Literature DB >> 7820586

Neuronal activity in normal and deafferented forelimb somatosensory cortex of the awake cat.

I Salimi1, H H Webster, R W Dykes.   

Abstract

Three hundred and seventy-three neurons were recorded from the forelimb representation in the primary somatosensory cortex of unanesthetized, quietly resting adult cats. Of these, 177 were studied from 2 days to 3 weeks after transection of the radial, median and ulnar nerves. Following deafferentation the proportion of cells without receptive fields increased from 24 to 82%, however, the average rate of spontaneous activity did not change nor did the probability of encountering a neuron with a receptive field as a function of depth. Receptive field sizes increased dramatically following deafferentation and the response changed from a reliable short-latency, brisk discharge to one that did not occur on every stimulus. After deafferentation the edges of the receptive field often could not be defined accurately. Spontaneous activity in 31% (n = 47) of the neurons from deprived cortex could be modulated by manipulations of the body but these changes were sufficiently slow and ill-defined that they were not classified as a receptive field. In some cases, manipulation of the body gradually reduced the discharge rate. This slow decline in activity was different from the abrupt inhibition of spontaneous activity elicited by somatic stimuli in another class of cells (n = 18). In other cases the manipulation produced a gradual increase in the discharge rate. After deafferentation antidromically identified corticothalamic and pyramidal tract neurons did not display behaviors different from their counterparts in normal cortex. However, the mean latency for synaptic activation from the ventroposterior thalamus increased from 2.7 ms to 4.6 ms. The lost forelimb receptive fields were rarely replaced by inputs from adjacent body parts over the two-week duration of this study. Most responses to somatic stimuli obtained from cortical neurons in the deafferented cortex were clearly abnormal.

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Year:  1994        PMID: 7820586     DOI: 10.1016/0006-8993(94)91469-9

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


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