Mechanisms of modulation of GABA-induced currents in isolated cerebellar cells by tacrine

Kolbaev, Sergey N.; Шаронова, И. Н.; Воробьев, В. С.; Skrebitskii, V. G.

doi:10.1007/bf02434947

Cited by 4 publications

(4 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, to determine whether increased levels of the inhibitory neurotransmitter GABA could prevent domoic acid-induced excitotoxicity, as it has been proposed in in vivo studies [ 8 ], the cultures were pretreated with this neurotransmitter. The studied concentrations of the NMDA and AMPA/KA receptor antagonists (100 μ M of APV and 20 μ M of NBQX) and the agonist (10 μ M of GABA) were selected based on findings from the literature [ 9 , 14 , 30 ]. These concentrations of APV, NBQX, and GABA did not induce any changes in the mRNA levels of studied genes in the control cultures (Figures 4 – 6 ).…”

Section: Resultsmentioning

confidence: 99%

Domoic Acid-Induced Neurotoxicity Is Mainly Mediated by the AMPA/KA Receptor: Comparison between Immature and Mature Primary Cultures of Neurons and Glial Cells from Rat Cerebellum

Högberg

Bal‐Price

2011

Journal of Toxicology

View full text Add to dashboard Cite

Domoic acid (DomA) is a naturally occurring shellfish toxin that can induce brain damage in mammalians. Neonates have shown increased sensitivity to DomA-induced toxicity, and prenatal exposure has been associated with e.g. decreased brain GABA levels, and increased glutamate levels. Here, we evaluated DomA-induced toxicity in immature and mature primary cultures of neurons and glial cells from rat cerebellum by measuring the mRNA levels of selected genes. Moreover, we assessed if the induced toxicity was mediated by the activation of the AMPA/KA and/or the NMDA receptor. The expression of all studied neuronal markers was affected after DomA exposure in both immature and mature cultures. However, the mature cultures seemed to be more sensitive to the treatment, as the effects were observed at lower concentrations and at earlier time points than for the immature cultures. The DomA effects were completely prevented by the antagonist of the AMPA/KA receptor (NBQX), while the antagonist of the NMDA receptor (APV) partly blocked the DomA-induced effects. Interestingly, the DomA-induced effect was also partly prevented by the neurotransmitter GABA. DomA exposure also affected the mRNA levels of the astrocytic markers in mature cultures. These DomA-induced effects were reduced by the addition of NBQX, APV, and GABA.

show abstract

Section: Resultsmentioning

confidence: 99%

Domoic Acid-Induced Neurotoxicity Is Mainly Mediated by the AMPA/KA Receptor: Comparison between Immature and Mature Primary Cultures of Neurons and Glial Cells from Rat Cerebellum

Högberg

Bal‐Price

2011

Journal of Toxicology

View full text Add to dashboard Cite

show abstract

“…For instance, a study on cultured rat dorsal root ganglion neurons has shown that Tb 3+ prolongs the opening time of the GABA A chloride channel (Ma & Narahashi, 1993;Narahashi, Ma, Arakawa, Reuveny, & Nakahiro, 1994). An increased GABA A sensitivity and enhanced chloride current after La 3+ administration is also reported for isolated cerebellar Purkyne cells (Kolbaev et al, 2002). It is therefore likely that Tb 3+ binds to the allosteric active site of the GABA A receptor-ion channel complex, extending its mean opening time by increasing the affinity of GABA .…”

Section: Anthanide S a S Modul Ator S Of Neuronal Ion Channel Phymentioning

confidence: 70%

Molecular neurochemistry of the lanthanides

Pałasz

Segovia

Skowronek

et al. 2019

Synapse

View full text Add to dashboard Cite

Lanthanides, once termed rare‐earth elements, are not as sparce in the environment as their traditional name suggests. Mean litospheric concentrations are in fact comparable to the physiologically fundamental elements such as iodine, cobalt, and selenium. Recent advances in medical technology have resulted in accumulation of lanthanides presenting potential exposure to both our central and peripheral nervous systems. Extensive and detailed studies on these peculiar active metals in the context of their influence on neural functions are therefore urgently required. Almost all neurochemical effects of trivalent lanthanide ions appear to result from the similarity of their radii to the key signaling ion calcium. Lanthanides, especially La3+ and Gd3+ block different types of calcium, potassium, and sodium channels in human and animal neurons, regulate neurotransmitter turnover and release, as well as synaptic activity. Lanthanides also act as modulators of several ionotropic receptors, e.g., GABA, NMDA, and kainate and can also affect numerous signaling mechanisms including NF‐κB and apoptotic‐related endoplasmic reticulum IRE1‐XBP1, PERK, and ATF6 pathways. Several lanthanide ions may cause oxidative neuronal injuries and functional impairment by promoting reactive oxygen species production. However, cerium and yttrium oxides have some unique and promising neuroprotective properties, being able to decrease free radical cell injury and even alleviate motor impairment and cognitive function in animal models of multiple sclerosis and mild traumatic brain damage, respectively. In conclusion, lanthanides affect various neurophysiological processes, altering a large spectrum of brain functions. Thus, a deeper understanding of their potential mechanistic roles during disease and as therapeutic agents requires urgent elucidation.

show abstract

“…Hence, the ion may bind to a superfi cial site near or at external orifi ces of the channel. Not only glutamate receptors, but also Á -aminobutyric acid type A [5][6][7] , glycine [8], and acetylcholine [9] receptors can be modulated by La 3+ . The multiplicity of the La 3+ action also suggests that more than one mechanism is likely to be involved in the modulation of synaptic currents by La…”

Section: +mentioning

confidence: 99%

“…Most studied properties are the effects of La 3+ on the Á -aminobutyric acid type A receptor function [5][6][7], and it has also been shown that La 3+ could modulate glycine currents in rat septal cholinergic neurons in culture [8] as well as acetylcholine-induced currents in guinea pig ileal smooth muscle cells [9] . Glutamate receptor induced responses can also be affected by La in various preparations, including rat dorsal root ganglia (DRG), cultured rat hippocampal and cortical neurons [10,11] , and rat dorsal horn neurons [12] .…”

Section: Introductionmentioning

confidence: 99%

Suppression of Kainate-Evoked AMPA Receptor Mediated Responses by Lanthanum in Rat Sacral Dorsal Commissural Neurons

Zhao

Wang²,

Lu³

et al. 2004

Neurosignals

View full text Add to dashboard Cite

The effect of lanthanum (La) on kainate (KA) responses in neurons acutely dissociated from the rat sacral dorsal commissural nucleus (SDCN) was investigated using the nystatin-perforated patch-recording configuration under voltage-clamp conditions. The responses to KA were mediated by activation of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in SDCN neurons. La³⁺ reversibly inhibited KA (100 µM) activated currents (I_KA) in a concentration-dependent manner over the range from 30 µM to 30 mM, with IC₅₀ values of 0.64 ± 0.06 mM at a holding potential (V_H) of –40 mV. Our further study indicated that the effects of La³⁺ on I_KA were voltage independent. Moreover, the inhibition was not use dependent and was not overcome by increasing the concentration of agonist. These findings indicate that La³⁺ is an efficacious inhibitor of AMPA receptor mediated responses which may contribute to its cytotoxic effect.

show abstract

Mechanisms of modulation of GABA-induced currents in isolated cerebellar cells by tacrine

Cited by 4 publications

References 14 publications

Domoic Acid-Induced Neurotoxicity Is Mainly Mediated by the AMPA/KA Receptor: Comparison between Immature and Mature Primary Cultures of Neurons and Glial Cells from Rat Cerebellum

Domoic Acid-Induced Neurotoxicity Is Mainly Mediated by the AMPA/KA Receptor: Comparison between Immature and Mature Primary Cultures of Neurons and Glial Cells from Rat Cerebellum

Molecular neurochemistry of the lanthanides

Suppression of Kainate-Evoked AMPA Receptor Mediated Responses by Lanthanum in Rat Sacral Dorsal Commissural Neurons

Contact Info

Product

Resources

About