Reconsolidation: Does the Past Linger on?

In Dr Kemenes’ response to my article (http://www.jneurosci.org/cgi/data/ 26/43/10935/DC1/1) he raises two important issues. In the first, Dr Kemenes argues that training stimulated cGMP is unlikely to participate in post-recall processing at 6 hr since the requirement of NO/cGMP in memory consolidation is completed at this time (Kemenes et al., 2002). While I concede that the levels of cGMP required to support consolidation have clearly declined below threshold by this time, I see no reason to exclude the possibility that interactions with the cAMP/PKA pathway require a different, and possibly lower, concentration of cGMP.

In his second point Dr Kemenes sought a reference for my assertion that PKG is capable of directly activating the cAMP/PKA pathway. My reference for this interaction comes from a study published in the Journal of Neuroscience (Moon et al., 1998); in this study a process is described by which PKG directly activates adenylyl cyclase, leading to increased stimulation of cAMP (see Figs. 8 and 9 in Moon et al.). The observations of Moon et al. were made in rats, and it remains to be determined whether this interaction also occurs in Lymnaea. However, should it be present in the snail, this interaction would provide an attractive mechanism by which a specific signaling molecule elicited during training could connect with conditioned stimulus (CS)- activated pathways to bring about the post-recall processing that underlies reconsolidation.

Kemenes I, Kemenes G, Andrew RJ, Benjamin PR, O’Shea M (2002) Critical Time-Window for NO-cGMP-Dependent Long-Term Memory Formation after One-Trial Appetitive Conditioning. J Neurosci 22:1414-1425.

Moon C, Jaberi P, Otto-Bruc A, Baehr W, Palczewski K, Ronnett GV (1998) Calcium-Sensitive Particulate Guanylyl Cyclase as a Modulator of cAMP in Olfactory Receptor Neurons. J Neurosci 18: 3195-3205.