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Updated: Jun 30, 2026

Rapid In Situ Hybridization using Oligonucleotide Probes on Paraformaldehyde-prefixed Brain of Rats with Serotonin Syndrome
Published on: September 23, 2015
An association between serotonin receptor 3B gene (HTR3B) and treatment-resistant schizophrenia (TRS) in a Japanese
Xiaofei Ji1, Nagahide Takahashi, Aleksic Branko
1Department of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan. xiaofei@med.nagoya-u.ac.jp
Abstract:
Genetic factors are thought to be involved in the development of treatment-resistant schizophrenia (TRS). Since several antipsychotic drugs inhibit the release of neurotransmitters via the serotonin receptors 3 (5-HT3), a dysfunction of this kind of receptor might be associated with the development of TRS. Thus, single-marker and haplotype analyses of the tag-single nucleotide polymorphisms (SNPs) of the 5-HT3B subunit gene (HTR3B) were performed in TRS (n = 101) and non-TRS (n = 244) patients. The deletion allele at the 3 bp-insertion/deletion polymorphism site (-100_-102delAAG) located in the putative HTR3B promoter region is significantly more frequent in the TRS group than the insertion allele by a single-marker comparison (p = 0.031). In addition, luciferase promoter assays showed that the deletion allele exhibited significantly higher transcriptional activity than the insertion allele in COS7 cells (p < 0.05). These results suggest that HTR3B is involved in the development of TRS in the Japanese population.
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