Inhibitory mechanisms influencing complex cell orientation selectivity and their modification at high resting discharge levels.
1. These experiments have investigated the contribution made by GABA-mediated inhibitory processes to the orientation tuning of complex cells in the cat's striate cortex. The GABA antagonist bicuculline has been ionophoretically applied to individual complex cells and the modifications produced in their orientation tuning documented. 2. In terms of the type of change produced in orientation tuning by the application of bicuculline, it seems that there are two categories of complex cells. 3. In one of these categories the orientation selectivity was eliminated during bicuculline application. The excitatory input to these cells would therefore appear to be non-orientation specific. Their orientation selectivity is presumably generated by a GABA-mediated inhibitory input. 4. In the other category of complex cells, although the orientation selectivity was decreased during bicuculline application, the cells retained a preference for a range of orientations that was generally centred around the original optimal orientation. It is suggested that for these cells the inhibitory input enhances the orientation tuning of an excitatory input that is already broadly orientation tuned. 5. Comparison of normal orientation tuning curves with those observed during the application of bicuculline provides a basis for estimating the orientation tuning of the GABA-mediated inhibitory input. In all cases, it is clear that at normal resting discharge levels, orientations either side of the optimal, and not those centred on the optimal, generate the most powerful inhibitory input. 6. These results would seem to be best explained by inhibitory interconnexions between cortical columns sensitive to different orientations. This type of lateral interaction between columns may serve to enhance the contrast in the orientation domain for the cortical representation of a specific stimulus orientation. 7. Increasing the resting discharge level of a complex cell, without blocking the action of GABA appeared to increase the gain of the inhibitory mechanisms acting on the cell. The normal excitatory responses to optimal or near optimal orientations were greatly reduced, or replaced by inhibitory responses, and non-optimal orientations produced only inhibitory responses. These inhibitory effects were blocked on the context of other observations in the literature. It is tentatively suggested that the interneurones providing the inhibitory drive to complex cells receive an input from recurrent collaterals of the recipient complex cells. Their other inputs would derive from neighbouring colums and from the afferent input to the parent column. The inputs from neighbouring columns would mediate the lateral inhibitory interactions in the orientation domain, and the recurrent collateral feed-back the decreased responsiveness at high resting discharge levels.
D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002415:Cats; D007395:Interneurons / Q000502:physiology; D009433:Neural Inhibition; D009434:Neural Pathways / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D009949:Orientation / Q000187:drug effects / Q000502:physiology*; D014793:Visual Cortex / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D005680:gamma-Aminobutyric Acid; D001640:Bicuculline