Wilkinson Lab Goals

1) To understand how the muscle spindle senses muscle stretch and how the sensitivity of muscle spindle afferents are controlled.

2) To understand how environmental conditions and/or disease states impair the function of the muscle spindle.

Current Research

  • Control of gamma motor neuron activity using optogenetics

We are currently developing an optogenetics technique to study the gamma motor neurons that innervate the muscle spindle and are vital for motor control. The length of the muscle spindle is controlled by gamma motor neurons innervating the intrafusal muscle fibers of the spindle. However, it has been challenging to study the gamma motor neurons since it is hard to specifically stimulate the small gamma but not the larger alpha motor neurons that control the force generating extrafusal fibers using electrical stimulation.  We express the blue light activated channelrhodopsin2 (ChR2) in ChAT positive motor neurons and use lower optical intensities of light to recruit the small gamma motor neurons first. We plan to use this technique to study gamma motor neuron function in vitro. This tool will also allow us to assay intrafusal fiber function in disease states.

  • Modulation of muscle spindle afferent excitability by glutamate 

Synaptic-like vesicles containing glutamate are found within muscle spindle afferent peripheral nerve endings. These vesicles are released in an activity dependent manner, with an increase in vesicle release following multiple stretches or high frequency vibration. This glutamate is thought to increase afferent sensitivity to stretch as exogenous glutamate can increase whole nerve firing rate during stretch. However, the effect on individual afferents has not been determined. We are characterizing the precise role of glutamate in the functioning of muscle spindle afferents, the sensory neurons responsible for proprioception or the ability to sense one’s body position. Currently, we are directly recording afferent activity and stretch response in muscles from both wild-type mice and those lacking a copy of the vesicular glutamate transporter 1 (VGLUT1) gene. Since the VGLUT1 gene encodes for a protein needed for glutamate packaging and release, we expect to see altered or aberrant stretch response in the afferents of mice that lack a single copy of this gene. Through direct recordings we hope to deepen our understanding of the role of glutamate in proprioception.