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. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: J Comput Neurosci. 2012 Jun 19;33(3):10.1007/s10827-012-0402-z. doi: 10.1007/s10827-012-0402-z

Figure 6. Effects of proctolin in model II on LP to PD synaptic transmission for a sample parameter set.

Figure 6

The response of the model with the parameter set shown in red in Fig. 5(a) to trains of low- and high-amplitude pulses in control and proctolin is compared to a biological recording (green traces) of the IPSPs in the PD neuron in one experiment (same as Fig. 3). (a) The model response to low-amplitude (20 mV) pulses in the presynaptic LP neuron in control shows no significant IPSP in the PD neuron. (b) The model response to high-amplitude (40 mV) presynaptic pulses shows synaptic depression in control. (c) A switch to synaptic facilitation by proctolin. A gradual increase of [Ca2+]i in presynaptic terminal due to the Ca2+ entry through MI channels allows for observed facilitation. (d) Although the increase in [Ca2+]i due to the MI channels is still present, the dominant effect on [Ca2+]i is due to ICa, resulting in depression as in control. (e) Steady-state activation of ICa in control and in proctolin. Proctolin shifts the activation curve to the left and changes its slope, which leads to enhanced synaptic strength of the LP to PD synapse in the biological range. (f) Activation time constant of ICa in control and in proctolin. Parameter values are: KCa = 1.7μM, ḡsyn = 10nS / μM4, ḡCa = 37.4nS, gm = 7.4nS, gMI = 2.68nS; τh = 1.23s, τCa = 9.57ms, τm = 14.3ms, Vh = 120mV, Sh = 49.8mV, Vm = 41.1mV, Sm = 1.91mV, V+ = 9.45mV, S+ = 4.44mV