Calcyon Forms a Novel Ternary Complex with Dopamine D1 Receptor through PSD-95 Protein and Plays a Role in Dopamine Receptor Internalization

Ha, Chang Man; Park, Daehun; Han, Jeong Kyu; Jang, June Ill; Park, Jae Yong; Hwang, Eun Mi; Seok, Heon; Chang, Sunghoe

doi:10.1074/jbc.m112.370601

Cited by 31 publications

(28 citation statements)

References 34 publications

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“…Finally, the interaction between dopamine and glutamate neurotransmission can be mirrored by the modulation of molecules belonging to synaptic plasticity pathways, such as PSD-95, that is modulated by antipsychotics [125,126] and by selective blockade of D2 receptors [127]. PSD-95 in turn regulates D1 receptor trafficking and internalization [128,129] and inhibits D1-NMDA receptor coupling [130].…”

Section: Dopamine-glutamate Interplay At the Psd And Mirna Dysfunctiomentioning

confidence: 98%

MicroRNAs in Schizophrenia: Implications for Synaptic Plasticity and Dopamine–Glutamate Interaction at the Postsynaptic Density. New Avenues for Antipsychotic Treatment Under a Theranostic Perspective

et al. 2014

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Despite dopamine-glutamate aberrant interaction that has long been considered a relevant landmark of psychosis pathophysiology, several aspects of these two neurotransmitters reciprocal interaction remain to be defined. The emerging role of postsynaptic density (PSD) proteins at glutamate synapse as a molecular "lego" making a functional hub where different signals converge may add a new piece of information to understand how dopamine-glutamate interaction may work with regard to schizophrenia pathophysiology and treatment. More recently, compelling evidence suggests a relevant role for microRNA (miRNA) as a new class of dopamine and glutamate modulators with regulatory functions in the reciprocal interaction of these two neurotransmitters. Here, we aimed at addressing the following issues: (i) Do miRNAs have a role in schizophrenia pathophysiology in the context of dopamine-glutamate aberrant interaction? (ii) If miRNAs are relevant for dopamine-glutamate interaction, at what level this modulation takes place? (iii) Finally, will this knowledge open the door to innovative diagnostic and therapeutic tools? The biogenesis of miRNAs and their role in synaptic plasticity with relevance to schizophrenia will be considered in the context of dopamine-glutamate interaction, with special focus on miRNA interaction with PSD elements. From this framework, implications both for biomarkers identification and potential innovative interventions will be considered.

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Section: Dopamine-glutamate Interplay At the Psd And Mirna Dysfunctiomentioning

confidence: 98%

MicroRNAs in Schizophrenia: Implications for Synaptic Plasticity and Dopamine–Glutamate Interaction at the Postsynaptic Density. New Avenues for Antipsychotic Treatment Under a Theranostic Perspective

et al. 2014

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“…Ca 2+ plays an important role not only in signaling pathways causing the activation of proteins such as protein kinase calcium-dependent (PKC) but also in the modulation of neurotransmitters release by exocytosis. It has been shown that this particular signaling pathways occurs primary in the prefrotal cortex and calcyon has been found co-localize with D1Rs in the dendritic spines on the pyramidal neurons [31]. The activation of this pathway in the medial prefrontal cortex is involved in impulsive choice in rats and neuropsychiatric disorders [32], in fact up-regulation of the interaction of calcyon and D1Rs has been found in schizophrenic patients [33].…”

Section: Aging and Disease • Volume 6 Number 5 October 2015 352mentioning

confidence: 99%

Dopamine Receptors and Neurodegeneration

Rangel‐Barajas¹,

Coronel²,

Florán³

2015

Aging and disease

187

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Dopamine (DA) is one of the major neurotransmitters and participates in a number of functions such as motor coordination, emotions, memory, reward mechanism, neuroendocrine regulation etc. DA exerts its effects through five DA receptors that are subdivided in 2 families: D1-like DA receptors (D1 and D5) and the D2-like (D2, D3 and D4). All DA receptors are widely expressed in the central nervous system (CNS) and play an important role in not only in physiological conditions but also pathological scenarios. Abnormalities in the DAergic system and its receptors in the basal ganglia structures are the basis Parkinson's disease (PD), however DA also participates in other neurodegenerative disorders such as Huntington disease (HD) and multiple sclerosis (MS). Under pathological conditions reorganization of DAergic system has been observed and most of the times, those changes occur as a mechanism of compensation, but in some cases contributes to worsening the alterations. Here we review the changes that occur on DA transmission and DA receptors (DARs) at both levels expression and signals transduction pathways as a result of neurotoxicity, inflammation and in neurodegenerative processes. The better understanding of the role of DA receptors in neuropathological conditions is crucial for development of novel therapeutic approaches to treat alterations related to neurodegenerative diseases.

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“…Out of the latter, calcyon density in SN was noted to be particularly high (Oakman and Meador-Woodruf, 2004). Furthermore, calcyon forms a ternary complex with D1 dopamine receptor (D(1)DR1) and thus regulates D(1)DR trafficking (Ha, 2012). Calcyon may also have a potential role as a partner of clathrin light chains implicated in endocytosis and synaptic plasticity in PD (Xiao, 2006, Heijtz, 2007).…”

Section: Discussionmentioning

confidence: 99%

Stress and corticosterone alter synaptic plasticity in a rat model of Parkinson’s disease

Hao

Shabanpoor

Metz

2017

Neuroscience Letters

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As a major influence on neuronal function and plasticity, chronic stress can affect the progression and symptoms of neurodegenerative conditions, such as Parkinson’s disease (PD). Here we investigated the influence of unilateral dopamine depletion and stress on dopamine-related hallmarks of stress response and neuronal plasticity in a rat model of PD. Animals received either restraint stress or a combination of adrenalectomy and corticosterone (CORT) supplementation to clamp circulating glucocorticoid levels for three weeks prior to unilateral nigrostriatal dopamine depletion. Rats were tested in skilled and gross motor function up to three weeks post-lesion. Midbrain mRNA expression assessments included markers of dopamine function and neuroplasticity, such as tyrosine hydroxylase (TH), synaptophysin (SYN), calcyon, and glucocorticoid receptor (GR). Along with impaired motor performance, stress and clamped CORT partially preserved TH expression in both substantia nigra (SN) and ventral tegmental area (VTA), but differentially modulated the expression of SYN, calcyon and GR mRNA in midbrain and cortical areas. Stress reduced synaptophysin mRNA expression in SN/VTA, and elevated calcyon mRNA optical density in both non-lesion and lesion hemispheres. Stress and CORT increased GR mRNA in the non-lesion SN/VTA, while in the lesion hemisphere GR mRNA was only elevated by CORT. In the motor cortex and striatum, however, GR was higher in both hemispheres under both experimental conditions. These findings suggest that stress and stress hormones differentially affect dopaminergic function and neuroplasticity in a rat model PD. The findings suggest a role for stress in motor and non-motor symptoms of PD and stress response.

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Calcyon Forms a Novel Ternary Complex with Dopamine D1 Receptor through PSD-95 Protein and Plays a Role in Dopamine Receptor Internalization

Cited by 31 publications

References 34 publications

MicroRNAs in Schizophrenia: Implications for Synaptic Plasticity and Dopamine–Glutamate Interaction at the Postsynaptic Density. New Avenues for Antipsychotic Treatment Under a Theranostic Perspective

MicroRNAs in Schizophrenia: Implications for Synaptic Plasticity and Dopamine–Glutamate Interaction at the Postsynaptic Density. New Avenues for Antipsychotic Treatment Under a Theranostic Perspective

Dopamine Receptors and Neurodegeneration

Stress and corticosterone alter synaptic plasticity in a rat model of Parkinson’s disease

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