Learn More
Several neurotransmitters, including acetylcholine, regulate neuronal tone by suppressing a non-inactivating low-threshold voltage-gated potassium current generated by the M-channel. Agonist dependent control of the M-channel is mediated by calmodulin, activation of anchored protein kinase C (PKC), and depletion of the phospholipid messenger(More)
All subtypes of KCNQ channel subunits (KCNQ1-5) require calmodulin as a co-factor for functional channels. It has been demonstrated that calmodulin plays a critical role in KCNQ channel trafficking as well as calcium-mediated current modulation. However, how calcium-bound calmodulin suppresses the M-current is not well understood. In this study, we(More)
β(1)- and β(2)-adrenergic receptors utilize different signaling mechanisms to control cardiac function. Recent studies demonstrated that β(2)-adrenergic receptors (β(2)ARs) colocalize with some ion channels that are critical for proper cardiac function. Here, we demonstrate that β(2)ARs form protein complexes with the pacemaker HCN4 channel, as well as with(More)
Neuronal excitability is strictly regulated by various mechanisms, including modulation of ion channel activity and trafficking. Stimulation of m1 muscarinic acetylcholine receptor (also known as CHRM1) increases neuronal excitability by suppressing the M-current generated by the Kv7/KCNQ channel family. We found that m1 muscarinic acetylcholine receptor(More)
Valproic acid (VPA) has been widely used for decades to treat epilepsy; however, its mechanism of action remains poorly understood. Here, we report that the anticonvulsant effects of nonacute VPA treatment involve preservation of the M-current, a low-threshold noninactivating potassium current, during seizures. In a wide variety of neurons, activation of(More)
Chronic experiments on hypophysectomized dogs with gastric and small intestinal fistulas as well as with hypothalamus-implanted electrodes have shown that blockade of alfa-adrenoreceptors by phentolamine increases the number of the excitatory motility responses while stimulating hypothalamic structures during rest of the gastrointestinal tract and decreases(More)
Chronic experiments in dogs showed that, after i.v. injection of oxytocin, the latency of activation of gastrointestinal motility by the stimulation of median hypothalamic structures was increased and inhibitory effects of posterior hypothalamic structures on the contractile activity of the digestive tract were intensified. The data obtained suggests that(More)
Light and electron microscopy and spectrophotometry were employed in study of the morphofunctional condition of the hypothalamo-hypophyseal neurosecretory system (HHNS) of intact rats after exposure to stress in injection of substance P. Injection of 12.5 mcg/100g of substance P decelerates the outflow of the neurosecretory substance in intact animals and(More)