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H. A. Brown, J. D. Allison, J. M. Samonds, A. B. Bonds; Nonlocal origin of response suppression from stimulation outside the classic receptive field in area 17 of the cat. Journal of Vision 2001;1(3):200. doi: https://doi.org/10.1167/1.3.200.
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© ARVO (1962-2015); The Authors (2016-present)
A stimulus located outside the Classic Receptive Field (CRF) of a striate cortical neuron markedly influences its behavior. To study this phenomenon, we recorded from two cortical sites, control and peripheral, with separate electrodes in cats anesthetized with Propofol and nitrous oxide. The receptive fields of each site were discrete (2–7.3í between centers). A baseline orientation tuning (OT) curve was recorded from a single cell at the control site. The OT curve was then remeasured by stimulating the cell's CRF while simultaneously stimulating the peripheral site with a stimulus optimized for that location. For 23/60 cells, the peripheral stimulus reduced the peak response and/or shifted the center of mass of the OT curve. For 18 of these 23 cells, we then reversibly blocked stimulus-driven activity at the peripheral site by iontophoretic application of GABA (0.5 M). For 6/18 cells (33%), the response returned to control levels, implying that for these cells the inhibitory influence came from the blocked site. The responses of nine cells remained reduced during inactivation of the peripheral site, suggesting that influence was generated outside the region of local block in Area 17. This is consistent with earlier findings that modulatory influences can originate from Area 18. Three cells (17%) had mixed results, suggesting multiple origins of influence. The response of each cell returned to reduced levels after dissipation of the GABA and returned to baseline values when the peripheral stimulus was removed. These findings support a cortical model in which orientation selectivity is modulated by an inhibitory network originating from beyond the receptive field that supplants convergence of excitatory geniculate neurons. The existence of cells that exhibit no change in peripherally inhibited responses during the GABA application suggests that peripheral mechanisms may arise from outside Area 17, presumably from other cortical areas (Area 18.)
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