Anmar Khadra

The paper develops a stochastic HH model to study intrinsic ionic mechanisms driving spontaneous firing in spPVINs, revealing how Ih and noise contribute to irregular bursting and circuit inhibition.

This study identifies astrocytic FMRP loss as the cause of spinal parvalbumin neuron dysfunction in FXS, revealing astrocyte-dependent circuit disruption.

The paper develops a machine learning framework to automatically quantify axonal and myelin features in electron microscopy images of gene-edited mice, showing correlations between myelin changes and mitochondrial density.

This study uses computational modeling to show that gap junctional coupling in molecular layer interneurons (MLIs) drives synchronization, primarily influenced by gap junction properties rather than dendritic properties.

This study investigates the role of dendritic and somatic currents in afterdepolarization potentials and spike-adding, revealing dendritic contributions and nonmonotonic spike-adding dynamics.

The paper develops biophysical and phenomenological models to explain in vivo burst firing in electrosensory pyramidal cells, showing how intrinsic conductances, Ca2+ dynamics, and synaptic noise interact to produce bursting activity.

This study develops a computational model of calcium signaling in oligodendrocyte precursor cells to understand how spontaneous and evoked responses are regulated by voltage, neurotransmitters, and calcium dynamics.

This study models how T cell receptor diversity affects viral immune escape, showing that lower diversity can increase escape despite constant mutation rates.

The paper shows burst firing in neural populations creates invariant representations of natural communication signals, demonstrated through recordings and computational modeling.

This study uses Monte Carlo simulations to show that TCR clustering and NP geometry affect the sensitivity-specificity trade-off in T cell responses to pMHC-coated nanoparticles.

This study investigates how action potentials contribute to scalp EEG by combining biophysical simulations and statistical modeling, finding that they account for at most 1% of the spectral density and that high-frequency EEG trends are mainly due to external noise and synaptic timescales.

The paper investigates how intrinsic spike frequency adaptation (I-SFA) and inhibitory circuit dynamics contribute to extrinsic-SFA (E-SFA) in primate lateral prefrontal cortex neurons during behavior.

This study shows that serotonin from dorsal raphe neurons regulates visual attention in mice by modulating neural activity and behavioral performance.

ElecFeX provides a user-friendly MATLAB-based toolkit for efficient feature extraction from single-cell electrophysiological recordings, enabling streamlined analysis of large datasets.

This study identifies a calcium-dependent mechanism that modulates spinal dorsal horn PVINs' electrical activity after nerve injury, showing that impaired calcium buffering increases SK channel activity and reduces intrinsic excitability.

The paper uses computational modeling to show that extrinsic synaptic input is the main factor causing spiking heterogeneity in sensory neurons in vivo.

This study develops a behavioral task to measure spatial and feature-based attention in mice using reverse correlation, showing attentional tuning improves with training and approaches ideal observer performance.

The paper develops a computational model to analyze Ca2+ flux contributions to spontaneous Ca2+ local transients in OPCs, revealing their stochastic nature and flux dependencies.

This study decomposes EEG changes during propofol-induced loss of consciousness into synchronous and asynchronous components, revealing that aperiodic activity, not rhythmic oscillations, drives spectral changes.