Abstract
Tourette’s Syndrome (TS) is a neuropsychiatric disorder, with onset in children. It is characterized by multiple motor and phonic tics. The pathophysiology of TS is not well understood. Previous studies suggested the etiology involving the abnormal dopaminergic neurotransmission, abnormalities in basal ganglia-related circuits and genetics in TS. In 2010, Ercan-Sencicek G, et al has identified a rare functional mutation in the Histidine Decarboxylase (HDC) gene in the family with high density of TS. HDC gene encodes L-Histidine decarboxylase, which is a rate-limiting step enzyme in histamine biosynthesis. HDC was found at high levels in mouse’s hypothalamus and striatum. Histamine receptors H2 and H3 are prominent in the striatum. H3 modulates dopamine signalling through dopamine receptors D1 and D2 in the striatum. Taken together, it is possible that the interactions between histamine and dopamine in the striatum contribute to TS.
DOI
10.58837/CHULA.CMJ.56.2.8
First Page
219
Last Page
226
Recommended Citation
Krusong, K.
(2012)
"Histaminergic neurotransmission and Tourette’s Syndrome,"
Chulalongkorn Medical Journal: Vol. 56:
Iss.
2, Article 8.
DOI: https://doi.org/10.58837/CHULA.CMJ.56.2.8
Available at:
https://digital.car.chula.ac.th/clmjournal/vol56/iss2/8