP‐protein kinase A and NMDA receptor signaling

Guo

Schroeder³

et al. 2004

Journal of Neurochemistry

136

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Antipsychotic drugs regulate gene transcription in striatal neurons by blocking dopamine D 2 -like receptors. Little is known about the underlying changes in chromatin structure, including covalent modifications at histone N-terminal tails that are epigenetic regulators of gene expression. We show that treatment with D 2 -like antagonists rapidly induces the phosphorylation of histone H3 at serine 10 and the acetylation of H3-lysine 14 in bulk chromatin from striatum and in nuclei of striatal neurons. We find that, in vivo, D 2 -like antagonistinduced H3 phospho-acetylation is inhibited by the NMDA receptor antagonist MK-801 and by the protein kinase A (PKA) inhibitor Rp-adenosine 3c¢,5c¢-cyclic monophosphorothioate triethylammonium salt but increased by the PKA activator Sp-adenosine 3c¢,5c¢-cyclic monophosphorothioate triethylammonium salt. Furthermore, in dissociated striatal cultures which lack midbrain and cortical pre-synaptic inputs, H3 phospho-acetylation was induced by glutamate, L- Robertson et al. 1991;Nguyen et al. 1992;Deutch et al. 1996) followed by increased transcription of neuropeptides, second and third messenger molecules, receptors, ion channels and other neurotransmission-related molecules (Merchant and Dorsa 1993;Fox et al. 1994;Delfs et al. 1995;Fitzgerald et al. 1995;Laprade and Soghomonian 1995;Schoots et al. 1995;Doucet et al. 1996;Moratalla et al. 1996;Eastwood et al. 1997;Healy and Meador-Woodruff 1997;Mijnster et al. 1998; Atkins et al. Abbreviations used: cAMP-PKA, cAMP-dependent protein kinase A; Rp-cAMPs, Rp-Adenosine 3c¢,5c¢-cyclic monophosphorothioate triethylammonium salt; Sp-cAMPs, Sp-Adenosine 3c¢,5c¢-cyclic monophosphorothioate triethylammonium salt.

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“…This aberrant high-frequency discharge is thought to be a critical determinant in the emergence of tremor and rigidity in Parkinson's disease (Taha et al, 1996;Wichmann and DeL ong, 1996). In rats that followed similar manipulations in dopamine levels, Kv3.1 mRNA is upregulated in GP neurons (Chesselet et al, 1998). This upregulation can be expected to alter the ratio of rapidly deactivating (Kv3.1/3.2) channels to slowly deactivating Kv2.1 channels in GP neurons.…”

Section: Slowly Deactivating Currents Are Attributable To Kv21 Channelsmentioning

confidence: 99%

Delayed Rectifier Currents in Rat Globus Pallidus Neurons Are Attributable to Kv2.1 and Kv3.1/3.2 K⁺Channels

1999

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The symptoms of Parkinson disease are thought to result in part from increased burst activity in globus pallidus neurons. To gain a better understanding of the factors governing this activity, we studied delayed rectifier K(+) conductances in acutely isolated rat globus pallidus (GP) neurons, using whole-cell voltage-clamp and single-cell RT-PCR techniques. From a holding potential of -40 mV, depolarizing voltage steps in identified GP neurons evoked slowly inactivating K(+) currents. Analysis of the tail currents revealed rapidly and slowly deactivating currents of similar amplitude. The fast component of the current deactivated with a time constant of 11. 1 +/- 0.8 msec at -40 mV and was blocked by micromolar concentrations of 4-AP and TEA (K(D) approximately 140 microM). The slow component of the current deactivated with a time constant of 89 +/- 10 microseconds at -40 mV and was less sensitive to TEA (K(D) = 0.8 mM) and 4-AP (K(D) approximately 6 mM). Organic antagonists of Kv1 family channels had little or no effect on somatic currents. These properties are consistent with the hypothesis that the rapidly deactivating current is attributable to Kv3.1/3.2 channels and the slowly deactivating current to Kv2.1-containing channels. Semiquantitative single-cell RT-PCR analysis of Kv3 and Kv2 family mRNAs supported this conclusion. An alteration in the balance of these two channel types could underlie the emergence of burst firing after dopamine-depleting lesions.

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Dopamine Control of Gene Expression in Basal Ganglia Nuclei: Striatal and Nonstriatal Mechanisms

Cited by 5 publications

References 6 publications

D₂Dopamine Receptors in Striatal Medium Spiny Neurons Reduce L-Type Ca²⁺Currents and Excitability via a Novel PLCβ1–IP₃–Calcineurin-Signaling Cascade

D₂Dopamine Receptors in Striatal Medium Spiny Neurons Reduce L-Type Ca²⁺Currents and Excitability via a Novel PLCβ1–IP₃–Calcineurin-Signaling Cascade

Dopamine D₂‐like antagonists induce chromatin remodeling in striatal neurons through cyclic AMP‐protein kinase A and NMDA receptor signaling

Delayed Rectifier Currents in Rat Globus Pallidus Neurons Are Attributable to Kv2.1 and Kv3.1/3.2 K⁺Channels

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Dopamine Control of Gene Expression in Basal Ganglia Nuclei: Striatal and Nonstriatal Mechanisms

Cited by 5 publications

References 6 publications

D2Dopamine Receptors in Striatal Medium Spiny Neurons Reduce L-Type Ca2+Currents and Excitability via a Novel PLCβ1–IP3–Calcineurin-Signaling Cascade

D2Dopamine Receptors in Striatal Medium Spiny Neurons Reduce L-Type Ca2+Currents and Excitability via a Novel PLCβ1–IP3–Calcineurin-Signaling Cascade

Dopamine D2‐like antagonists induce chromatin remodeling in striatal neurons through cyclic AMP‐protein kinase A and NMDA receptor signaling

Delayed Rectifier Currents in Rat Globus Pallidus Neurons Are Attributable to Kv2.1 and Kv3.1/3.2 K+Channels

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D₂Dopamine Receptors in Striatal Medium Spiny Neurons Reduce L-Type Ca²⁺Currents and Excitability via a Novel PLCβ1–IP₃–Calcineurin-Signaling Cascade

D₂Dopamine Receptors in Striatal Medium Spiny Neurons Reduce L-Type Ca²⁺Currents and Excitability via a Novel PLCβ1–IP₃–Calcineurin-Signaling Cascade

Dopamine D₂‐like antagonists induce chromatin remodeling in striatal neurons through cyclic AMP‐protein kinase A and NMDA receptor signaling

Delayed Rectifier Currents in Rat Globus Pallidus Neurons Are Attributable to Kv2.1 and Kv3.1/3.2 K⁺Channels