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Department of Nerve-Muscle Physiology was established in 1967.

Main research programs include investigation of the electrophysiological properties and mechanisms of the excitation-contraction coupling and synaptic transmission in smooth muscle, regulation of vascular tone and its importance in hypertension, Ca entry pathways, mechanisms of Ca-induced Ca release, Ca metabolism in smooth muscle cells during membrane depolarization and activation of cell-surface receptors for various excitatory and inhibitory neurotransmitters, modulatory effects of NO on smooth muscle contraction and Ca channels.

Important discoveries of the past are electrical low-resistance contacts between smooth muscle cells (cable properties), inhibition by apamin of the non-adrenergic non-cholinergic synaptic transmission, isolation and biophysical properties of Ca current in smooth muscle cells and other. In recent years signal transduction mechanisms which involve various membrane ion channels have been extensively characterized using patch-clamp recording techniques. Our research, teaching and training activities led to 25 PhD and 5 Doctor of Science degrees awarded. Many members of the department presently continue successful research or maintain close collaborative links with leading physiological laboratories abroad.

Current research program is entitled "Membrane and intracellular mechanisms of the regulation of contraction and ion channel activity in smooth muscle cells."(2001-2004)

• Mechanisms of the depolaruring action of acetelcholine on intestinal smooth muscle cells.
• Membrane and intracellular mechanisms of the inhibitory action of ATP on gostrointestinal smooth muscle cells.
• Role of endothelium in the regulation of intracellular Ca concentration in arteries.
• Investigation of intracellular calcium events in relation to ion channel activity and smooth muscle contraction and vascular tone.

Past research program entitled "Mechanisms of metabolic regulation of ion channels and contraction in smooth muscle cells" (1998-2000). Specific targets we aim to achieve include

• to investigate the effects of hypoxia, ATP, GTP and various protein kinases activators and blockers on the biophysical properties of L type voltage-gated Ca2+ channels;
• to investigate protein kinase-dependent regulation of Ca2+-activated K+ channels;
• to study mechanical properties of large and resistance arteries and the effects of hypoxia and protein kinases involvement in smooth muscle contraction/relaxation.