Next Article in Journal
Structural, Molecular, and Functional Alterations of the Blood-Brain Barrier during Epileptogenesis and Epilepsy: A Cause, Consequence, or Both?
Next Article in Special Issue
GABAA Receptor-Mediated Currents and Hormone mRNAs in Cells Expressing More Than One Hormone Transcript in Intact Human Pancreatic Islets
Previous Article in Journal
Approaches to Monitor Circuit Disruption after Traumatic Brain Injury: Frontiers in Preclinical Research
Previous Article in Special Issue
Molecular and Regulatory Mechanisms of Desensitization and Resensitization of GABAA Receptors with a Special Reference to Propofol/Barbiturate
Open AccessReview

TGF-β/Smad3 Signalling Modulates GABA Neurotransmission: Implications in Parkinson’s Disease

1
Unidad de Neurología Experimental, Hospital Universitario Ramón y Cajal—IRYCIS, ES-28034 Madrid, Spain
2
Servicio de Neurobiología-Investigación, Hospital Universitario Ramón y Cajal—IRYCIS, ES-28034 Madrid, Spain
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(2), 590; https://doi.org/10.3390/ijms21020590
Received: 16 December 2019 / Revised: 13 January 2020 / Accepted: 14 January 2020 / Published: 16 January 2020
(This article belongs to the Special Issue Pharmacology and Neurobiology of GABA Receptors)
γ-Aminobutiryc acid (GABA) is found extensively in different brain nuclei, including parts involved in Parkinson’s disease (PD), such as the basal ganglia and hippocampus. In PD and in different models of the disorder, an increase in GABA neurotransmission is observed and may promote bradykinesia or L-Dopa-induced side-effects. In addition, proteins involved in GABAA receptor (GABAAR) trafficking, such as GABARAP, Trak1 or PAELR, may participate in the aetiology of the disease. TGF-β/Smad3 signalling has been associated with several pathological features of PD, such as dopaminergic neurodegeneration; reduction of dopaminergic axons and dendrites; and α-synuclein aggregation. Moreover, TGF-β/Smad3 intracellular signalling was recently shown to modulate GABA neurotransmission in the context of parkinsonism and cognitive alterations. This review provides a summary of GABA neurotransmission and TGF-β signalling; their implications in PD; and the regulation of GABA neurotransmission by TGF-β/Smad3. There appear to be new possibilities to develop therapeutic approaches for the treatment of PD using GABA modulators. View Full-Text
Keywords: GABA; Parkinson’s disease; TGF-beta; Smad3; dopamine; synaptic plasticity; cognition GABA; Parkinson’s disease; TGF-beta; Smad3; dopamine; synaptic plasticity; cognition
Show Figures

Graphical abstract

MDPI and ACS Style

Muñoz, M.D.; de la Fuente, N.; Sánchez-Capelo, A. TGF-β/Smad3 Signalling Modulates GABA Neurotransmission: Implications in Parkinson’s Disease. Int. J. Mol. Sci. 2020, 21, 590.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop