Role of ?-aminobutyric acid (GABA) in the extrapyramidal motor system

1971 ◽  
Vol 14 (1) ◽  
Author(s):  
J.S. Kim ◽  
I.J. Bak ◽  
R. Hassler ◽  
Y. Okada
Keyword(s):  
Motor System ◽  
Aminobutyric Acid ◽  
Extrapyramidal Motor

Neurobiology of Anxiety Disorders

2020 ◽  
Author(s):  
Pooja Palkar ◽  
Eric Hollander
Keyword(s):  
Anxiety Disorders ◽  
Fear Conditioning ◽  
Endogenous Opioids ◽  
Aminobutyric Acid ◽  
Nmda Antagonists ◽  
Important Goal ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
New Learning

In recent years, advances in the fields of neuroimaging and experimental psychology increased our understanding of the basic mechanisms of classical conditioning and learning, contributing to our knowledge of the neurobiology of anxiety disorders. Research has shown that the amygdala is the cornerstone of fear circuitry and that abnormalities in amygdala pathways can affect the acquisition and expression of fear conditioning. Activation of the amygdala in response to disorder-relevant stimuli has been observed in anxiety disorders. The roles of the hippocampus, nucleus accumbens, periaqueductal gray, and insular and medial prefrontal cortices in response to fear have been identified as well. Neurotransmitters such as serotonin, dopamine, γ-aminobutyric acid, glutamate, and some neurosteroids play an important part in the neurobiology of anxiety disorders. Neuropeptides such as oxytocin, neuropeptide Y, galanin, and cholecystokinin have been shown to modulate stress response. Drugs such as N-methyl-d-aspartate (NMDA) antagonists and blockers of voltage-gated calcium channels in the amygdala are anxiolytic. Fear extinction, which entails new learning of fear inhibition, is the mechanism of effective antianxiety treatments such as d-cycloserine, a partial NMDA agonist. Extinction is thought to occur by the medial prefrontal cortex, which inhibits the lateral amygdala under hippocampal modulation. Harnessing extinction to delink neutral stimuli from aversive responses is an important goal of the psychotherapy and pharmacotherapy of anxiety disorders. Discovery of the role of microRNAs in the etiology of anxiety disorders and their possible utility as targets to treat these disorders is fascinating. In this review, we discuss the neurobiology of anxiety disorders, which will help us better manage them clinically. This review contains 5 figures, 6 tables, and 39 references. Key words: Amygdala, anxiety disorders, neurobiology, fear conditioning, neurocircuitry, neurotransmitters, neuropeptides, neurosteroids, endogenous opioids.

Tissue atrophy and elevated iron concentration in the extrapyramidal motor system in Friedreich ataxia: the IMAGE-FRDA study

2016 ◽  
Vol 87 (11) ◽  
pp. 1261-1263 ◽  
Author(s):  
Ian H Harding ◽  
Parnesh Raniga ◽  
Martin B Delatycki ◽  
Monique R Stagnitti ◽  
Louise A Corben ◽  
...  
Keyword(s):  
Motor System ◽  
Iron Concentration ◽  
Friedreich Ataxia ◽  
Extrapyramidal Motor

Combination Therapy of Extrapyramidal Disease with Trihexyphenidyl and L-Dopa

1979 ◽  
Vol 7 (1) ◽  
pp. 19-28 ◽  
Author(s):  
H Hökendorf
Keyword(s):  
Side Effects ◽  
Combination Therapy ◽  
Motor System ◽  
Good Control ◽  
Decarboxylase Inhibitor ◽  
System Disease ◽  
Extrapyramidal Disease ◽  
Extrapyramidal Motor

An electromyographic method was used to study the effect of combination therapy with L-dopa and trihexyphenidyl on tremor in thirty patients suffering from extrapyramidal motor system disease. In this method tremor activity was measured and documented so that the course of the disease could be followed objectively. L-dopa alone was slightly more effective against tremor than was trihexyphenidyl alone. The combination of the two drugs was more effective than either drug used alone, and its side-effects were mild and definitely fewer than had been reported with L-dopa combined with a decarboxylase inhibitor. Good control of tremor with L-dopa and trihexyphenidyl was obtained clinically and verified electromyographically.

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