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The Journal of Neuroscience, March 12, 2008, 28(11):2949-2958; doi:10.1523/JNEUROSCI.5539-07.2008

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 Previous Article

Development/Plasticity/Repair
Okadaic Acid-Sensitive Protein Phosphatases Constrain Phrenic Long-Term Facilitation after Sustained Hypoxia

Julia E. R. Wilkerson, Irawan Satriotomo, Tracy L. Baker-Herman, Jyoti J. Watters, and Gordon S. Mitchell

Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin 53706

Correspondence should be addressed to Julia E. R. Wilkerson, Department of Comparative Biosciences, University of Wisconsin, 2015 Linden Drive, Madison, WI 53706. Email: wilkersj{at}svm.vetmed.wisc.edu

Phrenic long-term facilitation (pLTF) is a serotonin-dependent form of pattern-sensitive respiratory plasticity induced by intermittent hypoxia (IH), but not sustained hypoxia (SH). The mechanism(s) underlying pLTF pattern sensitivity are unknown. SH and IH may differentially regulate serine/threonine protein phosphatase activity, thereby inhibiting relevant protein phosphatases uniquely during IH and conferring pattern sensitivity to pLTF. We hypothesized that spinal protein phosphatase inhibition would relieve this braking action of protein phosphatases, thereby revealing pLTF after SH. Anesthetized rats received intrathecal (C4) okadaic acid (25 nM) before SH (25 min, 11% O₂). Unlike (vehicle) control rats, SH induced a significant pLTF in okadaic acid-treated rats that was indistinguishable from rats exposed to IH (three 5 min episodes, 11% O₂). IH and SH with okadaic acid may elicit pLTF by similar, serotonin-dependent mechanisms, because intravenous methysergide blocks pLTF in rats receiving IH or okadaic acid plus SH. Okadaic acid did not alter IH-induced pLTF. In summary, pattern sensitivity in pLTF may reflect differential regulation of okadaic acid-sensitive serine/threonine phosphatases; presumably, these phosphatases are less active during/after IH versus SH. The specific okadaic acid-sensitive phosphatase(s) constraining pLTF and their spatiotemporal dynamics during and/or after IH and SH remain to be determined.

Key words: plasticity; pattern; phosphatase; control of breathing; motor neuron; hypoxia

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Received Aug. 17, 2007; revised Jan. 25, 2008; accepted Jan. 28, 2008.

Correspondence should be addressed to Julia E. R. Wilkerson, Department of Comparative Biosciences, University of Wisconsin, 2015 Linden Drive, Madison, WI 53706. Email: wilkersj{at}svm.vetmed.wisc.edu

This article has been cited by other articles:

				K.-Z. Lee, P. J. Reier, and D. D. Fuller Phrenic Motoneuron Discharge Patterns During Hypoxia-Induced Short-Term Potentiation in Rats J Neurophysiol, October 1, 2009; 102(4): 2184 - 2193. [Abstract] [Full Text] [PDF]

				P. M. MacFarlane, I. Satriotomo, J. A. Windelborn, and G. S. Mitchell NADPH oxidase activity is necessary for acute intermittent hypoxia-induced phrenic long-term facilitation J. Physiol., May 1, 2009; 587(9): 1931 - 1942. [Abstract] [Full Text] [PDF]

				J. H. Mateika and G. Narwani Intermittent hypoxia and respiratory plasticity in humans and other animals: does exposure to intermittent hypoxia promote or mitigate sleep apnoea? Exp Physiol, March 1, 2009; 94(3): 279 - 296. [Abstract] [Full Text] [PDF]

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