Journal club: The role of electrical coupling in generating and modulating oscillations in a neuronal network

by Christina Mouser, Amitabha Bose and Farzan Nadim
Mathematical Biosciences 278 (2016) 11–21

Melissa Coleman showed in her 1995 Nature paper that there is an electrical connection between MCN1 and LG. I was a grad student back then. I really liked that paper, but I have forgotten about this electrical connection.  This electrical synapse is voltage-sensitive. It gets stronger when LG was depolarized. It looks opposite to regular EPSPs which usually become smaller when depolarized. This voltage-sensitive electrical synapse seems to act as a positive feedback to LG activity.

   In this paper, Mouser et al. showed that this electrical coupling is very important for LG bursting by using a mathematical model. LG forms a Half-Center Oscillator with Int1 by forming mutually inhibitory synapses. This HCO configuration itself can generate a rhythm, which is influenced by periodic inhibition from pyrolic pacemaker (AB). However, the major finding in this paper is that the LG oscillation can also be generated without the reciprocal inhibition, but with the voltage-dependent electrical coupling between MCN1 and LG. This also indicates that the half-center configuration is not the main element that produces the rhythm; rather it is to form a pattern of activity in left-right alternation. For rhythmogenesis, some sorts of positive feedback system seems more important than mutual inhibition.

   I don't know how electrical coupling gets voltage-sensitive. I assume it not caused by changes in the coupling coefficient, but rather by overall depolarization at dendrites, which may trigger Ca influx and hence enhancing spike width.

Organization of spinal circuitry for rodent locomotion

Neuronal activity in the isolated mouse spinal cord during spontaneous deletions in fictive locomotion: Insights into locomotor CPG organization

by Guisheng Zhong, Natalia A Shevtsova, Ilya A Rybak, Ronald M Harris-Warrick

Journal of Physiology (2012)

Deletions are spontaneous errors in the rhythmic locomotor pattern when a set of synergist motoneurons (for example, flexor motoneurons on one side) loses rhythmic firing or falls silent during a time period when they are normally active. 

In the non-resetting deletions, the phase of the rhythm after the deletion did not change. The resetting deletions show rhythm resetting which was recognized by a shift in the phase of the motor bursts after the deletion. This study follows Rybak-McCrea model of the locomotor CPG, which has two functional levels: a half-center rhythm-generator and pattern formation networks. 

Deletions occur simultaneously in motor activity across more than one spinal segment. Spontaneous non-resetting deletions on one side are independent of the other side. The CPG can be functional within an isolated hemisegment. The reduction in locomotor frequency after simulated hemisection results mainly from the elimination of excitatory input to the rhythm-generating ipsilateral RG-F population from the contralateral RG-E population. The resumption of activity an integer number of cyces later does not require input from other parts of the spinal cord. Each hemicord contains an independent rhythmogenic network that can function in the absence of the other hemicord, although the left and right networks are normally coupled via commissural interneurons.

Among V2a interneurons, there are deletion-sensitive types and insensitive type (type I and II V2a interneurons). Type I V2a does not respond to non-locomotory firing in iL2, whereas type II V2a does. Both neurons were depolarized by synaptic drive. The type I V2a interneurons are involved in rhythm generation and/or coordination between left and right networks via the CINs. In contrast, the type II V2a interneurons do not belong to rhythm generator networks, but can be components of the pattern gormation network and/or last-order interneurons that directly project to motoneurons. Commissural interneurons (CINs) send their axons to the opposite side of the cord and coordinate left-right alternation. CINs were not affected by motoneuronal deletion. There was asymmetry in deletion: During all of the flexor deletions, the ipsilateral extensor root showed sustained activity with no interruptions at the times of the missing flexor bursts. In contrast, during all extensor deletions, the ipsilateral flexor root continued unperturbed bursting.

Their computational model combines the Rybak-McCrea concept of the two-level locomotor CPG (Rybak et al., 2006a,b; McCrea and Rybak, 2007,2008) with the Duysens-Pearson concept of an asymmetric rhythm generator with a dominant flexor half-centre (Pearson and Duysens, 1976).