Abstract
Activity-dependent modification of neural network output usually results from changes in neurotransmitter release and/or membrane conductance. In Xenopus frog tadpoles, spinal locomotor network output is adapted by an ultraslow afterhyperpolarization (usAHP) mediated by an increase in Na+ pump current. Here we systematically explore how the interval between two swimming episodes affects the second episode, which is shorter and slower than the first episode. We find the firing reliability of spinal rhythmic neurons to be lower in the second episode, except for excitatory descending interneurons (dINs). The sodium/proton antiporter, monensin, which potentiates Na+ pump function, induced similar effects to short inter-swim intervals. A usAHP induced by supra-threshold pulses reduced neuronal firing reliability during swimming. It also increased the threshold current for spiking and introduced a delay to the first spike in a train, without reducing subsequent firing frequency. This delay was abolished by ouabain or zero K+ saline, which eliminate the usAHP. We present evidence for an A-type K+ current in spinal CPG neurons which is inactivated by depolarization and de-inactivated by hyperpolarization, and accounts for the prolonged delay. We conclude that the usAHP attenuates neuronal responses to excitatory network inputs by both membrane hyperpolarization and enhanced de-inactivation of an A-current.
Highlights
Activity-dependent modification of neural network output usually results from changes in neurotransmitter release and/or membrane conductance
Data obtained from studies across a range of species, developmental stages and functional brain areas have revealed that Na+ pump function can be modified by neural network activity[2,3,4,5,6,7,8]
Swimming frequency in episode 2 was significantly lowered for all three inter-swim intervals: to 66.8 ± 2.9% of episode 1 for the 5 s interval (p < 0.05; Fig. 1D; top); 69.1 ± 4.5% for the 15s interval (p < 0.05; n = 5; Fig. 1D; middle); and 76.6 ± 4.2% for the 30s interval (p < 0.05; n = 5 ; Fig. 1D; bottom). These data suggest that the excitability of the swim central pattern generator (CPG) network in the second episode has been lowered in an interval-dependent manner
Summary
Activity-dependent modification of neural network output usually results from changes in neurotransmitter release and/or membrane conductance. Data obtained from studies across a range of species (from flies to mice), developmental stages (from embryos to adults) and functional brain areas (from sensory to motor systems) have revealed that Na+ pump function can be modified by neural network activity[2,3,4,5,6,7,8] This is due to the fact that the Na+ pumps of constituent neurons sense and respond to the increase in intracellular Na+ ion concentration that accompanies intense action potential firing. Besides increasing the excitation threshold, another dramatic effect of the usAHP is to introduce a delay to the first spike in a train so that the number of spikes for a given suprathreshold input is reduced This delay displays many of the hallmarks of an A-type K+ current (IA) being brought into play by the usAHP via enhanced deinactivation at more negative membrane potentials. Our data support the conclusion that the usAHP reduces locomotor network excitability by enhancing IA and shifting the membrane potential away from the threshold for firing in a sub-set of CPG neurons
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