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. Author manuscript; available in PMC: 2011 Jan 30.
Published in final edited form as: Ann N Y Acad Sci. 2010 Jun;1198:252–259. doi: 10.1111/j.1749-6632.2010.05499.x

Figure 2.

Figure 2

Working model of cellular mechanisms giving rise to pLTF. Intermittent activation of serotonergic 5-HT2 receptors during hypoxic episodes activates protein kinase C (PKC). This, in turn, initiates new BDNF protein synthesis and increases NADPH oxidase (NOX) activity. After BDNF binds its high affinity receptor, TrkB, downstream signaling molecules include ERK MAP kinases. Although less clear, we suggest that ERK activity increases synaptic strength between descending respiratory pre-motor neurons and phrenic motor neurons, thereby expressing pLTF. Protein phosphatases (PP2A/5) normally constrain pLTF. However, ROS formation via NADPH oxidase activity inhibits these phosphatases and relieves their inhibitory constraint to pLTF. When this pathway is activated chronically, we propose that increased gene transcription occurs (i.e. in the cell nucleus), enhancing the expression of elements critical in this form of plasticity. For further detail, see ztext.

340×241mm (600 × 600 DPI)