Learn More
Auditory evoked responses recorded from the CA3 region of the rat hippocampus show diminished response to repeated stimuli, suggesting the activity of an inhibitory gating mechanism. The effects on this putative gating mechanism of two GABAB receptor antagonists, CGP35348 and CGP46381, were characterized in a conditioning testing paradigm. Both compounds,(More)
Hormones may produce long-term effects on excitability by regulating K+ channel gene expression. Previous studies demonstrated that administration of dexamethasone, a glucocorticoid receptor agonist, to adrenalectomized rats, rapidly induces Kv1.5 K+ channel expression in the ventricle of the hear. Here, RNase protection assays and Northern blots are used(More)
Hypertension-induced cardiac hypertrophy is associated with alterations in ventricular action potentials. To understand molecular mechanisms underlying this electrical abnormality, expression of cardiac voltage-gated K+ channel subunit genes was examined in ventricles of renovascular hypertensive rats. While generating a rat Kv4.3 probe, we discovered a(More)
Adaptive supersensitivity in the guinea pig vas deferens has been shown previously to be associated with decreases in transmembrane potential, Na+/K+-ATPase activity, [3H]ouabain binding sites, and density of the alpha 2 subunit of the pump. One of several procedures that induce adaptive supersensitivity in the guinea pig vas deferens is neurotransmitter(More)
Regulation of voltage-gated K+ channel genes represents an important mechanism for modulating cardiac excitability. Here we demonstrate that expression of two K+ channel mRNAs is reciprocally controlled by cell-cell interactions between adult cardiac myocytes. It is shown that culturing acutely dissociated rat ventricular myocytes for 3 h results in a(More)
Adaptive supersensitivity has been demonstrated previously in the guinea pig vas deferens after chronic treatment with reserpine, postganglionic denervation, or preganglionic denervation. The magnitude of the change in sensitivity was similar regardless of the method of induction; the underlying mechanism was identified as a partial depolarization secondary(More)
Previously, we reported that cell-cell contact regulates K(+) channel mRNA expression in cultured adult rat cardiac myocytes. Here we show that exposing cardiac myocytes to tyrosine kinase inhibitors (genistein, tyrphostin A25), but not inactive analogs, prevents downregulation of Kv1.5 mRNA and upregulation of Kv4.2 mRNA normally observed when they are(More)
The biosynthetic enzyme peptidylglycine alpha-amidating monooxygenase catalyzes the formation of a variety of biologically active alpha-amidated peptides from respective COOH-terminal glycine-extended peptide precursors. Peptidylglycine alpha-amidating monooxygenase activity is dependent on copper, ascorbate, and molecular oxygen and is inhibited by the(More)
  • 1