Ionic Mechanism Underlying Rebound Depolarization in Medial Prefrontal Cortex Pyramidal Neurons

Kurowski, Przemysław; Grzelka, Katarzyna; Szulczyk, Paweł

doi:10.3389/fncel.2018.00093

Cited by 12 publications

(8 citation statements)

References 140 publications

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“…Postinhibitory rebound is involved in a variety of basic brain processes such as rhythmic recurrent activity [76] and short-term plasticity [77]. This phenomenon relies on several mechanisms occurring in response to hyperpolarization such as activation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels and deinactivation of low voltage-activated T-type calcium channels and persistent sodium channels [78][79][80][81]. In our conditions, postinhibitory rebound occurred in response to washout of MU and consecutive removal of tonic hyperpolarization.…”

Section: Plos Onementioning

confidence: 86%

Comparative study between radiofrequency-induced and muscimol-induced inhibition of cultured networks of cortical neuron

et al. 2022

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Previous studies have shown that spontaneously active cultured networks of cortical neuron grown planar microelectrode arrays are sensitive to radiofrequency (RF) fields and exhibit an inhibitory response more pronounced as the exposure time and power increase. To better understand the mechanism behind the observed effects, we aimed at identifying similarities and differences between the inhibitory effect of RF fields (continuous wave, 1800 MHz) to the γ-aminobutyric acid type A (GABAA) receptor agonist muscimol (MU). Inhibition of the network bursting activity in response to RF exposure became apparent at an SAR level of 28.6 W/kg and co-occurred with an elevation of the culture medium temperature of ~1°C. Exposure to RF fields preferentially inhibits bursting over spiking activity and exerts fewer constraints on neural network bursting synchrony, differentiating it from a pharmacological inhibition with MU. Network rebound excitation, a phenomenon relying on the intrinsic properties of cortical neurons, was observed following the removal of tonic hyperpolarization after washout of MU but not in response to cessation of RF exposure. This implies that hyperpolarization is not the main driving force mediating the inhibitory effects of RF fields. At the level of single neurons, network inhibition induced by MU and RF fields occurred with reduced action potential (AP) half-width. As changes in AP waveform strongly influence efficacy of synaptic transmission, the narrowing effect on AP seen under RF exposure might contribute to reducing network bursting activity. By pointing only to a partial overlap between the inhibitory hallmarks of these two forms of inhibition, our data suggest that the inhibitory mechanisms of the action of RF fields differ from the ones mediated by the activation of GABAA receptors.

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Section: Plos Onementioning

confidence: 86%

Comparative study between radiofrequency-induced and muscimol-induced inhibition of cultured networks of cortical neuron

et al. 2022

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“…Postinhibitory rebound is involved in a variety of basic brain processes such as rhythmic recurrent activity (Sanchez-Vives and McCormick, 2000) and short-term plasticity (Winograd et al, 2008). This phenomenon relies on several mechanisms occurring in response to hyperpolarization such as activation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels and deinactivation of low voltage-activated T-type calcium channels and persistent sodium channels (Boehme et al, 2011; Ferrante et al, 2017; Kurowski et al, 2018; Wu et al, 2005). In our conditions, postinhibitory rebound occurred in response to washout of MU and consecutive removal of tonic hyperpolarization.…”

Section: Discussionmentioning

confidence: 99%

Comparative study between radiofrequency-induced and muscimol-induced inhibition of cultured networks of cortical neuron

Lemercier

Garenne

Gannes

et al. 2022

Preprint

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Previous studies have shown that spontaneously active cultured networks of cortical neuron grown planar microelectrode array are sensitive to radiofrequency (RF) fields and exhibit an inhibitory response more pronounced as the exposure time and power increase. To better understand the mechanism behind the observed effects, we aimed at identifying similarities and dissimilarities between the inhibitory effect of RF fields (continuous wave, 1800 MHz) to the γ-Aminobutyric acid type A (GABA A) receptor agonist muscimol (MU). Inhibition of network bursting activity in response to RF exposure became apparent at an SAR level of 28.6 W/kg and co occurred with an elevation of the culture medium temperature of ~1 degree Celsius. Differently to a pharmacological inhibition with MU, exposure to RF fields preferentially inhibits bursting over spiking activity and exerts less constrains on neural network bursting synchrony. Network rebound excitation, a phenomenon relying on intrinsic properties of cortical neurons, was observed consecutively to the removal of tonic hyperpolarization after washout of MU but not in response to cessation of RF exposure which implies that hyperpolarization is not the main driving force mediating the inhibitory effects of RF fields. At the level of single neurons, network inhibition induced by MU and RF fields occurred with reduced action potential (AP) half-width. As change in AP waveform tightly influence efficiency of synaptic transmission, the narrowing effect on AP seen under RF exposure might contribute to reduce network bursting activity. By pointing only to a partial overlap between the inhibitory hallmarks of these two forms of inhibition, our data suggest that the inhibitory mechanisms of action of RF fields differ from the ones mediated by the activation of GABA A receptor. The rapid onset of the inhibitory effect of RF fields and its reversibility strikingly similar to MU are in favour of a mechanism interacting with fast operating targets at the membrane such as ion channels.

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“…Although several channels, for instance, inwardly-rectifying potassium channels ( Wang et al, 2016 ), low-threshold TTX-resistant sodium channels ( Kurowski et al, 2018 ), persistent sodium channels ( Sangrey and Jaeger, 2010 ), and high-threshold calcium channels ( Zheng and Raman, 2009 ) have been confirmed to be involved in regulating RD by hyperpolarizing RMP, decreasing neuronal input resistances, or enhancing synaptic inhibition that contributes to post-inhibitory depolarizations, currents mediated by HCN channels and T-type calcium channels are recognized as pivotal ionic factors underlying RD ( Boehme et al, 2011 ; Engbers et al, 2011 ). With respect to the role of I T in RD, pharmacological blockade of T-type calcium channels by using blockers such as NiCl 2 , mibefradil, or NNC 55-0396 could produce a significant block on the total number of spikes generated in RD ( Alvina et al, 2009 ).…”

Section: Discussionmentioning

confidence: 99%

“…Rebound depolarization (RD) is a transient membrane depolarization (sometimes accompanied by a series of spikes) following hyperpolarizing pulses. It has been observed in various brain regions, which include the hippocampus ( Surges et al, 2006 ), auditory midbrain ( Sun et al, 2020 ), medial prefrontal cortex ( Kurowski et al, 2018 ), thalamus ( Wang et al, 2016 ; Zhu et al, 2018 ), and deep spinal dorsal horn ( Rivera-Arconada and Lopez-Garcia, 2015 ), among others. RD substantially relies on channels with hyperpolarization-dependent activation or de-inactivation features.…”

Section: Introductionmentioning

confidence: 99%

Electrophysiological and Morphological Features of Rebound Depolarization Characterized Interneurons in Rat Superficial Spinal Dorsal Horn

Zhu

Yan

Cao

et al. 2021

Front. Cell. Neurosci.

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Substantia gelatinosa (SG) neurons, which are located in the spinal dorsal horn (lamina II), have been identified as the “central gate” for the transmission and modulation of nociceptive information. Rebound depolarization (RD), a biophysical property mediated by membrane hyperpolarization that is frequently recorded in the central nervous system, contributes to shaping neuronal intrinsic excitability and, in turn, contributes to neuronal output and network function. However, the electrophysiological and morphological properties of SG neurons exhibiting RD remain unclarified. In this study, whole-cell patch-clamp recordings were performed on SG neurons from parasagittal spinal cord slices. RD was detected in 44.44% (84 out of 189) of the SG neurons recorded. We found that RD-expressing neurons had more depolarized resting membrane potentials, more hyperpolarized action potential (AP) thresholds, higher AP amplitudes, shorter AP durations, and higher spike frequencies in response to depolarizing current injection than neurons without RD. Based on their firing patterns and morphological characteristics, we propose that most of the SG neurons with RD mainly displayed tonic firing (69.05%) and corresponded to islet cell morphology (58.82%). Meanwhile, subthreshold currents, including the hyperpolarization-activated cation current (Ih) and T-type calcium current (IT), were identified in SG neurons with RD. Blockage of Ih delayed the onset of the first spike in RD, while abolishment of IT significantly blunted the amplitude of RD. Regarding synaptic inputs, SG neurons with RD showed lower frequencies in both spontaneous and miniature excitatory synaptic currents. Furthermore, RD-expressing neurons received either Aδ- or C-afferent-mediated monosynaptic and polysynaptic inputs. However, RD-lacking neurons received afferents from monosynaptic and polysynaptic Aδ fibers and predominantly polysynaptic C-fibers. These findings demonstrate that SG neurons with RD have a specific cell-type distribution, and may differentially process somatosensory information compared to those without RD.

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Ionic Mechanism Underlying Rebound Depolarization in Medial Prefrontal Cortex Pyramidal Neurons

Cited by 12 publications

References 140 publications

Comparative study between radiofrequency-induced and muscimol-induced inhibition of cultured networks of cortical neuron

Comparative study between radiofrequency-induced and muscimol-induced inhibition of cultured networks of cortical neuron

Comparative study between radiofrequency-induced and muscimol-induced inhibition of cultured networks of cortical neuron

Electrophysiological and Morphological Features of Rebound Depolarization Characterized Interneurons in Rat Superficial Spinal Dorsal Horn

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