Biochemical and Pharmacological Studies in the Helix pomatia—Snail Memory Model

Kynurenic acid (KYNA) is a byproduct of the kynurenine pathway, which breaks down the amino acid tryptophan. KYNA acts as an antagonist of glutamate ionotropic excitatory amino acid (EAA) receptors and α7 nicotinic acetylcholine receptors (nAChRs). There is evidence that KYNA plays a significant role in various pathological conditions and the ageing process. It has also been suggested that KYNA contributes to memory impairment. This study investigated the impact of L-kynurenine, D-cycloserine, and Cerebrolysin on KYNA synthesis in the liver homogenate of Helix pomatia snails in vitro and in their ganglia in vivo. Furthermore, a memory model was established using these snails, wherein tentacle shortening served as an indicator of memory activity. In vitro experiments on Helix pomatia demonstrated the significant impact of L-kynurenine and anti-dementia drugs on KYNA synthesis. KYNA levels increased significantly in the presence of L-kynurenine, a bio-precursor, in liver homogenate. However, KYNA formation decreased when anti-dementia drugs, including Cerebrolysin or D-cycloserine, were administered to the snails’ liver homogenate. L-kynurenine has been shown to impair memory in vivo in snails, but an anti-dementia drug has been demonstrated to reverse this effect. Significant inhibition of tentacle lowering was observed in response to L-kynurenine treatment, which corresponded with elevated KYNA levels in the central nervous system. Administering D-cycloserine or Cerebrolysin alongside L-kynurenine reversed its effects. The Helix pomatia memory model is a valuable tool for studying learning and memory in various conditions and in the presence of different pharmacological agents. A drug or natural extract that blocks KYNA synthesis could be considered an anti-dementia agent. It may also protect against ageing and delay damage to the central nervous system related to memory.