Oral movements induced by interference with nigral GABA neurotransmission: Relationship to tardive dyskinesias

1988 ◽  
Vol 100 (3) ◽  
pp. 459-469 ◽  
Author(s):  
Lars M Gunne ◽  
Susan E Bachus ◽  
Karen Gale
Author(s):  
Sandra Godinho ◽  
Margarida V. Garrido ◽  
Oleksandr V. Horchak

Abstract. Words whose articulation resembles ingestion movements are preferred to words mimicking expectoration movements. This so-called in-out effect, suggesting that the oral movements caused by consonantal articulation automatically activate concordant motivational states, was already replicated in languages belonging to Germanic (e.g., German and English) and Italic (e.g., Portuguese) branches of the Indo-European family. However, it remains unknown whether such preference extends to the Indo-European branches whose writing system is based on the Cyrillic rather than Latin alphabet (e.g., Ukrainian), or whether it occurs in languages not belonging to the Indo-European family (e.g., Turkish). We replicated the in-out effect in two high-powered experiments ( N = 274), with Ukrainian and Turkish native speakers, further supporting an embodied explanation for this intriguing preference.


1988 ◽  
Vol 8 (3) ◽  
pp. 224-236 ◽  
Author(s):  
Kunihiko Endo ◽  
Hideo Makishita ◽  
Yoshio Tanizaki ◽  
Morihiro Sugishita ◽  
Nobuo Yanagisawa
Keyword(s):  

1992 ◽  
Vol 12 (2) ◽  
pp. 334-346 ◽  
Author(s):  
Anke M. Mans ◽  
Kelli M. Kukulka ◽  
Keith J. McAvoy ◽  
Norman C. Rokosz

The regional distribution of binding sites on the GABAA receptor and their kinetic parameters were measured by quantitative autoradiography in brains from normal rats and rats with a portacaval shunt, a model of portal systemic encephalopathy in which GABA neurotransmission may be altered. The ligands used were [3H]flunitrazepam (a benzodiazepine-site agonist), [3H]-Ro 15-1788 (a benzodiazepine-site antagonist), [3H]muscimol (a GABA-site agonist), and [35S] t-butylbicyclo-phosphorothionate (35S-TBPS, a convulsant that binds to a site near the chloride channel). Some brains were analyzed by computerized image analysis and three-dimensional reconstruction. The regional distribution of binding of the benzodiazepines was very similar, but the patterns obtained with [3H]muscimol and [35S]TBPS were different in many areas, suggesting a heterogeneous distribution of several subtypes of the GABAA receptor. The kinetic parameters were determined in brain regions for [3H]flunitrazepam, [3H]Ro15-1788, and [3H]muscimol. For each ligand, the Kd showed a significant heterogeneity among brain regions (at least threefold), contrary to conclusions drawn from earlier studies. In portacaval shunted rats, binding of all four ligands was essentially unchanged from that in control rats, indicating that, if there was an abnormality in GABA neurotransmission during portal systemic shunting, it was not reflected by altered binding to the main sites on the GABAA receptor.


2011 ◽  
Vol 104 (3) ◽  
pp. 423-428 ◽  
Author(s):  
René A. de Wijk ◽  
Anke M. Janssen ◽  
Jon F. Prinz

2020 ◽  
Vol 21 (2) ◽  
pp. 590 ◽  
Author(s):  
Mª Muñoz ◽  
Nerea de la Fuente ◽  
Amelia Sánchez-Capelo

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.


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