Involvement of NMDA and GABA(A) receptors in modulation of spontaneous activity in hippocampal culture: Interrelations between burst firing and intracellular calcium signal

Teplov, Ilia Y.; Зинченко, В. П.; Kosenkov, Artem M.; Gaidin, Sergei G.; Nenov, Miroslav N.; Сергеев, А. И.

doi:10.1016/j.bbrc.2021.02.149

Cited by 9 publications

(16 citation statements)

References 37 publications

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“…The present work and our previous study showed that PDSs in neuronal networks are accompanied by high-amplitude [Ca 2+ ] i oscillations [ 32 , 45 ]. This paroxysmal activity occurs spontaneously in some cultures or can be induced by different types of exposure, shifting the E/I balance toward excitation.…”

Section: Discussionsupporting

confidence: 68%

“…Blockade of GABA(A)Rs leads to the disinhibition of neuronal networks, promoting the generation of high-amplitude synchronous [Ca 2+ ] i oscillations in all neurons ( Figure 2 A,B and Figure 3 A). These oscillations are caused by the activation of ionotropic glutamate receptors since NMDAR antagonists decrease the amplitude, whereas AMPAR antagonists completely suppress the synchronous [Ca 2+ ] i changes in neurons [ 31 , 32 ]. As can be seen in Figure 3 A, the frequency and amplitude of [Ca 2+ ] i oscillations changed insignificantly in the control experiment during 30 min of bicuculline exposure.…”

Section: Resultsmentioning

confidence: 99%

“…Hence, it may be concluded that L-type VGCC plays a pivotal role in maintaining Ca 2+ inflow during the oscillations, and the duration of the Ca 2+ pulse possibly determines the number of PDSs in a cluster. It was shown (including in our studies) that the generation of each subsequent PDS may occur both during the depolarizing plateau (high membrane potential) and during the decrease in potential to values close to resting membrane potential [ 13 , 32 , 47 ]. Thus, it is unlikely that the generation of each subsequent PDS in a cluster is determined by membrane potential.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, it is unlikely that the generation of each subsequent PDS in a cluster is determined by membrane potential. In turn, the level of [Ca 2+ ] i increases during each cluster [ 32 , 50 ], whereas, in the case of single APs generating between the clusters, [Ca 2+ ] i changes are not observed in the soma of neurons [ 51 ]. Notably, PDS is terminated when [Ca 2+ ] i decays.…”

Section: Discussionmentioning

confidence: 99%

“…Notably, PDS is terminated when [Ca 2+ ] i decays. Moreover, as with the blockade of L-type VGCC, NMDAR antagonists also decrease the [Ca 2+ ] i oscillation amplitude [ 32 ]. Therefore, it can be suggested that the level of [Ca 2+ ] i determines the number of PDSs in a cluster.…”

Section: Discussionmentioning

confidence: 99%

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Role of L-Type Voltage-Gated Calcium Channels in Epileptiform Activity of Neurons

Laryushkin

Maiorov

Зинченко

et al. 2021

IJMS

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Epileptic discharges manifest in individual neurons as abnormal membrane potential fluctuations called paroxysmal depolarization shift (PDS). PDSs can combine into clusters that are accompanied by synchronous oscillations of the intracellular Ca2+ concentration ([Ca2+]i) in neurons. Here, we investigate the contribution of L-type voltage-gated calcium channels (VGCC) to epileptiform activity induced in cultured hippocampal neurons by GABA(A)R antagonist, bicuculline. Using KCl-induced depolarization, we determined the optimal effective doses of the blockers. Dihydropyridines (nifedipine and isradipine) at concentrations ≤ 10 μM demonstrate greater selectivity than the blockers from other groups (phenylalkylamines and benzothiazepines). However, high doses of dihydropyridines evoke an irreversible increase in [Ca2+]i in neurons and astrocytes. In turn, verapamil and diltiazem selectively block L-type VGCC in the range of 1–10 μM, whereas high doses of these drugs block other types of VGCC. We show that L-type VGCC blockade decreases the half-width and amplitude of bicuculline-induced [Ca2+]i oscillations. We also observe a decrease in the number of PDSs in a cluster and cluster duration. However, the pattern of individual PDSs and the frequency of the cluster occurrence change insignificantly. Thus, our results demonstrate that L-type VGCC contributes to maintaining the required [Ca2+]i level during oscillations, which appears to determine the number of PDSs in the cluster.

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Section: Discussionsupporting

confidence: 68%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Role of L-Type Voltage-Gated Calcium Channels in Epileptiform Activity of Neurons

Laryushkin

Maiorov

Зинченко

et al. 2021

IJMS

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Semiconducting carbon nanotubes decrease neuronal bursting in a network of rat hippocampal neuronsin vitrowhile increasing intrinsic excitability of single neurons

Kishore

Chakraborty

Vasnik

et al. 2023

Preprint

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The diverse electrical, chemical and structural properties of the functional derivatives of carbon nanotubes (CNTs) have shown biomedical possibilities for neuroprosthesis or neural interfaces. However, the studies have been generally confined to metallic CNTs that affect cell viability unless chemically functionalized for biocompatibility. Here, we explored the effects of semiconducting single-walled carbon nanotubes (ssw-CNT), on the active electrical properties of dissociated hippocampal neurons in-vitro using multielectrode array, calcium imaging and whole-cell patch clamp recordings. The findings show that ssw-CNT treatment regulates neural network excitability from burst to tonic firing by changing the calcium dynamics. However, at a single neuronal level, ssw-CNT increases neuronal excitability.

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Inhibition of 14‐3‐3 proteins increases the intrinsic excitability of mouse hippocampal CA1 pyramidal neurons

Logue,

Vilmont,

Zhang

et al. 2024

Eur J of Neuroscience

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Abstract14‐3‐3 proteins are a family of regulatory proteins that are abundantly expressed in the brain and enriched at the synapse. Dysfunctions of these proteins have been linked to neurodevelopmental and neuropsychiatric disorders. Our group has previously shown that functional inhibition of these proteins by a peptide inhibitor, difopein, in the mouse brain causes behavioural alterations and synaptic plasticity impairment in the hippocampus. Recently, we found an increased cFOS expression in difopein‐expressing dorsal CA1 pyramidal neurons, indicating enhanced neuronal activity by 14‐3‐3 inhibition in these cells. In this study, we used slice electrophysiology to determine the effects of 14‐3‐3 inhibition on the intrinsic excitability of CA1 pyramidal neurons from a transgenic 14‐3‐3 functional knockout (FKO) mouse line. Our data demonstrate an increase in intrinsic excitability associated with 14‐3‐3 inhibition, as well as reveal action potential firing pattern shifts after novelty‐induced hyperlocomotion in the 14‐3‐3 FKO mice. These results provide novel information on the role 14‐3‐3 proteins play in regulating intrinsic and activity‐dependent neuronal excitability in the hippocampus.

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Involvement of NMDA and GABA(A) receptors in modulation of spontaneous activity in hippocampal culture: Interrelations between burst firing and intracellular calcium signal

Cited by 9 publications

References 37 publications

Role of L-Type Voltage-Gated Calcium Channels in Epileptiform Activity of Neurons

Role of L-Type Voltage-Gated Calcium Channels in Epileptiform Activity of Neurons

Semiconducting carbon nanotubes decrease neuronal bursting in a network of rat hippocampal neuronsin vitrowhile increasing intrinsic excitability of single neurons

Inhibition of 14‐3‐3 proteins increases the intrinsic excitability of mouse hippocampal CA1 pyramidal neurons

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