Dopaminergic Control of Corticostriatal Long-Term Synaptic Depression in Medium Spiny Neurons Is Mediated by Cholinergic Interneurons

Wang, Zhongfeng; Li, Kai; Day, Michelle; Ronesi, Jennifer A.; Yin, Henry H.; Ding, Jun; Tkatch, Tatiana; Lovinger, David M.; Surmeier, D. James

doi:10.1016/j.neuron.2006.04.010

Cited by 460 publications

(470 citation statements)

References 49 publications

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“…Using intracellular loading with the patch pipette, we also showed that inhibition of translation in the postsynaptic cell did not block striatal LTD, although the same treatment blocked a different form of LTD in the hippocampus. The latter experiment demonstrates that cycloheximide is easily loaded into the postsynaptic neuron, and we know from past studies that larger molecules, such as Alexa Fluor 594, can be loaded easily into medium spiny neurons via the patch pipette (Wang et al, 2006). Thus, the lack of effect of postsynaptic cycloheximide loading on striatal LTD is not likely attributable to the inability of the drug to reach the relevant sites in the postsynaptic neuron.…”

Section: Discussionmentioning

confidence: 81%

The Role of Protein Synthesis in Striatal Long-Term Depression

Yin¹,

Davis²,

Ronesi³

et al. 2006

J. Neurosci.

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Long-term depression (LTD) at the corticostriatal synapse is postsynaptically induced but presynaptically expressed, the depression being a result of retrograde endocannabinoid signaling that activates presynaptic cannabinoid CB 1 receptors and reduces the probability of glutamate release. To study the role of protein synthesis in striatal LTD, we used a striatum-only preparation in which the presynaptic cell body is cut off, leaving intact only its axons, whose terminals synapse on medium spiny neurons. LTD (duration Ͼ150 min) was induced in this preparation, thus providing evidence that transcription in the presynaptic cell nucleus is not necessary for this form of plasticity. The maintenance of striatal LTD, however, was blocked by bath application of protein translation inhibitors but not by the same inhibitors loaded into the postsynaptic cell. These results suggest that local translation is critical for the expression of striatal LTD, distinguishing this form of mammalian synaptic plasticity from other forms that require postsynaptic protein synthesis. Possible roles of axonal or glial translation in striatal LTD are considered.

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Section: Discussionmentioning

confidence: 81%

The Role of Protein Synthesis in Striatal Long-Term Depression

Yin¹,

Davis²,

Ronesi³

et al. 2006

J. Neurosci.

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“…It is generally agreed that this LTD depends on activation of both D1-and D2-class receptors [9]. However, opinions differ with respect to the cell types that express this plasticity (striatopallidal vs. striatonigral), the sites of dopaminergic action (spines on postsynaptic MSN vs. presynaptic cholinergic interneurons), and the signaling mechanisms [66][67]. NMDAR-dependent striatal LTP can also be induced by high-frequency stimulation of corticostriatal glutamatergic inputs.…”

Section: Functional Evidencementioning

confidence: 99%

Dopaminergic signaling in dendritic spines

Yao

Spealman

Zhang

2008

Biochemical Pharmacology

109

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Dopamine regulates movement, motivation, reward, and learning and is implicated in numerous neuropsychiatric and neurological disorders. The action of dopamine is mediated by a family of seven-transmembrane G protein-coupled receptors encoded by at least five dopamine receptor genes (D1, D2, D3, D4, and D5), some of which are major molecular targets for diverse neuropsychiatric medications. Dopamine receptors are present throughout the soma and dendrites of the neuron, but accumulating ultrastructural and biochemical evidence indicates that they are concentrated in dendritic spines, where most of the glutamatergic synapses are established. By modulating local channels, receptors, and signaling modules in spines, this unique population of postsynaptic receptors is strategically positioned to control the excitability and synaptic properties of spines and mediate both the tonic and phasic aspects of dopaminergic signaling with remarkable precision and versatility. The molecular mechanisms that underlie the trafficking, targeting, anchorage, and signaling of dopamine receptors in spines are, however, largely unknown. The present commentary focuses on this important subpopulation of postsynaptic dopamine receptors with emphases on recent molecular, biochemical, pharmacological, ultrastructural, and physiological studies that provide new insights about their regulatory mechanisms and unique roles in dopamine signaling. The Central Dopaminergic Systems: An OverviewDopamine (DA) is a prototypical slow neurotransmitter that plays pivotal roles in a variety of cognitive, motivational, neuroendocrine, and motor functions [1][2]. Two major groups of DAcontaining neurons in the mammalian brain reside in the substantia nigra pars compacta (SN) and the ventral tegmental area (VTA) [3]. SN neurons form the nigrostriatal pathway, which projects mainly to the dorsal part of striatum where they control postural reflexes and initiation of movements. VTA neurons give rise to two pathways: the mesolimbic pathway, which projects to the subcortical and limbic nuclei, and the mesocortical pathway, which projects mainly to the cingulate, entorhinal and medial prefrontal cortices. Dysfunction of dopaminergic transmission in these major pathways has been implicated in an array of neurological and neuropsychiatric disorders, including Parkinson's disease, Huntington's diseases, schizophrenia, attention-deficit hyperactivity disorder (ADHD), and drug addiction [1][2]. Drugs targeting dopaminergic mechanisms are widely used to manage these and other conditions.The action of DA is mediated by a family of seven-transmembrane G protein-coupled receptors (GPCRs) encoded by at least five DA receptor genes (D1, D2, D3, D4, and D5) in the mammalian brain [4]. These receptors are classified into two subfamilies, the D1-class and Corresponding author: Wei-Dong Yao, Ph.D., Department of Psychiatry, Harvard Medical School, Beth Israel Deaconess Medical Center, New England Primate Research Center, One Pine Hill Drive, P.O. Box 9102, Southborough,...

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“…Dopaminergic inputs to the ventral striatum arise from the ventral tegmentum (VTA) and substantia nigra (SN), which themselves are recipients of cholinergic projections from PM neurons. Activation of a variety of pre-and postsynaptic dopamine receptors strongly regulates the release of ACh and the excitability of striatal cholinergic interneurons (Maurice et al, 2004;Wang et al, 2006). In addition, local circuits of opiate peptide and GABAergic neurons influence the net levels of striatal cholinergic tone.…”

Section: A Cholinergic Pathways Within the Ventral Striatummentioning

confidence: 99%

“…Nevertheless, recent progress in dissecting the interaction of cholinergic circuits with dopaminergic and glutamatergic inputs to the striatum inspires considerable hope that we may be approaching a bona fide understanding of how ACh works at least in one region that is known to effect in schizophrenia and that is particularly high in ACh tone (see below and Cragg, 2006;Calabresi et al, 2000;Wilson, 2006;Wonnacott, 2005 for reviews; Wang et al, 2006).…”

Section: A Cholinergic Pathways Within the Ventral Striatummentioning

confidence: 99%

Cholinergic Circuits and Signaling in the Pathophysiology of Schizophrenia

Berman

Talmage

Role

2007

International Review of Neurobiology

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Central cholinergic signaling has long been associated with aspects of memory, motivation, and mood, each affected functions in neuropsychiatric disorders such as schizophrenia. In this chapter, we review evidence related to the core hypothesis that dysregulation of central cholinergic signaling contributes to the pathophysiology of schizophrenia. Although central cholinergic circuits are resistant to simplification-particularly when one tries to parse the contributions of various classes of cholinergic receptors to disease related phenomena-the potential role of ACh signaling in Schizophrenia pathophysiology deserves careful consideration for prospective therapeutics. The established role of cholinergic circuits in attentional tuning is considered along with recent work on how the patterning of cholinergic activity may modulate corticostriatal circuits affected in schizophrenia.

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Dopaminergic Control of Corticostriatal Long-Term Synaptic Depression in Medium Spiny Neurons Is Mediated by Cholinergic Interneurons

Cited by 460 publications

References 49 publications

The Role of Protein Synthesis in Striatal Long-Term Depression

The Role of Protein Synthesis in Striatal Long-Term Depression

Dopaminergic signaling in dendritic spines

Cholinergic Circuits and Signaling in the Pathophysiology of Schizophrenia

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