Area 18 contribution to spatial integration of receptive fields of area 17 cells in the cat

Abstract

A stimulus placed outside the classic receptive field (CRF) of an Area 17 cell does not evoke an excitatory response. However if the CRF is stimulated to excite the cell, a second stimulus placed in the periphery can modulate this baseline activity. Does the integration of modulating influences arise in Area 17 alone? In cats paralyzed and anesthetized with Propofol and N2O, we investigated whether modulation of the response of Area 17 cells by peripheral stimulation originated from Area 18. We inserted a tungsten electrode in Area 17 (“central”) and a multi-barrel injection and recording pipette in Area 18 (“peripheral”) and identified sites with non-overlapping RFs. Optimal stimulus parameters for the Area 17 cell were determined and a control orientation tuning (OT) curve was measured. We then optimized stimulation parameters for the Area 18 site and verified that iontophoretic administration of GABA (0.5 M) silenced the response to that stimulus. To determine the influence of the peripheral site on the response of the Area 17 cell, both sites were stimulated simultaneously and the OT curve was remeasured. In 6/12 cases, peripheral stimulation suppressed the central response and GABA was administered to block the Area 18 activity. If the suppression were originating from Area 18, the blockade would eliminate the peripheral influence and the response of the Area 17 cell would return to control levels. In 4/6 cells, the OT curve returned to control levels during the Area 18 blockade indicating that Area 18 activity was responsible for most, if not all of the peripheral influence of Area 17 cells. The response of each cell returned to suppressed levels after GABA reuptake and returned to control values when the peripheral stimulus was removed. This result supports our hypothesis that Area 18 makes a major contribution to the widespread integration of information by Area 17 receptive fields.

Footnotes

 Supported by NIH EYR0103778, NIH Training Grant EY07135