Modifying spiking precision in conductance-based neuronal models.

The temporal precision of a neuron's spiking can be characterized by calculating its "jitter," defined as the standard deviation of the timing of individual spikes in response to repeated presentations of a stimulus. Sub-millisecond jitters have been measured for neurons in a variety of experimental systems and appear to be functionally important in some instances. We have investigated how modifying a neuron's maximal conductances affects jitter using the leaky integrate-and-fire (LIF) model and an eight-conductance Hodgkin-Huxley type (HH8) model. We observed that jitter can be largely understood in the LIF model in terms of the neuron's filtering properties. In the HH8 model we found the role of individual conductances in determining jitter to be complicated and dependent on the model's spiking properties. Distinct behaviors were observed for populations with slow (<11.5 Hz) and fast (>11.5 Hz) spike rates and appear to be related to differences in a particular channel's activity at times just before spiking occurs.

Laminar circuit organization and response modulation in mouse visual cortex.

The mouse has become an increasingly important animal model for visual system studies, but few studies have investigated local functional circuit organization of mouse visual cortex. Here we used our newly developed mapping technique combining laser scanning photostimulation (LSPS) with fast voltage-sensitive dye (VSD) imaging to examine the spatial organization and temporal dynamics of laminar circuit responses in living slice preparations of mouse primary visual cortex (V1). During experiments, LSPS using caged glutamate provided spatially restricted neuronal activation in a specific cortical layer, and evoked responses from the stimulated layer to its functionally connected regions were detected by VSD imaging. In this study, we first provided a detailed analysis of spatiotemporal activation patterns at specific V1 laminar locations and measured local circuit connectivity. Then we examined the role of cortical inhibition in the propagation of evoked cortical responses by comparing circuit activity patterns in control and in the presence of GABAa receptor antagonists. We found that GABAergic inhibition was critical in restricting layer-specific excitatory activity spread and maintaining topographical projections. In addition, we investigated how AMPA and NMDA receptors influenced cortical responses and found that blocking AMPA receptors abolished interlaminar functional projections, and the NMDA receptor activity was important in controlling visual cortical circuit excitability and modulating activity propagation. The NMDA receptor antagonist reduced neuronal population activity in time-dependent and laminar-specific manners. Finally, we used the quantitative information derived from the mapping experiments and presented computational modeling analysis of V1 circuit organization. Taken together, the present study has provided important new information about mouse V1 circuit organization and response modulation.