Immediate expansion of receptive fields of neurons in area 3b of macaque monkeys after digit denervation



Publication Details

Calford, M. B. & Tweedale, R. (1991). Immediate expansion of receptive fields of neurons in area 3b of macaque monkeys after digit denervation. Somatosensory and Motor Research, 8 (3), 249-260.


The short-term effect of total or partial single-digit denervation on receptive fields (Rds) of neurons in somatosensory cortex (area 3b) was examined in five macaque monkeys. In two animals, after denervation by amputation, it was found that electrode positions that initially recorded neurons with Rds on the amputated digit had new Rds extending from the wound. Often the new fields were on adjacent digits. Neurons with initial Rds that were partially amputated, or in some cases close to but not on the amputated digit, showed considerable expansion of the remaining RF. In three monkeys local anesthesia was used to provide a temporary denervation. In these experiments electrodes were placed in equivalent positions in both cortices. The effect on cortex contralateral to the denervation was similar to that seen with amputation. However, after esthesia returned to the digit, the expanded Rds contracted. In cortex ipsilateral to the denervation, Rds were on the opposite unaffected hand. These also rapidly expanded and then contracted, with the same time course as their counterparts in cortex contralateral to the denervation. Because of the rapidity of the expansion and its temporary nature with short-term denervation, the basis of the effect is probably an unmasking of existing but normally unexpressed connections, which are normally inhibited by the intact output from the denervated area. The wide arborization fields of thalamocortical afferents provide a potential source for the unmasked sensitivity. A mechanism for the inhibition that normally suppresses the expression of large Rds is not readily apparent. However, work in other species suggests that peripheral C fibers provide the primary source of input to central inhibitory circuits.

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