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GABAergic and cholinergic modulation of repetition suppression in inferior temporal cortex

Neurons in many brain areas of different species reduce their response when a stimulus is repeated. Such adaptation or repetition suppression is prevalent in inferior temporal (IT) cortex. The mechanisms underlying repetition suppression in IT are still poorly understood. Studies in rodents and in-v...

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Detalles Bibliográficos
Autores principales: Kuravi, Pradeep, Vogels, Rufin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6120963/
https://www.ncbi.nlm.nih.gov/pubmed/30177749
http://dx.doi.org/10.1038/s41598-018-31515-1
Descripción
Sumario:Neurons in many brain areas of different species reduce their response when a stimulus is repeated. Such adaptation or repetition suppression is prevalent in inferior temporal (IT) cortex. The mechanisms underlying repetition suppression in IT are still poorly understood. Studies in rodents and in-vitro experiments suggest that acetylcholine and GABA can contribute to repetition suppression by interacting with fatigue-related or local adaptation mechanisms. Here, we examined the contribution of cholinergic and GABAergic mechanisms to repetition suppression in macaque IT, using an adaptation paradigm in which familiar images were presented successively with a short interstimulus interval. We found that intracortical local injections of acetylcholine and of the GABA(A) receptor antagonist Gabazine both increased repetition suppression in awake macaque IT. The increased repetition suppression was observed for both spiking activity and local field potential power. The latter was present mainly for frequencies below 50 Hz, spectral bands that typically do not show consistent repetition suppression in IT. Although increased with drug application, repetition suppression remained stimulus selective. These findings agree with the hypothesis that repetition suppression of IT neurons mainly results from suppressed input from upstream and other IT neurons but depend less on intrinsic neuronal fatigue.