Bursting

Bursting, or burst firing, is an extremely diverse general phenomenon of the activation patterns of neurons in the central nervous system and spinal cord where periods of rapid action potential spiking are followed by G0 phase quiescent periods. Bursting is thought to be important in the operation of robust central pattern generators, the transmission of neural codes, and some neuropathologies such as epilepsy. The study of bursting both directly and in how it takes part in other neural phenomena has been very popular since the beginnings of cellular neuroscience and is closely tied to the fields of neural synchronization, neural coding, plasticity, and attention. Bursting, or burst firing, is an extremely diverse general phenomenon of the activation patterns of neurons in the central nervous system and spinal cord where periods of rapid action potential spiking are followed by G0 phase quiescent periods. Bursting is thought to be important in the operation of robust central pattern generators, the transmission of neural codes, and some neuropathologies such as epilepsy. The study of bursting both directly and in how it takes part in other neural phenomena has been very popular since the beginnings of cellular neuroscience and is closely tied to the fields of neural synchronization, neural coding, plasticity, and attention. Observed bursts are named by the number of discrete action potentials they are composed of: a doublet is a two-spike burst, a triplet three and a quadruplet four. Neurons that are intrinsically prone to bursting behavior are referred to as bursters and this tendency to burst may be a product of the environment or the phenotype of the cell. Neurons typically operate by firing single action potential spikes in relative isolation as discrete input postsynaptic potentials combine and drive the membrane potential across the threshold. Bursting can instead occur for many reasons, but neurons can be generally grouped as exhibiting input-driven or intrinsic bursting. Most cells will exhibit bursting if they are driven by a constant, subthreshold input and particular cells which are genotypically prone to bursting (called bursters) have complex feedback systems which will produce bursting patterns with less dependence on input and sometimes even in isolation. In each case, the physiological system is often thought as being the action of two linked subsystems. The fast subsystem is responsible for each spike the neuron produces. The slow subsystem modulates the shape and intensity of these spikes before eventually triggering quiescence. Input-driven bursting often encodes the intensity of input into the bursting frequency where a neuron then acts as an integrator. Intrinsic bursting is a more specialized phenomenon and is believed to play a much more diverse role in neural computation. Bursts differ from tonic firing, rapid spiking at similar rates to bursting but continuing for long periods of time, in that bursting involves a physiological 'slow subsystem' that eventually depletes as the bursting continues and then must be replenished before the cell can burst again (compare refractory period). During the bursting event, this slow subsystem modulates the timing and intensity of the emitted spikes and is thought to be important in the computational aspects of the resulting burst pattern. There are many discovered mechanisms of slow subsystems including voltage- and Ca2+- gated currents and spiking interplay between dendrites and the cell body. The slow subsystem also is connected to endogenous bursting patterns in neurons, where the pattern can be maintained completely by internal mechanism without any synaptic input. This process also relies on calcium channels, which depolarize the neuron by allowing an influx of calcium ions. So long as internal calcium ion concentrations remain at an elevated level, the neuron will continue to undergo periods of rapid spiking. However, elevated calcium ion levels also trigger a second messenger cascade within the cell which lower calcium influx and promote calcium efflux and buffering. As calcium concentrations decline, the period of rapid bursting ceases, and the phase of quiescence begins. When calcium levels are low, the original calcium channels will reopen, restarting the process and creating a bursting pattern.