Central pattern generator

Central pattern generators (CPGs) are self-organizing biological neural circuits that produce rhythmic outputs in the absence of rhythmic input. They are the source of the tightly-coupled patterns of neural activity that drive rhythmic and stereotyped motor behaviors like walking, swimming, breathing, or chewing. The ability to function without input from higher brain areas still requires modulatory inputs, and their outputs are not fixed. Flexibility in response to sensory input is a fundamental quality of CPG-driven behavior. To be classified as a rhythmic generator, a CPG requires:

CPGs are found in humans and most other vertebrates, and in some invertebrates.

CPG neurons can have different intrinsic membrane properties (see schematic). Some neurons fire bursts of action potentials, either endogenously or in the presence of neuromodulatory substances. Other neurons are bistable and generate plateau potentials that can be triggered by a depolarizing current pulse, and terminated by a hyperpolarizing current pulse. Many CPG neurons fire after being released from inhibition (postinhibitory rebound). Another common feature of CPG neurons is a decrease in the frequency of firing during a constant depolarization (spike frequency adaptation).

Rhythm generation in CPG networks depends on the intrinsic properties of CPG neurons and their synaptic connections. There are two general mechanisms for rhythm generation: pacemaker/follower and reciprocal inhibition (see schematic).

In a network driven by a pacemaker, one or more neurons act as a core oscillator (pacemaker) that drives other, non-bursting neurons (follower) into a rhythmic pattern. Examples of pacemaker driven networks include the pyloric rhythm of the crustacean stomatogastric ganglion and the vertebrate respiratory rhythms.

In a network driven by reciprocal inhibition, two (groups of) neurons reciprocally inhibit each other. Such networks are known as half-center oscillators. The neurons are not rhythmically active when isolated, but they can produce alternating patterns of activity when coupled by inhibitory connections. (The neurons can also produce activity patterns of other relative phasing, including synchrony, depending on the synaptic properties). The transitions between activated and inhibited states can occur via a number of mechanisms. For example, spike-frequency adaptation in the bursting neuron(s) may slowly release the other neuron(s) from inhibition. Reciprocal inhibition is a core feature of many CPGs, including those involved in locomotion.  

Gap junctions also contribute to rhythmic oscillations and neuronal synchrony in CPGs. They act as low-pass filter allowing slow membrane voltage fluctuations to pass more effectively across cells. In neonatal mice, blocking gap junctions results in decreased rhythmic activity and can completely abolish drug induced fictive locomotion. In zebrafish, motor neurons retrogradely control swim frequency via gap junctions.

CPG networks have extensive recurrent synaptic connections including reciprocal excitation and reciprocal inhibition. Synapses in CPG networks are subject to short-term activity dependent modifications. Short-term synaptic depression and facilitation of synapses can play a role in transitions between active and inactive phases of bursting and termination of bursts.