Vestibular evoked myogenic responses to amplitude modulated sounds

Auditory Steady State Responses ASSR allow objective assessment of hearing thresholds. At high stimulation levels artifactual responses have been reported in subjects with severe to profound deafness. Relatively large amplitude ‘steady state’ responses to amplitude modulated tones were measured from the Sternocleidomastoid muscle at 500 Hz. Response thresholds were similar to those of Vestibular Evoked Myogenic Potentials and scaled with neck muscle tension. ‘Steady-state’ myogenic responses showed broad tuning to modulation frequency. Reduced amplitude responses were measured at the inion indicating volume conduction from the SCM. While dependant on neck tension, such responses are a potential source of artifacts when recording ASSR

Ongoing epileptiform activity in the post-ischemic hippocampus is associated with a permanent shift of the excitatory-inhibitory synaptic balance in CA3 pyramidal neurons.

International audienceIschemic strokes are often associated with late-onset epilepsy, but the underlying mechanisms are poorly understood. In the hippocampus, which is one of the regions most sensitive to ischemic challenge, global ischemia induces a complete loss of CA1 pyramidal neurons, whereas the resistant CA3 pyramidal neurons display a long-term hyperexcitability several months after the insult. The mechanisms of this long-term hyperexcitability remain unknown despite its clinical implication. Using chronic in vivo EEG recordings and in vitro field recordings in slices, we now report spontaneous interictal epileptiform discharges in the CA3 area of the hippocampus from post-ischemic rats several months after the insult. Whole-cell recordings from CA3 pyramidal neurons, revealed a permanent reduction in the frequency of spontaneous and miniature GABAergic IPSCs and a parallel increase in the frequency of spontaneous and miniature glutamatergic postsynaptic currents. Global ischemia also induced a dramatic loss of GABAergic interneurons and terminals together with an increase in glutamatergic terminals in the CA3 area of the hippocampus. Altogether, our results show a morpho-functional reorganization in the CA3 network several months after global ischemia, resulting in a net shift in the excitatory-inhibitory balance toward excitation that may constitute a substrate for the generation of epileptiform discharges in the post-ischemic hippocampus