Differential Classical Conditioning of the Gill-Withdrawal Reflex In Aplysia Recruits Both Nmda Receptor-Dependent Enhancement and Nmda Receptor-Dependent Depression Of the Reflex
Differential classical conditioning of the gill-withdrawal response (GWR) in Aplysia can be elicited by training in which a conditioned stimulus (CS) delivered to one side of the siphon (the CS+) is paired with a noxious unconditioned stimulus (US; tail shock), while a second conditioned stimulus (the CS-), delivered to a different siphon site, is unpaired with the US. NMDA receptor(NMDAR) activation has been shown previously to be critical for nondifferential classical conditioning in Aplysia. Here, we used a semi-intact preparation to test whether differential classical conditioning of the GWR also depends on activation of NMDARs. Differential training produced conditioned enhancement of the reflexive response to the CS+ and a reduction in the response to the CS-. Comparison of the results after differential training with those after training in which only the two CSs were presented (CS-alone experiments) indicated that the decrement in the response to CS-after differential training was not caused by habituation. Surprisingly, differential training in the NMDAR antagonist APV(DL-2-amino-5-phosphonovalerate) blocked not only the conditioned enhancement of the GWR, but also the conditioning-induced depression of the GWR. We suggest that differential conditioning involves an NMDAR-dependent, competitive interaction between the separate neural pathways activated by the CS+ and CS-.
Jami, Shekib A., William G. Wright, and David L. Glanzman. "Differential classical conditioning of the gill-withdrawal reflex in Aplysia recruits both NMDA receptor-dependent enhancement and NMDA receptor-dependent depression of the reflex." The Journal of neuroscience 27.12 (2007): 3064-3068. doi: 10.1523/JNEUROSCI.2581-06.2007
Society for Neuroscience
This article was originally published in Journal of Neuroscience, volume 27, issue 12, in 2007. DOI: 10.1523/JNEUROSCI.2581-06.2007