Plasticity in striatal dopamine release is governed by release-independent depression and the dopamine transporter

Condon, Mark D.; Platt, Nicola J.; Zhang, Yan-Feng; Roberts, Bradley M.; Clements, Michael A.; Vietti‐Michelina, Stefania; Tseu, Min-Yee; Brimblecombe, Katherine R.; Threlfell, Sarah; Mann, Edward O.; Cragg, Stephanie J.

doi:10.1038/s41467-019-12264-9

Cited by 63 publications

(58 citation statements)

References 72 publications

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“…The DA system is therefore also sensitive to a local presynaptic modulation from other neurotransmitters (like acetylcholine or endocannabinoids) ( Xu et al., 2018 ). DAT exerts a main presynaptic master control on DA release as recently demonstrated ( Condon et al., 2019 ; Walters et al., 2020 ). DA release is in fact directly modulated at the presynaptic terminals by a Rho-dependent internalization of DAT.…”

Section: Section 1: Dopamine Receptorsmentioning

confidence: 79%

Dopamine Receptor Subtypes, Physiology and Pharmacology: New Ligands and Concepts in Schizophrenia

Martel¹,

McArthur²

2020

Front. Pharmacol.

177

125

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Dopamine receptors are widely distributed within the brain where they play critical modulator roles on motor functions, motivation and drive, as well as cognition. The identification of five genes coding for different dopamine receptor subtypes, pharmacologically grouped as D1- (D1 and D5) or D2-like (D2S, D2L, D3, and D4) has allowed the demonstration of differential receptor function in specific neurocircuits. Recent observation on dopamine receptor signaling point at dopamine—glutamate-NMDA neurobiology as the most relevant in schizophrenia and for the development of new therapies. Progress in the chemistry of D1- and D2-like receptor ligands (agonists, antagonists, and partial agonists) has provided more selective compounds possibly able to target the dopamine receptors homo and heterodimers and address different schizophrenia symptoms. Moreover, an extensive evaluation of the functional effect of these agents on dopamine receptor coupling and intracellular signaling highlights important differences that could also result in highly differentiated clinical pharmacology. The review summarizes the recent advances in the field, addressing the relevance of emerging new targets in schizophrenia in particular in relation to the dopamine – glutamate NMDA systems interactions.

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Section: Section 1: Dopamine Receptorsmentioning

confidence: 79%

Dopamine Receptor Subtypes, Physiology and Pharmacology: New Ligands and Concepts in Schizophrenia

Martel¹,

McArthur²

2020

Front. Pharmacol.

177

125

View full text Add to dashboard Cite

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“…GABA B receptor activation slightly promotes the ratio of evoked DA release by high-frequency trains over single pulse release (see Figure 1 ) [ 36 , 37 , 39 ], consistent with a reduction in the initial release probability of DA, and consequently, a slight relief of short-term depression. We have recently revealed that mechanisms that determine axonal excitability, particularly potassium-dependent processes, strongly gate short-term plasticity of DA release [ 82 ]. Tonic activation of GABA B receptors on DA axons might plausibly provide a persistent axonal permeability to potassium through activation of Kir3-type potassium channels, and we therefore hypothesise that tonic GABA B activity might facilitate changes to short-term plasticity of DA release in response to conditions that change the driving force on potassium entry.…”

Section: Gaba B Receptor Modulation Of Da Axonamentioning

confidence: 99%

Axonal Modulation of Striatal Dopamine Release by Local γ-Aminobutyric Acid (GABA) Signalling

Roberts

Lopes

Cragg

2021

Cells

Self Cite

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Striatal dopamine (DA) release is critical for motivated actions and reinforcement learning, and is locally influenced at the level of DA axons by other striatal neurotransmitters. Here, we review a wealth of historical and more recently refined evidence indicating that DA output is inhibited by striatal γ-aminobutyric acid (GABA) acting via GABAA and GABAB receptors. We review evidence supporting the localisation of GABAA and GABAB receptors to DA axons, as well as the identity of the striatal sources of GABA that likely contribute to GABAergic modulation of DA release. We discuss emerging data outlining the mechanisms through which GABAA and GABAB receptors inhibit the amplitude as well as modulate the short-term plasticity of DA release. Furthermore, we highlight recent data showing that DA release is governed by plasma membrane GABA uptake transporters on striatal astrocytes, which determine ambient striatal GABA tone and, by extension, the tonic inhibition of DA release. Finally, we discuss how the regulation of striatal GABA-DA interactions represents an axis for dysfunction in psychomotor disorders associated with dysregulated DA signalling, including Parkinson’s disease, and could be a novel therapeutic target for drugs to modify striatal DA output.

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“…Mounting evidence has demonstrated that DAT represents a critical regulator of terminal release and plasticity via regulation of the temporal dynamics of dopamine in the extracellular space (Condon, Platt, & Zhang, 2019). DAT is a low capacity, high affinity transporter expressed on dopamine neurons and can be found on dopamine cell bodies, their dendrites, and their axonal projections (Ciliax et al., 1995; Freed et al., 1995).…”

Section: Homosynaptic Regulation At the Terminalmentioning

confidence: 99%

Direct dopamine terminal regulation by local striatal microcircuitry

Nolan

Zachry

Johnson

et al. 2020

Journal of Neurochemistry

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Regulation of axonal dopamine release by local microcircuitry is at the hub of several biological processes that govern the timing and magnitude of signaling events in reward-related brain regions. An important characteristic of dopamine release from axon terminals in the striatum is that it is rapidly modulated by local regulatory mechanisms. These processes can occur via homosynaptic mechanisms-such How to cite this article: NolanSO, Zachry JF, Johnson AR,

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Plasticity in striatal dopamine release is governed by release-independent depression and the dopamine transporter

Cited by 63 publications

References 72 publications

Dopamine Receptor Subtypes, Physiology and Pharmacology: New Ligands and Concepts in Schizophrenia

Dopamine Receptor Subtypes, Physiology and Pharmacology: New Ligands and Concepts in Schizophrenia

Axonal Modulation of Striatal Dopamine Release by Local γ-Aminobutyric Acid (GABA) Signalling

Direct dopamine terminal regulation by local striatal microcircuitry

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