Neural parameters contributing to temperature compensation in the flight CPG of the locust, Locusta migratoria

Elevated thoracic temperature increases the wingbeat frequency of flying locusts. We investigated the extent to which temperature-induced changes in resting membrane potential and postsynaptic potential amplitude contribute to the effects of increased temperature on the frequency of the central flight rhythm. Flight neurons were hyperpolarized by changing the K+ concentration of the superfusing saline from 10 mM to 2 mM. 5 min of low-K+ superfusion hyperpolarized flight motoneurons from -42.8 mV to -50.1 mV with a concomitant decrease of the frequency of the central flight rhythm from 11.6 Hz to 10.5 Hz. The amplitude of postsynaptic potentials was halved after 10 min of zero Ca2+/high Mg2+ superfusion, but the frequency of the central rhythm did not change significantly. GABAergic inhibitory connections were reduced in amplitude using picrotoxin. This treatment increased the frequency of the central rhythm from 11.6 Hz to 12.9 Hz, and increased the thermosensitivity of the rhythm frequency. We conclude that the excitatory effect of increased temperature on rhythm frequency is not mediated by temperature effects on membrane potential and/or synaptic potential amplitude. We propose that the inhibitory effect of temperature-induced hyperpolarization of the membrane potential compensates for the excitatory effect of temperature on rhythm frequency (e.g. via increased conduction velocity). We further suggest that some measure of temperature compensation is afforded by equal effects on the amplitudes of excitatory and inhibitory postsynaptic potentials, such that the net effect on the level of excitation is zero.