Spinal Noradrenergic Overdrive Promotes Reversible Motor Unit Aging and Sarcopenia

Aging in mice (1–25 months) drives progressive spinal motor neuron hyperexcitability, linked to enhanced activity-dependent norepinephrine release and impaired autoregulation.

• Why it matters: Motor unit degeneration contributes to sarcopenia, but how age alters spinal noradrenergic control of motor neurons, NMJs, and muscle fibers is not well defined.
• What they did: Using patch-clamp recordings from 135 lumbar motor neurons in 81 mice, the study measured NE dynamics (optogenetics, voltammetry, microdialysis/HPLC) and tested aged mice with retrograde chemogenetic inhibition of descending noradrenergic neurons.
• The result: In aged mice, NE release increased at 20–40 Hz and NE storage rose while 2A-adrenergic receptor and NET expression fell; suppressing descending noradrenergic input increased hindlimb muscle mass, fiber size, NMJ innervation, and motor neuron soma size.

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