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Differential regulation of ventral spinal atypical PKC and ERK MAP kinase following hypocapnia‐induced respiratory neural inactivity
Author(s) -
Broytman Oleg,
Strey Kristi A,
BakerHerman Tracy L
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.799.7
Subject(s) - hypocapnia , protein kinase c , mapk/erk pathway , chemistry , neuroplasticity , respiratory system , phrenic nerve , microbiology and biotechnology , endocrinology , kinase , anesthesia , medicine , biology , neuroscience , biochemistry , hypercapnia
Hypocapnia‐induced respiratory neural inactivity elicits mechanisms of plasticity that enhance phrenic motor output once activity is restored, an effect known as inactivity‐induced phrenic motor facilitation (iPMF). Since atypical protein kinase C (aPKC) activity is necessary for iPMF, we tested the hypothesis that iPMF is associated with increased aPKC expression in spinal regions associated with the phrenic motor nucleus. Anesthetized and ventilated rats were exposed to 30 min of hypocapnia (5–10 mmHg below baseline) to reversibly stop respiratory neural activity. Following hypocapnia, ventral C3–C5 was fractionated into membrane‐enriched, cytoplasm‐enriched and nucleus‐enriched fractions. Total and phosphorylated aPKC increased in membrane‐enriched (47 +/− 10 and 39 +/− 11%, respectively, p<0.05), but decreased in cytoplasm‐enriched fractions (−77 +/− 5 and −74 +/− 6%, respectively, p<0.05) post‐hypocapnia. In contrast, there were no significant changes in membrane or cytoplasmic expression of phosphorylated ERK (−41 +/− 14 and −12 +/− 10%, respectively, p>0.05), a kinase implicated in other forms of spinal plasticity. Phospho‐ERK was increased in nuclear fractions post‐hypocapnia (97 +/− 17%, p<0.05), suggesting a possible role for ERK in longer‐lasting forms of plasticity elicited by neural inactivity. These data support a prominant role for aPKC in iPMF following hypocapnia ( NIH HL69064).