Thomas M. Bartol

The paper investigates how presynaptic vesicle density changes during LTP and links it to axonal bouton enlargement.

The paper models synaptic spine head morphology using graph grammars to simulate actin dynamics and their effects on membrane shape.

The paper shows that synaptic vesicle clusters become less dense and more dispersed during long-term potentiation, with increased mobility and a transition from compact to loose organization.

The paper uses Monte Carlo simulations to show that geometric complexity in rod synapses slows glutamate diffusion, affecting synaptic responses and receptor kinetics.

The paper develops a spatial model of CaMKII autophosphorylation in synaptic spines to show that CaM-trapping prolongs phospho-CaMKII lifetime by hindering dephosphorylation.

This study shows that long-term potentiation (LTP) increases synaptic information storage capacity in adult rat hippocampus by expanding the range of synapse sizes and improving precision.

The paper introduces a method to measure synaptic information storage capacity (SISC) using 3DEM data from rat hippocampus and finds regional and LTP-dependent variations in SISC.

The paper develops a mesoscale model of presynaptic release dynamics by characterizing molecular mechanisms and applying model reduction to create an efficient phenomenological framework.

The paper abstracts a detailed 3D reaction-diffusion model of a chemical synapse into a compact state space for neuromorphic hardware emulation with preserved input-output dynamics.

The paper analyzes mitochondrial morphology in mouse cerebellum neurons using 3D TEM data to quantify structural features that influence metabolic output.

The paper investigates the role of presynaptic endoplasmic reticulum in modulating short-term plasticity in hippocampal synapses using computational modeling.

The paper develops a rule-based computational model of CaMKII holoenzyme to explore how Ca2+/CaM binding stabilizes autophosphorylation and regulates synaptic plasticity.

The paper investigates nanoscale synaptic changes during two LTD protocols, showing NMDAR-dependent LTD reorganizes PSD-95 to enhance synaptic facilitation.

The paper shows that neuroligin-1 alignment with AMPA receptor nanodomains is critical for synaptic transmission efficiency, as disrupting this alignment reduces transmission.