Cancer survivors rank sensorimotor disability among the most distressing long-term consequences on chemotherapy. disorders in gait, balance and skilled movements are commonly assigned to chemotoxic damage of peripheral sensory neurons without consideration of the deterministic role played by neural circuits that translate sensory information into movement.
Compounding sensorimotor circuit dysfunction in cOIN. The diagram on the right shows key stages in translation of propriosensory signals in a spinal circuit:
Propriosensory neurons (blue object) encode and conduct signals from the periphery into the spinal cord, where synaptic potentials are produced in α motoneurons (orange object) either mono- or polysynaptically through interneurons (in). Records linked to corresponding recording sites in the circuit are displayed in temporal sequence from left to right for both control and cOIN rats
Black circles plot instantaneous firing rates (pulses per second [pps]) of corresponding spike (action potential) intervals. Dashed vertical lines mark onset of movement (3 mm from resting length: Lo) shown in bottom trace divided into dynamic and static phases, respectively, by dark gray (150-ms duration after stretch command onset) and light gray (1-s duration after the dynamic phase) bars.
Chemotherapy for cancer impairs all muscle propriosensory neurons. Representative cases of spiking activity in control (gray) and cOIN (purple) as a measure of sensory encoding in Ia (A), Iun (B), Ib (C), and II (D) propriosensors.
Chemotherapy for cancer impairs cutaneous sensory encoding.
Representative cases of receptive fields (circles on paw traces in left column; A–D), spiking activity in control (gray; E, G, I, and K) and cOIN (purple; F, H, J, and L) as a measure of cutaneous sensory encoding. Black circles plot instantaneous firing rates (pulses per second [pps]) of corresponding spike (action potential) intervals.
