Artificial gravity loading increases the effects of the glutamate transporter inhibitors on the glutamate release and uptake in rat brain nerve terminals

2006 ◽  
Vol 18 (3-4) ◽  
pp. 230-233 ◽  
Author(s):  
Tatiana Borisova ◽  
Natalia Krisanova ◽  
Nina Himmelreich
Keyword(s):  
Rat Brain ◽  
Glutamate Release ◽  
Glutamate Transporter ◽  
Artificial Gravity ◽  
Nerve Terminals ◽  
Brain Nerve Terminals

Release of neurotransmitters from rat brain nerve terminals after chronic ethanol ingestion: differential effects in cortex and hippocampus

2003 ◽  
Vol 8 (3) ◽  
pp. 287-294 ◽  
Author(s):  
JOSEFA SABRIÀ ◽  
DÁMASO TORRES ◽  
MANEL PASTÓ ◽  
JOSEP PERALBA ◽  
ABDELLAH ALLALI-HASSANI ◽  
...  
Keyword(s):  
Rat Brain ◽  
Chronic Ethanol ◽  
Ethanol Ingestion ◽  
Nerve Terminals ◽  
Differential Effects ◽  
Brain Nerve Terminals

Permanent dynamic transporter-mediated turnover of glutamate across the plasma membrane of presynaptic nerve terminals: arguments in favor and against

2016 ◽  
Vol 27 (1) ◽  
pp. 71-81 ◽  
Author(s):  
Tatiana Borisova
Keyword(s):  
Plasma Membrane ◽  
Glutamate Uptake ◽  
Glutamate Release ◽  
Glutamate Transporter ◽  
Long Term Potentiation ◽  
Nerve Terminals ◽  
Model Calculations ◽  
New Vision ◽  
Ambient Glutamate ◽  
Energy Deprivation

AbstractMechanisms for maintenance of the extracellular level of glutamate in brain tissue and its regulation still remain almost unclear, and criticism of the current paradigm of glutamate transport and homeostasis has recently appeared. The main premise for this study is the existence of a definite and non-negligible concentration of ambient glutamate between the episodes of exocytotic release in our experiments with rat brain nerve terminals (synaptosomes), despite the existence of a very potent Na+-dependent glutamate uptake. Glutamate transporter reversal is considered as the main mechanisms of glutamate release under special conditions of energy deprivation, hypoxia, hypoglycemia, brain trauma, and stroke, underlying an increase in the ambient glutamate concentration and development of excitotoxicity. In the present study, a new vision on transporter-mediated release of glutamate as one of the main mechanisms involved in the maintenance of definite concentration of ambient glutamate under normal energetical status of nerve terminals is forwarded. It has been suggested that glutamate transporters act effectively in outward direction in a non-pathological manner, and this process is thermodynamically synchronized with uptake and provides effective outward glutamate current, thereby establishing and maintaining permanent and dynamic glutamatein/glutamateout gradient and turnover across the plasma membrane. In this context, non-transporter tonic glutamate release by diffusion, spontaneous exocytosis, cystine-glutamate exchanger, and leakage through anion channels can be considered as a permanently added ‘new’ exogenous substrate using two-substrate kinetic model calculations. Permanent glutamate turnover is of value for tonic activation of post/presynaptic glutamate receptors, long-term potentiation, memory formation, etc. Counterarguments against this mechanism are also considered.

scholarly journals Neurotoxic Potential of Lunar and Martian Dust: Influence on Em, Proton Gradient, Active Transport, and Binding of Glutamate in Rat Brain Nerve Terminals

Astrobiology ◽  
2013 ◽  
Vol 13 (8) ◽  
pp. 679-692 ◽  
Author(s):  
Natalia Krisanova ◽  
Ludmila Kasatkina ◽  
Roman Sivko ◽  
Arseniy Borysov ◽  
Anastasiya Nazarova ◽  
...  
Keyword(s):  
Rat Brain ◽  
Active Transport ◽  
Proton Gradient ◽  
Nerve Terminals ◽  
Brain Nerve Terminals

Widespread Inhibition of Sodium Channel–dependent Glutamate Release from Isolated Nerve Terminals by Isoflurane and Propofol

2001 ◽  
Vol 95 (6) ◽  
pp. 1460-1466 ◽  
Author(s):  
Ratnakumari Lingamaneni ◽  
Martin L. Birch ◽  
Hugh C. Hemmings
Keyword(s):  
Cerebral Cortex ◽  
Guinea Pig ◽  
Rat Brain ◽  
Glutamate Release ◽  
Brain Regions ◽  
Rat Striatum ◽  
Nerve Terminals ◽  
Na Channels ◽  
Rat Brain Regions ◽  
Ca2 Channels

Background Controversy persists concerning the mechanisms and role of general anesthetic inhibition of glutamate release from nerve endings. To determine the generality of this effect and to control for methodologic differences between previous studies, the authors analyzed the presynaptic effects of isoflurane and propofol on glutamate release from nerve terminals isolated from several species and brain regions. Methods Synaptosomes were prepared from rat, mouse, or guinea pig cerebral cortex and also from rat striatum and hippocampus. Release of endogenous glutamate evoked by depolarization with 20 microm veratridine (which opens voltage-dependent Na+ channels by preventing inactivation) or by 30 mm KCl (which activates voltage-gated Ca2+ channels by membrane depolarization) was monitored using an on-line enzyme-linked fluorometric assay. Results Glutamate release evoked by depolarization with increased extracellular KCl was not significantly inhibited by isoflurane up to 0.7 mM ( approximately 2 minimum alveolar concentration; drug concentration for half-maximal inhibition [IC50] > 1.5 mM) [corrected] or propofol up to 40 microm in synaptosomes prepared from rat, mouse, or guinea pig cerebral cortex, rat hippocampus, or rat striatum. Lower concentrations of isoflurane or propofol significantly inhibited veratridine-evoked glutamate release in all three species (isoflurane IC50 = 0.41-0.50 mm; propofol IC50 = 11-18 microm) and rat brain regions. Glutamate release was evoked by veratridine or increased KCl (from 5 to 35 mM) to assess the involvement of presynaptic ion channels as targets for drug actions [corrected]. Conclusions Isoflurane and propofol inhibited Na+ channel-mediated glutamate release evoked by veratridine with greater potency than release evoked by increased KCl in synaptosomes prepared from three mammalian species and three rat brain regions. These findings are consistent with a greater sensitivity to anesthetics of presynaptic Na+ channels than of Ca2+ channels coupled to glutamate release. This widespread presynaptic action of general anesthetics is not mediated by potentiation of gamma-aminobutyric acid type A receptors, though additional mechanisms may be involved.

Effects of new fluorinated analogues of GABA, pregabalin bioisosters, on the ambient level and exocytotic release of [3H]GABA from rat brain nerve terminals

2017 ◽  
Vol 25 (2) ◽  
pp. 759-764 ◽  
Author(s):  
T. Borisova ◽  
N. Pozdnyakova ◽  
E. Shaitanova ◽  
I. Gerus ◽  
M. Dudarenko ◽  
...  
Keyword(s):  
Rat Brain ◽  
Nerve Terminals ◽  
Ambient Level ◽  
Brain Nerve Terminals
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