MicrocircuitDB: Coincident glutamatergic depolarization effects on Cl- dynamics (Lombardi et al, 2021)

Accession:266823

"... we used compartmental biophysical models of Cl- dynamics simulating either a simple ball-and-stick topology or a reconstructed CA3 neuron. These computational experiments demonstrated that glutamatergic co-stimulation enhances GABA receptor-mediated Cl- influx at low and attenuates or reverses the Cl- efflux at high initial [Cl-]i. The size of glutamatergic influence on GABAergic Cl--fluxes depends on the conductance, decay kinetics, and localization of glutamatergic inputs. Surprisingly, the glutamatergic shift in GABAergic Cl--fluxes is invariant to latencies between GABAergic and glutamatergic inputs over a substantial interval..."
Reference:
1 . Lombardi A, Jedlicka P, Luhmann HJ, Kilb W (2021) Coincident glutamatergic depolarizations enhance GABAA receptor-dependent Cl- influx in mature and suppress Cl- efflux in immature neurons PLOS Comp Bio

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Model Information (Click on a link to find other models with that property)

Model Type:	Synapse; Dendrite;
Brain Region(s)/Organism:
Cell Type(s):	Hippocampus CA3 pyramidal GLU cell;
Channel(s):
Gap Junctions:
Receptor(s):	GabaA; AMPA; NMDA;
Gene(s):
Transmitter(s):	Gaba; Glutamate;
Simulation Environment:	NEURON;
Model Concept(s):	Short-term Synaptic Plasticity; Synaptic Plasticity; Chloride regulation;
Implementer(s):	Jedlicka, Peter [jedlicka at em.uni-frankfurt.de]; Kilb, Werner [wkilb at uni-mainz.de];

Search NeuronDB for information about: Hippocampus CA3 pyramidal GLU cell; GabaA; AMPA; NMDA; Gaba; Glutamate;