CA1 pyramidal neuron: nonlinear a5-GABAAR controls synaptic NMDAR activation (Schulz et al 2018)


The study shows that IPSCs mediated by a5-subunit containing GABAA receptors are strongly outward-rectifying generating 4-fold larger conductances above -50?mV than at rest. Experiments and modeling show that synaptic activation of these receptors can very effectively control voltage-dependent NMDA-receptor activation in a spatiotemporally controlled manner in fine dendrites of CA1 pyramidal cells. The files contain the NEURON code for Fig.8, Fig.S8 and Fig.S9 of the paper. The model is based on the model published by Bloss et al., 2017. Physiological properties of GABA synapses were modified as determined by optogenetic activation of inputs during voltage-clamp recordings in Schulz et al. 2018. Other changes include stochastic synaptic release and short-term synaptic plasticity. All changes of mechanisms and parameters are detailed in the Methods of the paper. Simulation can be run by starting start_simulation.hoc after running mknrndll. The files that model the individual figures have to be uncommented in start_simulation.hoc beforehand.

Model Type: Neuron or other electrically excitable cell; Dendrite; Synapse

Region(s) or Organism(s): Hippocampus; Mouse

Cell Type(s): Hippocampus CA1 pyramidal GLU cell

Currents: I h; I A

Receptors: GabaA; GabaB; AMPA; NMDA

Transmitters: Gaba; Glutamate

Simulation Environment: NEURON

Implementer(s): Schulz, Jan M [j.schulz at unibas.ch]

References:

Schulz JM, Knoflach F, Hernandez MC, Bischofberger J. (2018). Dendrite-targeting interneurons control synaptic NMDA-receptor activation via nonlinear a5-GABAA receptors. Nature communications. 9 [PubMed]


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