SummaryMotor function deteriorates with advancing age, increasing the risk of adverse health outcomes. While it is well established that skeletal muscles and neuromuscular junctions (NMJs) degenerate with increasing age, the effect of aging on α‐motor neurons and their innervating synaptic inputs remains largely unknown. In this study, we examined the soma of α‐motor neurons and innervating synaptic inputs in the spinal cord of aged rhesus monkeys and mice, two species with vastly different lifespans. We found that, in both species, α‐motor neurons retain their soma size despite an accumulation of large amounts of cellular waste or lipofuscin. Interestingly, the lipofuscin profile varied considerably, indicating that α‐motor neurons age at different rates. Although the rate of aging varies, α‐motor neurons do not atrophy in old age. In fact, there is no difference in the number of motor axons populating ventral roots in old mice compared to adult mice. Moreover, the transcripts and proteins associated with α‐motor neurons do not decrease in the spinal cord of old mice. However, in aged rhesus monkeys and mice, there were fewer cholinergic and glutamatergic synaptic inputs directly abutting α‐motor neurons, evidence that aging causes α‐motor neurons to shed synaptic inputs. Thus, the loss of synaptic inputs may contribute to age‐related dysfunction of α‐motor neurons. These findings broaden our understanding of the degeneration of the somatic motor system that precipitates motor dysfunction with advancing age.
The inability to specifically identify and manipulate synaptic glial cells remains a major obstacle to understanding fundamental aspects of synapse formation, stability and repair. Using a combinatorial gene expression approach, we discovered molecular markers that allow us to specifically label perisynaptic Schwann cells (PSCs), glial cells at neuromuscular synapses. Using these markers, we demonstrate that PSCs fully-differentiate postnatally and have a unique molecular signature that includes genes predicted and known to play critical roles at synapses. These findings will serve as a springboard for unprecedented approaches for studying molecular determinants of PSC differentiation and function at neuromuscular synapses and possibly synapseassociated glia throughout the CNS.
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