Showing papers by "Sacha B. Nelson published in 1997"

Synaptic depression and cortical gain control

Abstract: Cortical neurons receive synaptic inputs from thousands of afferents that fire action potentials at rates ranging from less than 1 hertz to more than 200 hertz. Both the number of afferents and their large dynamic range can mask changes in the spatial and temporal pattern of synaptic activity, limiting the ability of a cortical neuron to respond to its inputs. Modeling work based on experimental measurements indicates that short-term depression of intracortical synapses provides a dynamic gain-control mechanism that allows equal percentage rate changes on rapidly and slowly firing afferents to produce equal postsynaptic responses. Unlike inhibitory and adaptive mechanisms that reduce responsiveness to all inputs, synaptic depression is input-specific, leading to a dramatic increase in the sensitivity of a neuron to subtle changes in the firing patterns of its afferents.

A Quantitative Description of Short-Term Plasticity at Excitatory Synapses in Layer 2/3 of Rat Primary Visual Cortex

Abstract: Cortical synapses exhibit several forms of short-term plasticity, but the contribution of this plasticity to visual response dynamics is unknown. In part, this is because the simple patterns of stimulation used to probe plasticity in vitro do not correspond to patterns of activity that occur in vivo. We have developed a method of quantitatively characterizing short-term plasticity at cortical synapses that permits prediction of responses to arbitrary patterns of stimulation. Synaptic responses were recorded intracellularly as EPSCs and extracellularly as local field potentials in layer 2/3 of rat primary visual cortical slices during stimulation of layer 4 with trains of electrical stimuli containing random mixtures of frequencies. Responses exhibited complex dynamics that were well described by a simple three-component model consisting of facilitation and two forms of depression, a stronger form that decayed exponentially with a time constant of several hundred milliseconds and a weaker, but more persistent, form that decayed with a time constant of several seconds. Parameters obtained from fits to one train were used to predict accurately responses to other random and constant frequency trains. Control experiments revealed that depression was not caused by a decrease in the effectiveness of extracellular stimulation or by a buildup of inhibition. Pharmacological manipulations of transmitter release and postsynaptic sensitivity suggested that both forms of depression are mediated presynaptically. These results indicate that firing evoked by visual stimuli is likely to cause significant depression at cortical synapses. Hence synaptic depression may be an important determinant of the temporal features of visual cortical responses.

Functional signatificance of synaptic depression between cortical neurons

Abstract: Intracortical synapses exhibit several forms of short-term plasticity that cause synaptic efficacy at any given time to depend on the previous history of presynaptic activity. We have measured synaptic transmission between layer 4 and layer 2/3 in slices of rat visual cortex and used the data to construct an accurate mathematical description of intracortical short-term synaptic plasticity. These data show rapid synaptic facilitation and three forms of synaptic depression differing in their rates of onset and recovery. The dominant effect seen is overall synaptic depression that causes steady-state synaptic efficacy to decrease as a function of presynaptic firing rate. At high rates, the steady-state efficacy is inversely proportional to firing rate which implies that cortical synapses do not convey information about the magnitude of sustained high firing rates. However, this same dependence means that, for transient signals, synapses convey information about fractional rather than absolute changes in presynaptic firing rates. We explore the functional significance of this result including its implications for spike-rate adaptation and mechanisms that produce directional selectivity in visually responsive neurons.

Modeling visual cortical contrast adaptation effects

Abstract: We demonstrate model visual cortical circuits which exhibit robust contrast adaptation properties, consistent with physiological observations in V1. The adaptation mechanism we employ is activity-dependent synaptic depression at thalamocortical and local intra-cortical synapses. Model contrast response functions (CRF) shift so that cells remain maximally responsive to changes around the recent average stimulus contrast level. Hysteresis effects for both stimulus contrast and orientation are achieved; orientation hysteresis is weaker, and depends exclusively on intracortical adaptation. Following stimulation of the receptive field (RF) surround, RFs dynamically expand to “fill in” for the missing stimulation in the RF center; in our model this expansion results from adaptation of local inhibitory synapses, triggered by excitation from long range horizontal projections. All adaptation effects are achieved using the same synaptic depression mechanisms.