Abstract

Previous studies in postnatal mouse demonstrating high levels of alpha7 nicotinic acetylcholine receptors on layer IV somatosensory cortical neurons coincident with the onset of functional synaptic transmission led us to investigate whether the number and/or the localization of these receptors could be regulated by activity. Accordingly, we examined alpha-bungarotoxin binding in mouse somatosensory cortex following removal of all of the vibrissae on one side of the face, either by vibrissal follicle cauterization or daily plucking beginning on the day of birth. Following vibrissa plucking, the levels of [125I]alpha-bungarotoxin binding on postnatal day 6 were significantly higher (23 +/- 7%) in the denervated cortex (contralateral to the peripheral manipulation) than the intact cortex. Cauterization also resulted in significantly higher (14 +/- 3%) [125I]alpha-bungarotoxin binding in the contralateral vs. the ipsilateral cortex. In contrast, there was no difference in [125I]alpha-bungarotoxin binding in the left and right cortices of unoperated control animals. At postnatal day 14, levels of [125I]alpha-bungarotoxin binding in layer IV were very low in control animals as well as in animals subjected to whisker plucking or cautery. These findings suggest that reducing activity in the somatosensory pathway regulates the density of alpha7 nicotinic acetylcholine receptors during the first postnatal week. However, the normal decrease in receptor density that is seen during the second postnatal week of development proceeds despite altered sensory activity.

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