AI Article Synopsis

  • The Suk-Saiyasna remedy, an herbal treatment that contains cannabis, has seen a resurgence in Thailand after a relaxation of drug laws, prompting a study into its effects on rodent behavior.
  • The study tested various doses of the remedy on mice to assess sedative-like effects, analyzing behaviors like anxiety, depression, and motor coordination using specific tests.
  • Results showed that the remedy significantly increased sleeping time and decreased activity, suggesting it may work through GABAA and cannabinoid CB1 receptors to produce a sedative-hypnotic effect in rodents.

Article Abstract

The Suk-Saiyasna remedy, an herbal treatment, was historically used but ceased due to its cannabis content. After a relaxation of drug control laws in Thailand, its use re-emerged. This study examines the Suk-Saiyasna remedy's impact on rodent behavior and its receptor effects. This study was conducted to assess the sedative-like effects of the remedy on mice. The mice were divided into groups receiving 0.6, 3, 30, and 60 mg/kg extracts, with negative controls for comparison. We also investigated the impact on receptors, utilizing negative controls and pretreatment with receptor blockers, followed by either a negative control or a 60 mg/kg extract. Furthermore, this study investigated the behavioral aspects of mice, including anxiolytic effects, antidepressant-like effects, and motor coordination, utilizing the elevated plus-maze, open-field, and rotarod performance tests. The Suk-Saiyasna remedy ( < 0.05) decreased significantly in the latent period and increased sleeping time in the treated groups. Moreover, the Suk-Saiyasna remedy also showed efficacy in reaction to GABAA receptors and cannabinoid CB1 receptors ( < 0.05). In addition, positive effects were observed regarding the animal behavior in the arena, as the animal activity, behavior, and muscle coordination were reduced ( < 0.05). The Suk-Saiyasna remedy may be involved in a sedative-hypnotic-like effect in rodents under normal conditions through the modulation of GABAergic neurons and induction of the cannabinoid CB1 receptor mechanism.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10880918PMC
http://dx.doi.org/10.4103/JAPTR.JAPTR_355_23DOI Listing

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