CRCNS: Multi-Scale Models of Proprioceptive Encoding for Sensorimotor Control

Information from muscle spindle sensory afferents play a critical role in sensorimotor control of movement. Altered muscle spindle function is implicated in sensorimotor impairments, including spasticity in stroke, cerebral palsy, spinal cord injury, and other neural injuries, as well as in dystonia, hypotonia, and Parkinson’s disease. In neurological disorders, muscle spindle function can be altered at many levels of neuromuscular organization. For example, muscle fiber types and muscle tissue stiffness change following stroke and spinal cord injury, which could change the transduction of movement to the muscle spindle. Autonomic dysfunction and altered neuromodulators secretion is associated with spinal cord injury as well as Parkinson’s disease, which could affect the input-output properties of both sensory and motor neurons. Teasing apart these multi-scale factors and their impact on sensorimotor control is challenging if not impossible during behavior. However current muscle spindle models are largely phenomenological and do not have representations of mechanstic muscle and neuron properties. This limitations of current model reflect the fact that despite decades of work, the basic mechanisms of muscle spindle sensory encoding are not well understood. Classically, muscle spindle instantaneous firing rates (IFRs) are described to encode muscle length and velocity information necessary for movement. However, an overwhelming amount of evidence shows that muscle spindle IFRs have highly non-unique and history-dependent relationships to muscle length and velocity. These history-dependent properties have been attributed to characteristic of force generation in muscle contractile proteins, i.e. cross-bridges. Further, neuromodulators and neurotransmitters from the peripheral and autonomic nervous systems can alter muscle spindle IFRs (Bewick). Muscle spindle IFRs also depend upon the mechanical properties of the surrounding muscle and connective tissues as well as the activity level of the spindle-bearing muscle. Moreover, the ion channels responsible for mechanotransduction in primary muscle spindle afferents are only just being identified (REF).