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The development of the nervous system involves the overproduction of synapses but connectivity is refined by Hebbian activity-dependent axonal competition. The newborn skeletal muscle fibers are polyinnervated but, at the end of the competition process, some days later, become innervated by a single axon. We used quantitative confocal imaging of the autofluorescent axons from transgenic B6.Cg-Tg (Thy1-YFP)16 Jrs/J mice to investigate the possible cooperation of the muscarinic autoreceptors (mAChR, M 1 -, M 2 - and M 4 -subtypes) and the tyrosine kinase B (TrkB) receptor in the control of axonal elimination after the mice  Levator auris longus (LAL)  muscle had been exposed to several selective antagonist of the corresponding receptor pathways  in vivo . Our previous results show that M 1 , M 2  and TrkB signaling individually increase axonal loss rate around P9. Here we show that although the M 1  and TrkB receptors cooperate and add their respective individual effects to increase axonal elimination rate even more, the effect of the M 2  receptor is largely independent of both M 1  and TrkB receptors. Thus both, cooperative and non-cooperative signaling mechanisms contribute to developmental synapse elimination.