Figure 5.

CM-induced plasticity of synaptic connections between identified Lymnaea neurons is mediated via receptor tyrosine kinases. RPeD1 and VD2/3 were soma–soma paired in DM for 12 hr. DM was subsequently replaced with CM containing a receptor tyrosine kinase inhibitor. (1)Twelve hours after initial soma–soma pairing, DM was replaced with CM. The CM-induced synaptic plasticity was either blocked completely or reduced significantly in the presence of CM containing a receptor tyrosine kinase inhibitor [(2) Lavendustin A, 10 μm; (5) K252a, 0.1 μm]. CM containing the inactive forms of receptor tyrosine kinase inhibitors [(3) Lavendustin B, 10 μm] were, however, ineffective in perturbing the CM-induced excitatory synapse formation. Similarly, the addition of DMSO [(4) carrier solution, 1%] failed to affect CM-induced plasticity of synaptic connections between RPeD1 and VD2/3 pairs. The n values for each experiment are noted above the data bars.