Although synaptic output is known to be modulated by changes in presynaptic
calcium channels, additional pathways for
calcium entry into the presynaptic terminal, such as non-selective channels, could contribute to modulation of short term synaptic dynamics. We address this issue using computational modeling. The
neuropeptide proctolin modulates the inhibitory synapse from the lateral pyloric (LP) to the pyloric dilator (PD) neuron, two slow-wave bursting neurons in the pyloric network of the crab
Cancer borealis.
Proctolin enhances the strength of this synapse and also changes its dynamics. Whereas in control saline the synapse shows depression independent of the amplitude of the presynaptic LP signal, in
proctolin, with high-amplitude presynaptic LP stimulation the synapse remains depressing while low-amplitude stimulation causes facilitation. We use simple
calcium-dependent release models to explore two alternative mechanisms underlying these modulatory effects. In the first model,
proctolin directly targets
calcium channels by changing their activation kinetics which results in gradual accumulation of
calcium with low-amplitude presynaptic stimulation, leading to facilitation. The second model uses the fact that
proctolin is known to activate a non-specific
cation current I ( MI ). In this model, we assume that the MI channels have some permeability to
calcium, modeled to be a result of slow conformation change after binding
calcium. This generates a gradual increase in
calcium influx into the presynaptic terminals through the modulatory channel similar to that described in the first model. Each of these models can explain the modulation of the synapse by
proctolin but with different consequences for network activity.