PMID- 19416672 OWN - NLM STAT- MEDLINE DCOM- 20090526 LR - 20220309 IS - 1090-2430 (Electronic) IS - 0014-4886 (Print) IS - 0014-4886 (Linking) VI - 217 IP - 1 DP - 2009 May TI - Daily intermittent hypoxia augments spinal BDNF levels, ERK phosphorylation and respiratory long-term facilitation. PG - 116-23 LID - 10.1016/j.expneurol.2009.01.017 [doi] AB - Acute intermittent hypoxia (AIH) elicits a form of respiratory plasticity known as long-term facilitation (LTF). We hypothesized that: 1) daily AIH (dAIH) preconditioning enhances phrenic and hypoglossal (XII) LTF in a rat strain with low constitutive LTF expression; 2) dAIH induces brain-derived neurotrophic factor (BDNF), a critical protein for phrenic LTF (pLTF) in the cervical spinal cord; and 3) dAIH increases post-AIH extracellular regulated kinase (ERK) activation. Phrenic and XII motor output were monitored in anesthetized dAIH- or sham-treated Brown Norway rats with and without acute AIH. pLTF was observed in both sham (18+/-9% baseline; 60 min post-hypoxia; p<0.05; n=18) and dAIH treated rats (37+/-8%; p<0.05; n=14), but these values were not significantly different (p=0.13). XII LTF was not observed in sham-treated rats (4+/-5%), but was revealed in dAIH pretreated rats (48+/-18%; p<0.05). dAIH preconditioning increased basal ventral cervical BDNF protein levels (24+/-8%; p<0.05), but had no significant effect on ERK phosphorylation. AIH increased BDNF in sham (25+/-8%; p<0.05), but not dAIH-pretreated rats (-7+/-4%), and had complex effects on ERK phosphorylation (ERK2 increased in shams whereas ERK1 increased in dAIH-treated rats). Thus, dAIH elicits metaplasticity in LTF, revealing XII LTF in a rat strain with no constitutive XII LTF expression. Increased BDNF synthesis may no longer be necessary for phrenic LTF following dAIH preconditioning since BDNF concentration is already elevated. FAU - Wilkerson, Julia E R AU - Wilkerson JE AD - Department of Comparative Biosciences, University of Wisconsin, School of Veterinary Medicine, Madison, WI 53706, USA. FAU - Mitchell, Gordon S AU - Mitchell GS LA - eng GR - T32 HL007654-18/HL/NHLBI NIH HHS/United States GR - R01 HL080209/HL/NHLBI NIH HHS/United States GR - T32 HL007654-20/HL/NHLBI NIH HHS/United States GR - T32 HL007654/HL/NHLBI NIH HHS/United States GR - T32 HL007654-16/HL/NHLBI NIH HHS/United States GR - HL80209/HL/NHLBI NIH HHS/United States GR - R01 HL080209-01/HL/NHLBI NIH HHS/United States GR - HL 07654/HL/NHLBI NIH HHS/United States GR - T32 HL007654-19/HL/NHLBI NIH HHS/United States GR - R01 HL080209-03/HL/NHLBI NIH HHS/United States GR - R01 HL080209-02/HL/NHLBI NIH HHS/United States GR - T32 HL007654-17/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20090203 PL - United States TA - Exp Neurol JT - Experimental neurology JID - 0370712 RN - 0 (Brain-Derived Neurotrophic Factor) RN - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases) SB - IM MH - Animals MH - Blood Gas Analysis/methods MH - Blood Pressure MH - Body Mass Index MH - Brain-Derived Neurotrophic Factor/*metabolism MH - Extracellular Signal-Regulated MAP Kinases/*metabolism MH - Hypoglossal Nerve/physiopathology MH - *Hypoxia/metabolism/pathology/physiopathology MH - Long-Term Potentiation/*physiology MH - Male MH - Phosphorylation/physiology MH - Phrenic Nerve/physiopathology MH - Radioimmunoassay/methods MH - Rats MH - *Respiration MH - Spinal Cord/*metabolism MH - Time Factors MH - Vagotomy/methods PMC - PMC2691872 MID - NIHMS115682 EDAT- 2009/05/07 09:00 MHDA- 2009/05/27 09:00 PMCR- 2010/05/01 CRDT- 2009/05/07 09:00 PHST- 2008/07/04 00:00 [received] PHST- 2009/01/23 00:00 [revised] PHST- 2009/01/27 00:00 [accepted] PHST- 2009/05/07 09:00 [entrez] PHST- 2009/05/07 09:00 [pubmed] PHST- 2009/05/27 09:00 [medline] PHST- 2010/05/01 00:00 [pmc-release] AID - S0014-4886(09)00039-9 [pii] AID - 10.1016/j.expneurol.2009.01.017 [doi] PST - ppublish SO - Exp Neurol. 2009 May;217(1):116-23. doi: 10.1016/j.expneurol.2009.01.017. Epub 2009 Feb 3.