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Cerebral Cortex, Vol. 12, No. 1, 62-74, January 2002
© 2002 Oxford University Press

Contribution of GABAergic Inhibition to Receptive Field Structures of Monkey Inferior Temporal Neurons

Yi Wang1,2,3, Ichiro Fujita1,2,3, Hiroshi Tamura1 and Yusuke Murayama2

1 Division of Biophysical Engineering, Graduate School of Engineering Science, Osaka University, Toyonaka, Osaka 560-8531, , 2 Department of Cognitive Neuroscience, Osaka University Medical School, Suita, Osaka 565-0871 and , 3 Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Toyonaka, Osaka 560-8531, Japan

Ichiro Fujita, Laboratory for Cognitive Neuroscience, Division of Biophysical Engineering, Graduate School of Engineering Science, Osaka University, 1–3 Machikaneyama, Toyonaka, Osaka 565-8531, Japan. Email: fujita{at}bpe.es.osaka-u.ac.jp.

Receptive field (RF) structures of neurons in area TE of the monkey inferior temporal cortex were investigated under blockade of inhibition mediated by {gamma}-aminobutyric acid (GABA). Bicuculline methiodide, a GABAA receptor antagonist, was microiontophoretically administered to TE neurons. Blockade of inhibition enhanced responses to a particular range of visual stimuli not only at the RF center, but also at the periphery of or outside RFs where the stimuli originally evoked little or no response, enlarging the RFs. The strongest responses under normal and disinhibited conditions occurred at the RF center in most neurons. The largest increase in responses, reflecting the strongest inhibitory input, usually occurred at the RF center, but in some neurons it occurred in the periphery. A neuron had a silent region within its RF where some stimuli effective at adjacent locations could not elicit responses even under blockade of inhibition. We suggest that (i) afferent information to individual TE neurons originates from a wide retinotopic region beyond their normal RF; (ii) the afferent convergence is not necessarily complete throughout a RF; and (iii) GABAergic inhibition contributes to the generation of RF structures of TE neurons.


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