Search results for "Shunting inhibition"
showing 4 items of 4 documents
The relation between neuronal chloride transporter activities, GABA inhibition, and neuronal activity
2020
Abstract The intracellular chloride concentration [Cl−]i in neurons is regulated by a set of transmembrane transporters, with the Cl−-loader NKCC1 and the Cl−-extruder KCC2 as most relevant members. The expression of these transporters is tightly regulated, with the general trend that KCC2 expression is low in immature neurons, which are thus characterized by a high [Cl−]i. As [Cl−]i is the main factor determining the polarity of GABAergic responses, such a high [Cl−]i is related to depolarizing GABAergic responses. However, depolarizing GABAergic responses are not per se excitatory, but can also contribute to shunting inhibition. The excitatory/inhibitory action of GABAergic responses is m…
Modelling the spatial and temporal constrains of the GABAergic influence on neuronal excitability
2021
GABA (γ-amino butyric acid) is an inhibitory neurotransmitter in the adult brain that can mediate depolarizing responses during development or after neuropathological insults. Under which conditions GABAergic membrane depolarizations are sufficient to impose excitatory effects is hard to predict, as shunting inhibition and GABAergic effects on spatiotemporal filtering of excitatory inputs must be considered. To evaluate at which reversal potential a net excitatory effect was imposed by GABA (EGABAThr), we performed a detailed in-silico study using simple neuronal topologies and distinct spatiotemporal relations between GABAergic and glutamatergic inputs. These simulations revealed for GABAe…
Effect of depolarizing GABAA-mediated membrane responses on excitability of Cajal-Retzius cells in the immature rat neocortex
2011
In immature neurons activation of ionotropic GABA receptors induces depolarizing membrane responses due to a high intracellular Cl− concentration ([Cl−]i). However, it is difficult to draw conclusions about the functional consequences of subthreshold GABAergic depolarizations, since GABAergic membrane shunting and additional effects on voltage-dependent ion channels or action potential threshold must be considered. To systematically investigate factors that determine the GABAergic effect on neuronal excitability we performed whole cell patch-clamp recordings from Cajal-Retzius cells in immature rat neocortex, using [Cl−]i between 10 and 50 mM. The effect of focal GABA application was quant…
TRESK channel contributes to depolarization-induced shunting inhibition and modulates epileptic seizures.
2020
Glutamatergic and GABAergic synaptic transmission controls excitation and inhibition of postsynaptic neurons, whereas activity of ion channels modulates neuronal intrinsic excitability. However, it is unclear how excessive neuronal excitation affects intrinsic inhibition to regain homeostatic stability under physiological or pathophysiological conditions. Here, we report that a seizure-like sustained depolarization can induce short-term inhibition of hippocampal CA3 neurons via a mechanism of membrane shunting. This depolarization-induced shunting inhibition (DShI) mediates a non-synaptic, but neuronal intrinsic, short-term plasticity that is able to suppress action potential generation and…