Stimulation outside the receptive field of a primary visual cortical (V1) neuron reveals intracortical neural interactions. However, previous investigators implicitly or explicitly considered the extent of cortical spatial summation and, therefore, the size of the classical receptive field to be fixed and independent of stimulus characteristics or of surrounding context. On the contrary, we found that the extent of spatial summation in macaque V1 neurons depended on contrast, and was on average 2.3-fold greater at low contrast. This adaptive increase in spatial summation at low contrast was seen in cells throughout V1 and was independent of surround inhibition.
This study characterizes the spatial organization of excitation and inhibition that influences the visual responses of neurons in macaque monkey's primary visual cortex (V1). To understand the spatial extent of excitatory and inhibitory influences on V1 neurons, we performed area-summation experiments with suprathreshold contrast stimulation. The extent of spatial summation and the magnitude of surround suppression were estimated quantitatively by analyzing the spatial summation experiments with a difference of Gaussians (DOG) model. The average extent of spatial summation is approximately the same across layers except for layer 6 cells, which tend to sum more extensively than cells in the other layers. On average, the extent of length and width summation is approximately equal. Across the population, surround suppression is greatest in layer 4B and weakest in layer 6. Estimates of summation and suppression are compared for the DOG (subtractive) model and a normalization (divisive) model. The two models yield quantitatively similar estimates of the extent of excitation and inhibition. However, the normalization (divisive) model predicts weaker surround strength than the DOG model.
Sceniak, Michael P. and M. Bruce MacIver. Cellular actions of urethane on rat visual cortical neurons in vitro. J Neurophysiol 95: 3865-3874, 2006. First published March 1, 2006 doi:10.1152/jn.01196.2005. Urethane is widely used in neurophysiological experiments to anesthetize animals, yet little is known about its actions at the cellular and synaptic levels. This limits our ability to model systems-level cortical function using results from urethane-anesthetized preparations. The present study found that action potential discharge of cortical neurons in vitro, in response to depolarizing current, was strongly depressed by urethane and this was accompanied by a significant decrease in membrane resistance. Voltage-clamp experiments suggest that the mechanism of this depression involves selective activation of a Ba 2ϩ -sensitive K ϩ leak conductance. Urethane did not alter excitatory glutamate-mediated or inhibitory (GABA A -or GABA B -mediated) synaptic transmission. Neither the amplitude nor decay time constant of GABA A -or GABA B -mediated monosynaptic inhibitory postsynaptic currents (IPSCs) were altered by urethane, nor was the frequency of spontaneous IPSCs. These results are consistent with observations seen in vivo during urethane anesthesia where urethane produced minimal disruption of signal transmission in the neocortex.
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