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Curr Med Chem. 2018 Nov 11. doi: 10.2174/0929867325666181112094330. [Epub ahead of print]

An Update On The Neurochemistry Of Essential Tremor.

Author information

1
Section of Neurology, Hospital Universitario del Sureste, Arganda del Rey, Madrid. Spain.
2
University Institute of Molecular Pathology Biomarkers, UNEx. ARADyAL Instituto de Salud Carlos III, Cáceres. Spain.

Abstract

BACKGROUND:

The pathophysiology and neurochemical mechanisms of essential tremor (ET) are not fully understood, because only a few post-mortem studies have been reported, and the lack of a good experimental model for this disease.

OBJECTIVE:

The main aim of this review is to update data regarding the neurochemical features of ET. Alterations of certain catecholamine systems, the dopaminergic, serotonergic, GABAergic, noradrenergic, and adrenergic systems have been described, and are the object of this revision.

METHODS:

For this purpose, we performed a literature review on alterations of the neurotransmitter or neuromodulator systems (catecholamines, gammaaminobutyric acid or GABA, excitatory amino acids, adenosine, T-type calcium channels) in ET patients (both post-mortem or in vivo) or in experimental models resembling ET.

RESULTS AND CONCLUSION:

The most consistent data regarding neurochemistry of ET are related with the GABAergic and glutamatergic systems, with a lesser contribution of adenosine and dopaminergic and adrenergic systems, while there is not enough evidence of a definite role of other neurotransmitter systems in ET. The improvement of harmaline-induced tremor in rodent models achieved with T-type calcium channel antagonists, cannabinoid 1 receptor, sphingosine-1-phosphate receptor agonists, and gap-junction blockers, suggests a potential role of these structures in the pathogenesis of ET.

KEYWORDS:

Essential tremor; GABA; Neurochemistry; T-type calcium channels; adenosine; adrenaline; dopamine; glutamate; noradrenaline; serotonin

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