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Maternal Diabetes Increases a Large Conductance Ca2+‐activated K+ (BK) Current of Cardiac Motoneurons in the Nucleus Ambiguus (NA) of Neonatal Mice
Author(s) -
Lin Min,
Li Lihua,
Epstein Paul N.,
Wurster Robert D.,
Liu Yeqi,
Cheng Zixi Jack
Publication year - 2008
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.22.1_supplement.950.6
Subject(s) - charybdotoxin , endocrinology , iberiotoxin , medicine , chemistry , nucleus ambiguus , bk channel , brainstem , membrane potential , potassium channel , central nervous system , medulla oblongata , biochemistry
Maternal diabetes induces baroreflex dysfunction in the offspring. In a companion work (Lin et al. 2008, EB Abstract), we demonstrated that maternal diabetes altered the activity of Ca2+ and Ca2+—activated K+ channels of NA cardiac motoneurons in the neonatal mice of diabetic mothers. In the present study, neonatal mice from FVB control and OVE26 diabetic mothers (mated with FVB fathers) received tracer XRITC injections into the pericardial sac on postnatal days 7–9. Two days later, membrane currents of XRITC‐labeled NA cardiac motoneurons in brainstem slices were recorded using a whole‐cell patch technique. Compared with control, our data indicated that maternal diabetes significantly increased: 1) K+ channel activity of transient outward currents but not persistent currents evoked by voltage steps, 2) Cd2+ (calcium channel blocker cadmium)‐sensitive K+ channel conductance for transient outward currents but not persistent currents (n=8; p<0.05), 3) ChTX (BK channel blocker charybdotoxin)‐sensitive K+ channel conductance for both the transient and persistent outward currents, and the maximum values of ChTX‐sensitive transient and persistent currents at +40 mV (n=13; p<0.05). Thus, we conclude that the increased BK channel activity contributes to the decreased excitability of NA cardiac motoneurons in the neonatal mice of diabetic mothers. NIHRO1 HL‐79636.