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Venkatesh N Murthy

Publications and source records attributed to Venkatesh N Murthy.

5 recordsLinked to original sources

Synaptic activity of the AFD neuron in Caenorhabditis elegans correlates with thermotactic memory.

Thermotactic behavior in Caenorhabditis elegans is sensitive to both a worm's ambient temperature (T(amb)) and its memory of the temperature of its cultivation (T(cult)). The AFD neuron is part of a neural circuit that underlies thermotactic behavior. By monitoring the fluorescence of pH-sensitive green fluorescent protein localized to synaptic vesicles, we measured the rate of the synaptic release of AFD in worms cultivated at temperatures between 15 and 25 degrees C, and subjected to fixed, ambient temperatures in the same range. We found that the rate of AFD synaptic release is high if either T(amb) > T(cult) or T(amb) < T(cult), but AFD synaptic release is low if T(amb) congruent with T(cult). This suggests that AFD encodes a direct comparison between T(amb) and T(cult).

Action Potentials↗

Multiple forms of synaptic plasticity triggered by selective suppression of activity in individual neurons.

The rules by which neuronal activity causes long-term modification of synapses in the central nervous system are not fully understood. Whereas competitive or correlation-based rules result in local modification of synapses, homeostatic modifications allow neuron-wide changes in synaptic strength, promoting stability. Experimental investigations of these rules at central nervous system synapses have relied generally on manipulating activity in populations of neurons. Here, we investigated the effect of suppressing excitability in single neurons within a network of active hippocampal neurons by overexpressing an inward-rectifier potassium channel. Reducing activity in a neuron before synapse formation leads to a reduction in functional synaptic inputs to that neuron; no such reduction was observed when activity of all neurons was uniformly suppressed. In contrast, suppressing activity in a single neuron after synapses are established results in a homeostatic increase in synaptic input, which restores the activity of the neuron to control levels. Our results highlight the differences between global and selective suppression of activity, as well as those between early and late manipulation of activity.

Action Potentials↗

Gradients of substrate-bound laminin orient axonal specification of neurons.

Little is known about the influence of substrate-bound gradients on neuronal development, since it has been difficult to fabricate gradients over the distances typically required for biological studies (a few hundred micrometers). This article demonstrates a generally applicable technique for the fabrication of substrate-bound gradients of proteins with complex shapes, using laminar flows in microchannels. Gradients that range from pure laminin to pure BSA were formed in solution by using a network of microchannels, and these proteins were allowed to adsorb onto a homogeneous layer of poly-l-lysine. Rat hippocampal neurons were cultivated on these substrate-bound gradients. Analysis of optical images of these neurons showed that axon specification is oriented in the direction of increasing surface density of laminin. Linear gradients in laminin adsorbed from a gradient in solution having a slope of nabla [laminin] > about 0.06 microg (ml.microm)(-1) (defined by dividing the change of concentration of laminin in solution over the distance of the gradient) orient axon specification, whereas those with nabla [laminin] < about 0.06 microg (ml.microm)(-1) have no effect.

Animals↗

Rapid turnover of actin in dendritic spines and its regulation by activity.

Dendritic spines are motile structures that contain high concentrations of filamentous actin. Using hippocampal neurons expressing fluorescent actin and the method of fluorescence recovery after photobleaching, we found that 85 +/- 2% of actin in the spine was dynamic, with a turnover time of 44.2 +/- 4.0 s. The rapid turnover is not compatible with current models invoking a large population of stable filaments and static coupling of filaments to postsynaptic components. Low-frequency stimulation known to induce long-term depression in these neurons stabilized nearly half the dynamic actin in the spine. This effect depended on the activation of N-methyl-D-aspartate (NMDA) receptors and the influx of calcium. In neurons from mice lacking gelsolin, a calcium-dependent actin-binding protein, activity-dependent stabilization of actin was impaired. Our studies provide new information on the kinetics of actin turnover in spines, its regulation by neural activity and the mechanisms involved in this regulation.

Actins↗