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

Authors
  • muñoz, mª dolores
  • de la fuente, nerea
  • sánchez-capelo, amelia
Publication Date
Jan 16, 2020
Source
MDPI
Keywords
Language
English
License
Green
External links

Abstract

&gamma / -Aminobutiryc acid (GABA) is found extensively in different brain nuclei, including parts involved in Parkinson&rsquo / 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-&beta / /Smad3 signalling has been associated with several pathological features of PD, such as dopaminergic neurodegeneration / reduction of dopaminergic axons and dendrites / and &alpha / -synuclein aggregation. Moreover, TGF-&beta / /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-&beta / signalling / their implications in PD / and the regulation of GABA neurotransmission by TGF-&beta / /Smad3. There appear to be new possibilities to develop therapeutic approaches for the treatment of PD using GABA modulators.

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