ModelDB: Paradoxical GABA-mediated excitation (Lewin et al. 2012)

Paradoxical GABA-mediated excitation (Lewin et al. 2012)

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Citations

Accession:146504

"GABA is the key inhibitory neurotransmitter in the adult central nervous system, but in some circumstances can lead to a paradoxical excitation that has been causally implicated in diverse pathologies from endocrine stress responses to diseases of excitability including neuropathic pain and temporal lobe epilepsy. We undertook a computational modeling approach to determine plausible ionic mechanisms of GABAA-dependent excitation in isolated post-synaptic CA1 hippocampal neurons because it may constitute a trigger for pathological synchronous epileptiform discharge. In particular, the interplay intracellular chloride accumulation via the GABAA receptor and extracellular potassium accumulation via the K/Cl co-transporter KCC2 in promoting GABAA-mediated excitation is complex. ..."
Reference:
1 . Lewin N, Aksay E, Clancy CE (2012) Computational modeling reveals dendritic origins of GABA(A)-mediated excitation in CA1 pyramidal neurons. PLoS One 7:e47250 [PubMed]

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

Model Type:	Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s):	Hippocampus CA1 pyramidal GLU cell;
Channel(s):	I Na,p; I Na,t; I L high threshold; I T low threshold; I A; I K; I M; I h; I K,Ca; I Calcium; Na/Ca exchanger; Na/K pump; KCC2; NKCC1; Ca pump;
Gap Junctions:
Receptor(s):	GabaA;
Gene(s):
Transmitter(s):
Simulation Environment:	C or C++ program;
Model Concept(s):	Bursting; Detailed Neuronal Models; Epilepsy; Calcium dynamics; Markov-type model;
Implementer(s):	Clancy, Colleen E [ceclancy at ucdavis.edu];