Linking motor cortex activity and movement in the mouse orofacial system.

NIH RePORTER · NIH · R01 · $412,498 · view on reporter.nih.gov ↗

Abstract

Information flow through neural circuits is dynamic. The set of brain areas that are engaged in computation are ever changing according to behavioral demands. How circuits in the brain are functionally coupled and uncoupled on behavioral time scales so that information can be relayed to the appropriate place at the appropriate time remains a major outstanding question in systems neuroscience. This question is of particular relevance in the motor system. The production of movements is one of the most fundamental functions of the brain, and in mammals, flexible movements depend on the motor cortex. Neural activity in the motor is cortex complex, made up of control signals that drive movements in addition to activity related to motor planning, learning, and other cognitive processes. This wide array of signals is multiplexed within the same circuit and, often, within the same cells. How does the brain regulate which activity patterns are communicated to the periphery to drive movements and which are confined to local circuits for local cortical computation? An influential hypothesis proposed to explain why only some activity patterns generate movements – the null space model – provides a biologically plausible computational strategy for segregating cognitive signals from those that are transmitted to the periphery to produce movement. The null space model suggests that cognitive signals are restricted to patterns whose impact on downstream motor areas effectively cancel out – they are ‘output-null.’ Preliminary evidence suggests that activity patterns in the primate motor cortex may be consistent with the null space model, but thus far it has been challenging to establish a causal link between these neural activity patterns and behavior. In this proposal, we examine the flow of neural signals from the motor cortex to the motor neurons that control the musculature to determine whether the null space model accurately predicts which neural signals have a causal role in generating movements. Powerful, emerging methods for multi-regional physiology allow us to examine neural activity at each processing stage along this pathway, an essential requirement for understanding how cortical activity patterns are transformed into movements. Cell-type specific optogenetic perturbations allow us to disambiguate the neural signals that drive movements from those that are simply a consequence and will help to establish a causal relationship between neural activity and movements. Understanding how neural activity relates to behavior will ultimately help us better interpret the deficits expressed in movement disorders and motivate improved brain-machine interfaces and biomimetic control strategies for use in the next generation of artificial systems.

Key facts

NIH application ID
10367341
Project number
1R01NS121409-01A1
Recipient
BOSTON UNIVERSITY (CHARLES RIVER CAMPUS)
Principal Investigator
Michael Nicholas Economo
Activity code
R01
Funding institute
NIH
Fiscal year
2022
Award amount
$412,498
Award type
1
Project period
2022-02-01 → 2027-01-31