Motor neurons of the crustacean cardiac ganglion generate virtually identical, synchronized output despite the fact that each neuron uses distinct conductance magnitudes. As a result of this variability, manipulations that target ionic conductances have distinct effects on neurons within the same ganglion, disrupting synchronized motor neuron output that is necessary for proper cardiac function. We hypothesized that robustness in network output is accomplished via plasticity that counters such destabilizing influences. By blocking high-threshold K + conductances in motor neurons within the ongoing cardiac network, we discovered that compensation both resynchronized the network and helped restore excitability. Using model findings to guide experimentation, we determined that compensatory increases of both G A and electrical coupling restored function in the network. This is one of the first direct demonstrations of the physiological regulation of coupling conductance in a compensatory context, and of synergistic plasticity across cell- and network-level mechanisms in the restoration of output.
Neurons can communicate with each other by releasing chemicals called neurotransmitters, or by forming direct connections with each other known as gap junctions. These direct connections allow electrical impulses to flow from one neuron to another via pores in the membranes between the cells. Unlike communication via neurotransmitters, gap junctions are usually thought to be hard-wired and unchanging over the life of the animal.
Lane et al. recorded electrical activity in a network of neurons that generates rhythmic heart contractions in the Jonah crab. Neurons in this network usually all fire an electrical impulse at the same time, which is crucial to make sure that the whole heart contracts at the same time. The experiments show that drugs that block potassium channel pores in the membrane cause the neurons to fire too much and at different times to each other.
However, the network of neurons soon adapted to the changes caused by the drugs and returned to working as normal. Mimicking these changes in a computer model of the neuron network, together with experimental data, showed that changes to the gap junctions play a major role in restoring normal activity to the network.
The next step following on from this research is to understand how a network of neurons ‘senses’ that it is not working normally and changes its electrical activity.