Dataset Information

Cannabidiol displays proteomic similarities to antipsychotics in cuprizone-exposed human oligodendrocytic cell line MO3.13

ABSTRACT: We employed nano-chromatography coupled with mass spectrometry to investigate the proteomic response to benztropine,cannabidiol, clozapine, and haloperidol, both in healthy oligodendrocytic cells and in a cuprizone-based toxicity model, using the human oligodendrocyte precursor cell line MO3.13.

INSTRUMENT(S): Synapt MS

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Oligodendrocyte Precursor Cell, Cell Culture

DISEASE(S): Schizophrenia

SUBMITTER: Ana Caroline Brambilla Falvella

LAB HEAD: Daniel Martins-de-Souza

PROVIDER: PXD028419 | Pride | 2021-11-11

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	2020_12_03_Homo-sapiens_Revisado.fasta	Fasta
	2020_12_05_BENZ_VEI_Peptides.csv	Csv
	2020_12_05_BENZ_VEI_Proteins.csv	Csv
	2020_12_05_CBD_VEI_Peptides.csv	Csv
	2020_12_05_CBD_VEI_Proteins.csv	Csv

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Publications

Cannabidiol Displays Proteomic Similarities to Antipsychotics in Cuprizone-Exposed Human Oligodendrocytic Cell Line MO3.13.

Falvella Ana Caroline Brambilla ACB Smith Bradley Joseph BJ Silva-Costa Licia C LC Valença Aline G F AGF Crunfli Fernanda F Zuardi Antonio W AW Hallak Jaime E JE Crippa José A JA de Almeida Valéria V Martins-de-Souza Daniel D

Frontiers in molecular neuroscience 20210528

Cannabidiol, a compound of <i>Cannabis sativa</i>, has been proposed as an alternative treatment of schizophrenia. Preclinical and clinical data have suggested that cannabidiol shares more similarity with atypical antipsychotics than typical, both of which are customarily used to manage schizophrenia symptoms. While oligodendrocytes are known to be relevant targets of antipsychotics, the biochemical knowledge in this regard is still limited. Here we evaluated the molecular pathways modulated by ...[more]

PMID: 34122009

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Project description:Schizophrenia is a chronic mental illness that is among the world’s top twenty causes of years lost to disability according to the global burden of disease 2019 (10.1016/S0140-6736(20)30925-9). Positive symptoms, including hallucinations and delusions in schizophrenia, often improved with conventional antipsychotic medication, which exerts its therapeutic effects mainly by antagonizing the dopamine D2 receptors. Haloperidol was one of the first antipsychotics to be approved by the FDA, and it is since then widely used for the treatment of psychotic disorders including schizophrenia. Despite its high affinity for dopamine D2 receptors, it has been shown that haloperidol interacts with other receptors, such as dopamine D3 and D4 receptors, α-adrenergic receptor 1 and to some extent 5HT2A. Dopaminergic dysfunction is known for decades to be involved in the pathophysiology of schizophrenia, but only recently has the striatum been implicated in such devasting disorder. The dorsal striatum is a brain region involved in motor, cognitive and motivational functions, highly impacted by antipsychotic drugs. Particularly, it is well-recognized that chronic haloperidol administration has a tremendous impact on striatal synaptic plasticity, by changing the volume of dorsal striatum, the number of striatal neurons and the synaptic morphology, both in humans and rodents. Despite the overwhelming evidence correlating chronic haloperidol administration with striatum alterations, so far, the exact striatal synaptic mechanism by which haloperidol exerts its beneficial effects remains unclear. Although dopamine D2 receptor blockade can be achieved within hours after haloperidol administration, the onset of action is delayed by weeks. Thus, it is crucial to better understand the neuronal mechanism behind the delayed clinical effects of haloperidol to improve the treatment outcome. Using proteomic analysis and whole-cell patch-clamp recordings (Figure 1), we demonstrate for the first time a possible mechanism by which haloperidol may be contributing to its beneficial long-term therapeutic effect. Specifically, we demonstrate that modulation of D2-MSNs by chronic haloperidol administration leads to a slow remodeling of D1-neurons that may be responsible for its positive therapeutic effects.