Dendritic but not somatic GABAergic inhibition is decreased in experimental epilepsy

By Rosa Cossart, C. Dinocourt, J. Hirsch, Á. Merchán-Pérez, J. D. Felipe, Yehezkel Ben-Ari, M. Esclapez, Christophe Bernard. Nature Neuroscience, 2001

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Disynaptic inhibition between neocortical pyramidal cells mediated by Martinotti cells. (2007, background): “Indeed, a correlation was described between selective loss of hippocampal somatostatin-positive dendritic-targeting interneurons and epileptic states (Buckmaster and Jongen-Relo, 1999; Cossart et al., 2001).”
Three Groups of Interneurons Account for Nearly 100% of Neocortical GABAergic Neurons (2011, background): “Moreover, malfunction of these neurons has been implicated in a number of diseases ranging from epilepsy to schizophrenia, anxiety disorders and autism (Cossart et al., 2001; Noebels, 2003; Levitt et al., 2004; Cobos et al., 2005; GonzalezBurgos and Lewis, 2008).”
Epileptic fast activity can be explained by a model of impaired GABAergic dendritic inhibition (2002, background): “As suggested in (Cossart et al., 2001), this impairment of GABAergic dendritic inhibition in the epileptic tissue could be explained by a selective loss of inhibitory interneurons projecting to stratum lacunosum moleculare and controlling the excitability of pyramidal neuron's dendrites.”