Нейронные взрывы: механизмы и характеристики.

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 quiescent periods much longer than typical inter spike intervals. Bursting is thought to be important in the operation of robust central pattern generators, 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. and |Ca(2+) 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.

In isolation or in mathematical models bursting can be recognized since the environment and state of the neuron can be carefully observed and modulated. When observing neurons in the wild, however, bursting may be difficult to distinguish from normal firing patterns. In order to recognize bursting patterns in these contexts statistical methods are used to determine threshold parameters. Bursting is characterized by a coefficient of variation (CV) of the interspike intervals (ISI) that is larger than one, or a Fano factor of the spike count that is larger than one, because bursting leads to spike patterns that are more irregular than a Poisson process (which has a CV and Fano factor equal to unity). Alternatively, the serial correlation coefficient of the ISI sequence is positive for bursting patterns, because in this case short ISIs tend to be followed by more short ISIs (at least if the bursts consist of more than two spikes).

Some neurons, sometimes called resonators, exhibit sensitivity for specific input frequencies and fire either more quickly or exclusively when stimulated at that frequency. Intrinsically bursting neurons can use this band pass filtering effect in order to encode for specific destination neurons and multiplex signals along a single axon. When combined with burst dependent long term plasticity, such multiplexing can allow neurons to coordinate synaptic plasticity across hierarchical networks.

Burst synchronization refers to the alignment of bursting and quiescent periods in interconnected neurons. In general, if a network of bursting neurons is linked it will eventually synchronize for most types of bursting. Synchronization can also appear in circuits containing no intrinsically bursting neurons, however its appearance and stability can often be improved by including intrinsically bursting cells in the network. In order to perform this function, it uses intrinsically bursting neurons to convert promising single stimuli into longer lasting burst patterns as a way to better focus attention on new stimuli and activate important processing circuits. Once these circuits have been activated, the subicular signal reverts to a single spiking mode.

The pre Bötzinger complex (preBötC) is located in ventrolateral medulla and is proposed to generate the rhythm underlying inspiratory efforts in mammals. Since the frequency that the lungs need to operate at can vary according to metabolic demand, preBötC activity is modulated over a wide range of frequencies and is able to entrain the respiratory system to meet metabolic demand. While pacemaker neurons do not necessarily require intrinsically bursting neurons

Cerebellar Purkinje neurons have been proposed to have two distinct bursting modes: dendritically driven, by dendritic spikes, and somatically driven, wherein the persistent current is the burst initiator and the SK current is the burst terminator. Purkinje neurons may utilise these bursting forms in information coding to the deep cerebellar nuclei.