Fig. 6.

Schematic illustrating cellular mechanisms giving rise to phenotypically similar pathways to phrenic motor facilitation (pMF). Our findings indicate that spinal AMP-activated protein kinase (AMPK) activation cancels selective pathways to pMF, and possible mechanisms are suggested based on literature, such as 1) directly or indirectly (i.e., via tuberous sclerosis complex activation) AMPK-induced mammalian target of rapamycin complex inhibition (mTORC), and 2) phosphodiesterase (PDE)-induced cAMP downregulation. BDNF, brain-derived neurotrophic factor; TrkB, tyrosine receptor kinase B; EPAC, exchange protein activated by cAMP, mTOR, or mammalian target of rapamycin complex.