Tag Archives: GABA
GABA-ergic system in the experimental diabetes
H. L. Hayrapetyan, N. Kh. Khachatryan, R. R. Balagyozyan,
V. R. Balagyozyan, S. S. Mardanyan*, A. A. Antonyan
Department of Metabolism of Adenylic Compounds,
H. Buniatian Institute of Biochemistry of Armenian NAS, Yerevan, Armenia;
*e-mail: biochem@biochem.sci.am
Received: 09 September 2025; Revised: 22 October 2025;
Accepted: 30 January 2026; Available on-line: 23 February 2026
γ-Aminobutyric acid (GABA) is a non-proteinogenic amino acid, neurotransmitter and concurrently trophic factor in the non-neuronal peripheral tissues. GABA is involved in the pathophysiology of endocrine disorders, in particular, diabetes mellitus (DM). This review summarizes the effects of GABA-ergic system components on the development of experimental diabetes induced in laboratory animals. The beneficial effect of GABA-associated amino acids mixtures in the DM treatment is discussed.
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.