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Joseph, K.

Publications and source records attributed to Joseph, K..

2 recordsLinked to original sources

When a rose is not a rose: Pyramidal neurons respond differently in healthy and epileptic human neocortex

Epilepsy affects a huge number of patients by severe disruption of brain functions and is characterised by recurrent seizures, sometimes hard to be treated by medications. Seizure induced cellular consequences in ionic gradient and homeostasis are expected to result in electrophysiological differences between epileptic and non-epileptic neurons.\n\nIn the following work we demonstrate these differences in layer III cortical pyramidal neurons sourced from epileptic and non-epileptic human patient tissue. Although visually indistinguishable and featuring similar membrane potentials and latency to first spikes upon whole cell patch stimulation, epileptic pyramidal neurons display a larger rheobase and a smaller membrane resistance, responding less efficiently to electrical stimulation than their peri-tumorous equivalents. This decreased excitability contradicts results in comparable animal models of epilepsy and was further corroborated by detailed analysis of spiking characteristics and phase plot analysis of these events. Both point to an overexpression of K+ channels trying to compensate for the hyperexcited, epileptic network state. A computational model of a pyramidal neuron was utilized to give an estimate of the needful relative changes in K+ and Na+ conductances.

neuroscience

When the ostrich-algorithm fails: Blanking method affects spike train statistics

1.Electrophysiological recordings of neuronal tissue face particular challenges when attempted during electrical stimulation, both in vivo and in vitro. Electrical stimulation may produce undesired electronic artifacts and thus render the recorded signal only partially useful. A commonly used remedy for these artifacts is to temporarily ground the input during the stimulation pulses. In the following study, we quantify the effects of this method on the spike train count, which is called \"blanking\". Starting a from theoretical standpoint, we deduce a loss of countable action potentials, depending on: width of the blanking window, Frequency of stimulation and neuronal activity. Calculations are corroborated by actual high SNR single cell recordings. We have to state, for therapeutically relevant frequencies of 130 Hz and realistic blanking windows of 2 ms, up to 27% of actual existing spikes are lost. We strongly advice careful and controlled use of blanking circuits when spike rate quantification is attempted.

neuroscience