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 there is a lack of 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
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.