Spinal motoneuron excitability is homeostatically regulated through β-adrenergic neuromodulation in wild-type and presymptomatic SOD1 mice.

Interestingly, the treatment with Adrb2/Adrb3 agonists caused a significant shortening of the AHP half-decay time in WT MNs, and an almost significant shortening (p = 0.07) in SOD1 MNs ( Fig. 4K ).

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1D - E ) and Adrb3 was unaltered in Mmp9 + and showed a trend toward downregulation in Mmp9− MNs ( Fig. 1F - G ; all statistics are reported in Supplemental Excel Table 1 ).

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