Plasticity is an important property of the respiratory control system. One of the best-studied models of respiratory plasticity is pLTF (phrenic long-term facilitation). pLTF is a progressive increase in phrenic motor output lasting several hours following acute exposure to intermittent hypoxia. Similar to many other forms of neuroplasticity, pLTF is pattern-sensitive; it is induced by intermittent, but not sustained hypoxia of similar cumulative duration. Our understanding of the cellular/synaptic mechanisms underlying pLTF has increased considerably in recent years. Here, we review accumulating evidence suggesting that the pattern-sensitivity of pLTF arises substantially from differential reactive oxygen species formation and subsequent protein phosphatase inhibition during intermittent compared with sustained hypoxia in or near phrenic motor neurons. A detailed understanding of the cellular/synaptic mechanisms of pLTF may provide the rationale for new pharmacological approaches in the treatment of severe ventilatory control disorders, such as obstructive sleep apnoea and respiratory insufficiency either following spinal cord injury or during neurodegenerative diseases such as amyotrophic lateral sclerosis.
Respiratory plasticity following intermittent hypoxia: roles of protein phosphatases and reactive oxygen species
J.E.R. Wilkerson, P.M. MacFarlane, M.S. Hoffman, G.S. Mitchell; Respiratory plasticity following intermittent hypoxia: roles of protein phosphatases and reactive oxygen species. Biochem Soc Trans 1 November 2007; 35 (5): 1269–1272. doi: https://doi.org/10.1042/BST0351269
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