Abstract
Behavioral and histochemical studies demonstrated that endogenous tryptophan metabolites – kynurenines – play a role in the long-term retention of memory traces and the functioning of key components in the (GluR–LIMK1– F-actin) signaling cascade, which mediates these functions. Kynurenine deficiency induced by injections of allopurinol (a tryptophan oxygenase inhibitor) inhibited long-term memory, decreased the level of expression of LIMK1, and produced a paradoxical increase in the F-actin level in the cerebral ganglion in bees. These results are consistent with our previous data obtained in Drosophila with a mutation in the structural gene for tryptophan oxygenase, i.e., the vermilion mutation.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have