Voltage-independent sodium channels emerge for an expression of activity-induced spontaneous spikes in GABAergic neurons

Abstract

BackgroundCerebral overexcitation needs inhibitory neurons be functionally upregulated to rebalance excitation vs. inhibition. For example, the intensive activities of GABAergic neurons induce spontaneous spikes, i.e., activity-induced spontaneous spikes (AISS). The mechanisms underlying AISS onset remain unclear. We investigated the roles of sodium channels in AISS induction and expression at hippocampal GABAergic neurons by electrophysiological approach.ResultsAISS expression includes additional spike capability above evoked spikes, and the full spikes in AISS comprise early phase (spikelets) and late phase, implying the emergence of new spikelet component. Compared with the late phase, the early phase is characterized as voltage-independent onset, less voltage-dependent upstroke and sensitivity to TTX. AISS expression and induction are independent of membrane potential changes. Therefore, AISS’s spikelets express based on voltage-independent sodium channels. In terms of AISS induction, the facilitation of voltage-gated sodium channel (VGSC) activation accelerates AISS onset, or vice versa.ConclusionAISS expression in GABAergic neurons is triggered by the spikelets based on the functional emergence of voltage-independent sodium channels, which is driven by intensive VGSCs’ activities.

Activity-induced spontaneous spikes in GABAergic neurons suppress seizure discharges: an implication of computational modeling

“…Their features are similar those in cortical GABAergic neurons in the mice (Figure 3 and [12]). Subsequently, we have examined the role of these AISS-generated neurons from seizure-onset tissues of TLE patients in seizure self-termination by the computational simulation.…”

“…30% of GABAergic neurons are AISS-generated neurons [12]. Based on the properties of AISS-generated inhibitory neurons, such as their portions, spiking frequency and AISS-onset latency (Figure 3), we change these parameters and examine their influence on efficacies of seizure suppression in neuronal networks.…”

“…Intensive activities in GABAergic neurons induce their spontaneous action potentials, i.e., activity-induced spontaneous spikes (AISS) [12–14], especially in seizure-onset tissues [10]. A hypothesis is that overexcited neural networks trigger AISS generation in GABAergic neurons, which in turn suppresses the network overexcitation.…”

Coordinated Plasticity between Barrel Cortical Glutamatergic and GABAergic Neurons during Associative Memory

“…The wavelength at 488 nm excited GFP, and the wavelength at 575 nm excited YFP. GABAergic neurons showed basket shape and fast spiking with less adaptation in spike amplitudes and frequency [46–48]. Glutamatergic neurons showed pyramidal shape and regular spikes with the adaptation of spike amplitudes and frequency [49].…”

Associations of Unilateral Whisker and Olfactory Signals Induce Synapse Formation and Memory Cell Recruitment in Bilateral Barrel Cortices: Cellular Mechanism for Unilateral Training Toward Bilateral Memory

“…The wavelength at 488 nm excited GFP, and the wavelength at 575 nm excited YFP. GABAergic neurons showed basket shape and fast spiking with less adaptation in spike amplitude and frequency (Wang et al, 2008; DeFelipe et al, 2013; Lu et al, 2014). Glutamatergic neurons showed pyramidal shape and regular spikes with the adaptation of spike amplitude and frequency.…”