Biomedical subjects

David Tsay

Publications and source records attributed to David Tsay.

4 recordsLinked to original sources

PubMed2004

On the electrical function of dendritic spines.

Dendritic spines mediate most excitatory inputs in the brain, yet their function is still unclear. Imaging experiments have demonstrated their role in biochemical compartmentalization at individual synapses, yet theoretical studies have suggested that they could serve an electrical function in transforming synaptic inputs and transmitting dendritic spikes. Recent data indicate that spines possess voltage-dependent conductances and that these channels can be spine-specific. Although direct experimental investigations of the electrical properties of spines have not yet taken place, spines could play a significant electrical role, greatly influencing dendritic integration and the function of neural circuits.

Animals↗

PubMed2002

Calcium dynamics of spines depend on their dendritic location.

Dendritic spines are morphologically and functionally heterogeneous. To understand this diversity, we use two-photon imaging of layer 5 neocortical pyramidal cells and measure action potential-evoked [Ca(2+)]i transients in spines. Spine calcium kinetics are controlled by (i) the diameter of the parent dendrite, (ii) the length of the spine neck, and (iii) the strength of spine calcium pumps. These factors produce different calcium dynamics in spines from basal, proximal apical, and distal apical dendrites, differences that are more pronounced without exogenous buffers. In proximal and distal apical dendrites, different calcium dynamics correlate with different susceptibility to synaptic depression, and modifying calcium kinetics in spines changes the expression of long-term depression. Thus, the spine location apparently determines its calcium dynamics and synaptic plasticity. Our results highlight the precision in design of neocortical neurons.

Animals↗

PubMed2002

Calcium dynamics in spines: link to synaptic plasticity.

Dendritic spines are morphologically and functionally heterogeneous. Here, we use two-photon imaging of layer V pyramidal neurons in slices from mouse visual cortex to characterize differences in spine calcium dynamics between individual spines. By measuring action potential-evoked [Cell transients in spines, we find different calcium dynamics in spines from proximal apical and distal apical dendrites. Using a mathematical multi-compartmental model, we demonstrate that these differences are even more pronounced in the absence of exogenous calcium buffers. We also find that these different calcium dynamics cause different susceptibility to synaptic depression in proximal and distal apical synapses, and that modifying calcium decay kinetics in spines changes the expression of long-term depression. We conclude that the location of the spine determines its time window of calcium compartmentalization and degree of calcium-dependent synaptic plasty. Our results highlight the precision of the design of neocortical neurons.

Action Potentials↗

PubMed2002

Role of dendritic spines in action potential backpropagation: a numerical simulation study.

Two remarkable aspects of pyramidal neurons are their complex dendritic morphologies and the abundant presence of spines, small structures that are the sites of excitatory input. Although the channel properties of the dendritic shaft membrane have been experimentally probed, the influence of spine properties in dendritic signaling and action potential propagation remains unclear. To explore this we have performed multi-compartmental numerical simulations investigating the degree of consistency between experimental data on dendritic channel densities and backpropagation behavior, as well as the necessity and degree of influence of excitable spines. Our results indicate that measured densities of Na(+) channels in dendritic shafts cannot support effective backpropagation observed in apical dendrites due to suprathreshold inactivation. We demonstrate as a potential solution that Na(+) channels in spines at higher densities than those measured in the dendritic shaft can support extensive backpropagation. In addition, clustering of Na(+) channels in spines appears to enhance their effect due to their unique morphology. Finally, we show that changes in spine morphology significantly influence backpropagation efficacy. These results suggest that, by clustering sodium channels, spines may serve to control backpropagation.

Action Potentials↗