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It is known that trace amine-associated receptor 5 (TAAR5) is expressed in various regions of the central nervous system. However, very limited information is available on the behavioral effects of TAAR5 activation and the TAAR5 functional role, in general. We studied the effect of TAAR5 agonist (2-(alpha-naphthoyl) ethyltrimethylammonium iodide) systemic administration on animal behavior. The study was performed on male C57BL/6 mice. It was observed that α-NETA in 10 mg/kg dose caused specific impairment of motor behavior, similar to the manifestations of tardive dyskinesia in humans. It can be assumed that trace amines and TAAR5 may be involved in the human tardive dyskinesia pathogenesis.
This article was published in the following journal.
Name: Neuroscience letters
Tardive dyskinesia is a movement disorder that develops during the course of long-term treatment with neuroleptic agents and is characterized primarily by choreiform and athetotic movements. We report...
Pathogenesis of gallstone includes bile stasis due to defect in the gallbladder muscle contraction. Our aim of the study is to find out the role of 99mTc-HIDA scan in assessment of gallbladder dyskine...
There is accruing evidence of spontaneous dyskinesia in individuals with schizophrenia that is independent of medication exposure. Dyskinetic motor behavior is also present in individuals who are at h...
Tardive dyskinesia and tardive dystonia are caused by dopamine receptor blocking agents, mostly antipsychotics and sometimes antidepressants or calcium channel blockers. Duloxetine is a serotonin-nora...
Mutations of the PRRT2 gene are the most common cause for paroxysmal kinesigenic dyskinesia. However, patients with negative PRRT2 mutations are not rare. The aim of this study is to determine whether...
Prospective study to quantify the prevalence of possible tardive dyskinesia (TD) in outpatient psychiatry practices in the United States (US), as well as to describe the associated disease...
The purpose of this study is to determine whether fixed-doses of an investigational drug, SD-809 (deutetrabenazine), will reduce the severity of abnormal involuntary movements of tardive d...
The purpose of this study is to determine whether an investigational drug, SD-809 (deutetrabenazine), will reduce the severity of abnormal involuntary movements of tardive dyskinesia.
The goal of this study is to challenge the existing clinical practice of employing laparoscopic cholecystectomy as the treatment for gallbladder dyskinesia by comparing it to a regimen of ...
The purpose of this study is to evaluate the efficacy and safety of MT-5199 administered once daily for the treatment of Tardive Dyskinesia (TD) symptoms.
A motility disorder characterized by biliary COLIC, absence of GALLSTONES, and an abnormal GALLBLADDER ejection fraction. It is caused by gallbladder dyskinesia and/or SPHINCTER OF ODDI DYSFUNCTION.
Strains of mice arising from a parental inbred stock that was subsequently used to produce substrains of knockout and other mutant mice with targeted mutations.
Abnormal involuntary movements which primarily affect the extremities, trunk, or jaw that occur as a manifestation of an underlying disease process. Conditions which feature recurrent or persistent episodes of dyskinesia as a primary manifestation of disease may be referred to as dyskinesia syndromes (see MOVEMENT DISORDERS). Dyskinesias are also a relatively common manifestation of BASAL GANGLIA DISEASES.
Mice homozygous for the mutant autosomal recessive gene "scid" which is located on the centromeric end of chromosome 16. These mice lack mature, functional lymphocytes and are thus highly susceptible to lethal opportunistic infections if not chronically treated with antibiotics. The lack of B- and T-cell immunity resembles severe combined immunodeficiency (SCID) syndrome in human infants. SCID mice are useful as animal models since they are receptive to implantation of a human immune system producing SCID-human (SCID-hu) hematochimeric mice.
A strain of mice widely studied as a model for cystic fibrosis. These mice are generated from embryonic stem cells in which the CFTR (cystic fibrosis transmembrane conductance regulator) gene is inactivated by gene targeting. As a result, all mice have one copy of this altered gene in all their tissues. Mice homozygous for the disrupted gene exhibit many features common to young cystic fibrosis patients, including failure to thrive, meconium ileus, and alteration of mucous and serous glands.