Anxiogenic activity of quinolinic acid and kynurenine in the social interaction test in mice

Abstract

Quinolinic acid, a metabolite of tryptophan on the kynurenine pathway, shortened the duration of social contacts (sniffings) in C57BL/6 mice which had been previously isolated for 24 h. This effect was observed at the following time intervals after i.c.v. administration: 2-6, 22-26 and 32-36 min. Locomotion was significantly less inhibited and only during the first interval. L-Kynurenine sulphate was less active. It shortened the duration of contacts only during the 32-36 min interval after i.c.v. administration. Grooming was significantly reduced by quinolinic acid at 7-11, 12-16 and 17-21 min after administration. These effects of quinolinic acid in the social interaction test are similar to those of standard anxiogens and suggest that quinolinic acid belongs to the putative endogenous anxiogens (and not only to the endogenous convulsants). The same assumption about L-kynurenine based on data in other models of anxiety has been made previously.

Phenibut (β‐Phenyl‐GABA): A Tranquilizer and Nootropic Drug

“…In the social interaction test PEA, at 5 to 10 mg/kg i.p., decreased the number and the duration of contacts of previously isolated mice. PB and DZP prevented this effect of PEA (34). In a conflict situation of a dark-light chamber PEA reduced the movements of mice from one chamber to the other.…”

“…In these models the behavioral effects of PEA were typical of standard anxiogens (27,29,30,34). In the social interaction test PEA, at 5 to 10 mg/kg i.p., decreased the number and the duration of contacts of previously isolated mice.…”

Kynurenine Pathway in Autism Spectrum Disorders in Children

“…As stated earlier, KA exerts anxiolytic [33] and neuroprotective [29] effects, and KYN/KA reflects a neurotoxic potential and lowered KAT activity. Our finding of the serum KA being significantly lower in ASD children than in healthy controls thus suggests that the level of neuroprotection is lower in ASD children.…”

“…KA, 3-HAA, and QA do not cross the blood-brain barrier, and KYN and TRP are transported via the large neutral amino acid transporter system [32]. In contrast to KYN, KA exerts anxiolytic [33] and neuroprotective [29] effects. Consequently, KYN/KA reflects a neurotoxic potential and KAT activity, whereas the QA/KA ratio reflects NMDA receptor excitotoxicity.…”

Biological phenotypes underpin the physio‐somatic symptoms of somatization, depression, and chronic fatigue syndrome

“…QUIN increases brain inflammation, contributing to a neurotoxic environment as well as having apoptotic and neurodegenerative consequences (135,136). Moreover, kyn may cause anxiety in animals (137,138) and humans (139,140) while KYNA has anxiolytic effects (141,142). This suggests that lowered KYNA in somatization contributes to increased anxiety levels, concurrent to its effects on nociceptive processing.…”