bioRxiv Science⌕ Search

Biology subjects

Nelson, J. S. E.

Publications and source records attributed to Nelson, J. S. E..

2 recordsLinked to original sources

Spatio-temporal dynamics of lateral Na+ diffusion in apical dendrites of mouse CA1 pyramidal neurons

Sodium ions (Na+) are major charge carriers mediating neuronal excitation and play a fundamental role in brain physiology. Glutamatergic synaptic activity is accompanied by large transient Na+ increases, but the spatio-temporal dynamics of Na+ signals and properties of Na+ diffusion within dendrites are largely unknown. To address these questions, we employed multi-photon Na+ imaging combined with whole-cell patch-clamp in dendrites of CA1 pyramidal neurons in tissue slices from mice of both sexes. Fluorescence lifetime microscopy revealed a dendritic baseline Na+ concentration of ~10 mM. Using intensity-based line-scan imaging we found that local, glutamate-evoked Na+ signals spread rapidly within dendrites, with peak amplitudes decreasing and latencies increasing with increasing distance from the site of stimulation. Spread of Na+ along dendrites was independent of dendrite diameter, order or overall spine density in the ranges measured. Our experiments also show that dendritic Na+ readily invades spines and suggest that spine necks may represent a partial diffusion barrier. Experimental data were well reproduced by mathematical simulations assuming normal diffusion with a diffusion coefficient of [Formula]. Modeling moreover revealed that lateral diffusion is key for the clearance of local Na+ increases at early time points, whereas when diffusional gradients are diminished, Na+/K+-ATPase becomes more relevant. Taken together, our study thus demonstrates that Na+ influx causes rapid lateral diffusion of Na+ within spiny dendrites. This results in an efficient redistribution and fast recovery from local Na+ transients which is mainly governed by concentration differences. Significance statementActivity of excitatory glutamatergic synapses generates large Na+ transients in postsynaptic cells. Na+ influx is a main driver of energy consumption and modulates cellular properties by modulating Na+-dependent transporters. Knowing the spatio-temporal dynamics of dendritic Na+ signals is thus critical for understanding neuronal function. To study propagation of Na+ signals within spiny dendrites, we performed fast Na+ imaging combined with mathematical simulations. Our data shows that normal diffusion, based on a diffusion coefficient of 600 {micro}m2/s, is crucial for fast clearance of local Na+ transients in dendrites, whereas Na+ export by the Na+/K+-ATPase becomes more relevant at later time points. This fast diffusive spread of Na+ will reduce the local metabolic burden imposed by synaptic Na+ influx.

neuroscience↗

Atypical plume-like events drive glutamate accumulation in metabolic stress conditions

Neural glutamate homeostasis plays a key role in health and disease. In ischemic conditions, such as stroke, this homeostasis is severely disrupted since energy depletion and ion imbalances lead to more glutamate release and less uptake. We here used the fluorescent glutamate sensor SF-iGluSnFR(A184V) to probe the effects of chemical ischemia on extracellular glutamate dynamics in situ, using organotypic slice cultures from mouse cortex. SF-iGluSnFR imaging reported spontaneous glutamate release events, which indicate synchronous network activity, similar to calcium signals detected with GCaMP6f. In addition, glutamate imaging revealed local, asynchronous release events, which were atypically large and long-lasting and showed plume-like characteristics. Under baseline conditions plumes occurred with low frequency, were independent of network activity, and persisted in the presence of TTX. Plume induction was strongly favored by blocking glutamate uptake with TFB-TBOA, whereas blocking ionotropic glutamate receptors (iGluRs) suppressed plumes. Upon inducing chemical ischemia plumes became more pronounced and overly abundant, which resulted in large-scale accumulation of extracellular glutamate. Similar plumes were recently also observed in models of cortical spreading depression and migraine. We therefore propose that plumes represent a more general phenomenon induced by glutamate uptake dysfunction, which may contribute to glutamate-related excitotoxicity in various neurodegenerative and neurological disorders.

neuroscience↗