C. Mulle is the first author of a 1998 study testing the contribution of a kainate receptor subunit to signalling in the hippocampus. The investigators compared mice lacking the subunit with controls and measured responses in CA3 neurons.[ref]
Altered synaptic physiology and reduced susceptibility to kainate-induced seizures in GluR6-deficient mice by C. Mulle and others. Original byline and Abstract: receptor-subunit deletion
The deletion reduced sensitivity to kainic acid and removed a postsynaptic component evoked by repeated stimulation of the relevant inputs. The mutant mice also showed reduced susceptibility to the experimentally induced seizures.[ref]
Altered synaptic physiology and reduced susceptibility to kainate-induced seizures in GluR6-deficient mice by C. Mulle and others. Abstract: synaptic recordings and systemic-kainate comparison
A molecular perturbation was therefore connected to both a local physiological readout and a whole-animal response. The latter alone would not localize the changed signalling step; the neuron recordings supplied that additional resolution. The result concerns the tested genetic and experimental conditions, rather than showing that every kind of seizure uses the same mechanism.
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