Modulatory Effects of Jujuboside A on Amino Acid Neurotransmitter Profiles in Tic Disorder

Objective This study investigates the impact of jujuboside A (JuA) on the levels of glutamate (Glu) and gamma‐aminobutyric acid (GABA) in the extracellular fluid of the caudate putamen (CPu) in a rat model of tic disorder (TD). It also compares the therapeutic effects of JuA alone and in combination with Tiapride on TD. Method The Sprague–Dawley (SD) rats were randomly assigned to five distinct groups: the normal group, the model group, the JuA group, the Tiapride group, and the JuA + Tiapride group. The TD rat model was established through the induction method utilizing intraperitoneal injection of iminodipropionitrile (IDPN). Microdialysis technology was utilized to obtain extracellular fluid from the CPu of rats in each group, and high‐performance liquid chromatography (HPLC) was employed to ascertain the levels of Glu and GABA. The stereotypical behavior scores of rats in each group were observed and recorded. Immunohistochemistry was utilized to compare the expression levels of glutamate transporter‐1(GLT‐1) and glutamate/aspartate transporter (GLAST) proteins in the CPu tissue of rats across the different groups. Results In the TD rats, the Glu content in the CPu extracellular fluid was significantly increased, while the GABA content was significantly decreased, accompanied by a notable increase in stereotypical behavior scores. Both JuA and Tiapride reduced the Glu content and increased the GABA content in the CPu extracellular fluid of TD rats, improving stereotypical behaviors. The combination of JuA and Tiapride showed superior effects compared to either treatment alone, potentially related to the upregulation of GLT‐1 and GLAST protein expression in the CPu tissue. Conclusion JuA can improve stereotypical behaviors in TD rats by regulating the levels of Glu and GABA in the CPu extracellular fluid, possibly through the upregulation of GLT‐1 and GLAST protein expression. The combination of JuA and Tiapride offers enhanced therapeutic effects, providing a new approach for the treatment of TD.