[Participation of synaptotagmin in release of catecholamines in rat adrenal chromaffin cells].

Exocytosis is known to provide such a vital processes as the release of neurotransmitters in synaptic transmission or release of hormones during secretion. The main mechanism of exocytotic process occurs through the specialized protein complex called the SNARE-complex. Due to its activity the fusion of vesicular and plasma membrane occurs and fusion pore is formed through which a content of vesicles is released outside. It is believed that just synaptotagmins which are Ca2+ dependent proteins, responsible for initiation of the process of Ca(2+)-dependent exocytosis. Synaptotagmins are located at the membrane of the vesicles and can bind two or three Ca2+ ions. In our research, we studied the role of one of the most common isoform of synaptotagmines--synaptotagmin-1. For this we used an injection of antibodies arised to synaptotagmin-1 (anti-STg-1) into isolated rat adrenal chromaffin cells to depress the function of this protein. Catecholamine secretion was measured by amperometric method. Our results showed that an exclusion of synaptotagmin-1 function in tested cells resulted in significant suppression of secretion. These data allow us to conclude that synaptotagmin-1 is a key protein which is needed for Ca(2+)-dependent exocytosis in chromaffin cells.

Acetylcholine-induced calcium signalling in adrenaline- and noradrenaline-containing adrenal chromaffin cells.

Adrenal chromaffin cells secrete catecholamines in response to cholinergic receptor activation by acetylcholine (ACh). Characteristics of Ca(2+) transients induced by activation of nicotinic (nAChRs) and muscarinic (mAChRs) receptors were analyzed using Fura-2 fluorescent measurements on rat chromaffin cells. We first found two populations of chromaffin cells, which differently responded on AChR stimulation. In the first group (n-cells), consecutive ACh applications evoked persistent Ca(2+) transients, whereas desensitizing transients were observed in the other group (m-cells). The AChR agonists and antagonists precisely imitated or abolished the ACh action on n- and m-type cells, respectively. Cytochemical staining showed that n-cells contained adrenaline, whereas m-cells-noradrenaline. Thus, for the first time we found that nAChRs and mAChRs are differentially expressed in adrenergic and noradrenergic chromaffin cells, respectively. Our data suppose that chromaffin cells can be differentially regulated by incoming ACh signals and in such way release different substances-adrenaline and noradrenaline.

[Electrochemical studies of induced secretion of catecholamines from individual vesicles of rat chromaffin cells]. / Elektrokhimicheskie issledovaniia indutsiruemoi sekretsii katekholaminov iz odinochnykh vezikul khromaffinnykh kletok krysy.

Influence of agents inducing secretion: KCl-induced membrane depolarization and acetylcholine on catecholamine secretion from individual vesicles of rat chromaffin cells was studied by using amperometric methods. It has been shown that secretory components participating in these processes are different. An importance of cellular response on different kind of stimulation is discussed.