Tag Archives: exocytosis
The Department of Neurochemistry from 1925 untill the present day
N. Krisanova, N. Pozdnyakova*
Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine,
Department of Neurochemistry, Kyiv;
*e-mail: nataly.pozdniakova@gmail.com
Received: 11 June 2025; Revised: 14 August 2025;
Accepted: 30 October 2025; Available on-line: 2025
Activity in the Department of Neurochemistry from 1925 until the present day was described in particular. The main scientific areas of research at the Department of Biochemistry of the Nervous System until 1982 were following: study of the chemical topography of the nervous system; study of subcellular and suborganoid localization of neurospecific proteins; investigation of the effect of psychotropic agents on nitrogen, carbohydrate, and protein metabolism in the structures of the nervous system; studying membrane organization and function mechanisms of enzyme systems for active transport of sodium, potassium, and calcium in nerve cells. Since 1982, research in the Department has been focused primarily on the following areas: biogenesis of membrane and secretory proteins; research on neurospecific proteins; research on plasma membrane directly involved in the generation and transmission of nerve signals. Since 2010, the research of the Department of Neurochemistry was aimed at solving the following urgent problems: elucidation of the role of structural organization of membrane and lipid- protein interactions in the regulation of nerve signal transmission process; elucidation of the role of presynaptic receptors in the regulation of key stages of neurotransmission process and determination of the ways to modulate the neurotransmitter reception system; search and identification of natural membranotropic and neuroactive compounds, analysis of the molecular mechanisms of existing membranotropic and neuroactive drugs action; space biology, namely the development of a method for determining the toxicity of planetary dust; nanotechnology, namely the synthesis and analysis of the neuroactive effect of nanoparticles; environmental neurotoxicology, namely the study of the neurotoxic effects of environmental pollutants and the development of the ways to overcome their harmful impact.
Perinatal hypoxia and thalamus brain region: increased efficiency of antiepileptic drug levetiracetam to inhibit GABA release from nerve terminals
M. V. Dudarenko*, N. G. Pozdnyakova
Department of Neurochemistry, Palladin Institute of Biochemistry,
National Academy of Sciences of Ukraine, Kyiv;
*e-mail: marina.dudarenko@gmail.com
Received: 28 January 2022; Revised: 25 March 2022;
Accepted: 20 September 2022; Available on-line: 19 December 2022
Levetiracetam (LV), 2S-(2-oxo-1-pyrrolidiny1) butanamide, is an antiepileptic drug. The exact mechanisms of anticonvulsant effects of LV remain unclear. In this study, rats (Wistar strain) underwent hypoxia and seizures at the age of 10–12 postnatal days (pd). [3H]GABA release was analysed in isolated from thalamus nerve terminals (synaptosomes) during development at the age of pd 17–19 and pd 24–26 (infantile stage), pd 38–40 (puberty) and pd 66–73 (young adults) in control and after perinatal hypoxia. The extracellular level of [3H]GABA in the preparation of thalamic synaptosomes increased during development at the age of pd 38–40 and pd 66–73 as compared to earlier ones. LV did not influence the extracellular level of [3H]GABA in control and after perinatal hypoxia at all studied ages. Exocytotic [3H]GABA release in control increased at the age of pd 24–26 as compared to pd 17–19. After hypoxia, exocytotic [3H]GABA release from synaptosomes also increased during development. LV elevated [3H]GABA release from thalamic synaptosomes at the age of pd 66–73 after hypoxia and during blockage of GABA uptake by NO-711 only. LV realizes its antiepileptic effects at the presynaptic site through an increase in exocytotic release of [3H]GABA in thalamic synaptosomes after perinatal hypoxia at pd 66–73. LV exhibited a more significant effect in thalamic synaptosomes after perinatal hypoxia than in control ones. The action of LV is age-dependent, and the drug was inert at the infantile stage that can be useful for an LV application strategy in child epilepsy therapy.
Exocytotic steps in cell-free system after cholesterol deprivation in synaptosomal plasma membranes and synaptic vesicles
V. P. Gumenyuk, I. O. Trikash
Palladin Institute of Biochemistry, National Academy
of Sciences of Ukraine, Kyiv;
e-mail: trikash@biochem.kiev.ua
Using a cell-free system we investigated a specific role of cholesterol in exocytotic processes. To modulate the cholesterol content in membrane methyl-β-cyclodextrin was used as a cholesterol binding agent. The experimental conditions for cholesterol depletion from synaptosomal membrane structures were determined and depended on methyl-β-cyclodextrin concentration, time and mediums temperature. The role of cholesterol was studied on the stages of synaptic vesicles docking and Ca2+-stimulated fusion which are the components of multivesicular compound exocytosis. Using dynamic light scattering technique we have found that after cholesterol depletion from synaptic vesicles the process of their aggregation (docking) remains unchanged.
It was found that the rate of calcium-triggered fusion of synaptic vesicles depends on the membrane level of cholesterol. The decreasing level of synaptosomal plasma membrane cholesterol by 8% leads to suppression of the Ca2+-dependent membrane fusion with synaptic vesicles. But, under 25% reduction of plasma membrane cholesterol the level of membrane merging with synaptic vesicles did not differ from control; probably this is due to changes in physical properties of lipid bilayer and/or disturbances in function of membrane proteins driving this process.
In cholesterol depleted synaptosomes the exocytotic release of glutamate stimulated by calcium was decreased by 32%. Obtained data suggest that the cholesterol concenration in synaptosomal plasma membranes or synaptic vesicles is the crucial determinant for synaptic transmission efficiency in nerve terminals.
Activation of presynaptic ionotropic glutamate receptors stimulates gaba release from hippocampal and cortical rat brain nerve terminals
O. О. Krupko, A. S. Tarasenko, N. G. Himmelreich
Palladin Institute of Biochemistry, National Academy
of Sciences of Ukraine, Kyiv;
e-mail: olya_krupko@mail.ru
One of the pathways implicated in a fine-tuning control of neurosecretory process is the activation of presynaptic receptors. The present study was focused on the role of presynaptic glutamate receptor activation in the regulation of inhibitory synaptic transmission in the rat hippocampus and cortex. We aimed to clarify what types of ionotropic glutamate receptors are involved in the modulation of GABA secretion, and what mechanism underlies this modulation. We have revealed that specific agonists of kainate and NMDA receptors, kainate and NMDA, like glutamate, induced the release of [3H]GABA from hippocampal and cortical nerve terminals suggesting the involvement of both types in the regulation of GABAergic transmission. Our results indicate preferential involvement of vesicular, but not cytosolic, pool in response to glutamate receptor activation. This is based on the finding that NO-711 (a specific inhibitor of plasma membrane GABA transporters), fails to attenuate [3H]GABA release. We have concluded that presynaptic glutamate receptor-induced modulation of the strength of synaptic response is due to increasing the release probability of synaptic vesicles.