I. Salimi et al., NEURONAL-ACTIVITY IN NORMAL AND DEAFFERENTED FORELIMB SOMATOSENSORY CORTEX OF THE AWAKE CAT, Brain research, 656(2), 1994, pp. 263-273
Three hundred and seventy-three neurons were recorded from the forelim
b representation in the primary somatosensory cortex of unanesthetized
, quietly resting adult cats. Of these, 177 were studied from 2 days t
o 3 weeks after transection of the radial, median and ulnar nerves. Fo
llowing deafferentation the proportion of cells without receptive fiel
ds increased from 24 to 82%, however, the average rate of spontaneous
activity did not change nor did the probability of encountering a neur
on with a receptive field as a function of depth. Receptive field size
s increased dramatically following deafferentation and the response ch
anged from a reliable short-latency, brisk discharge to one that did n
ot occur on every stimulus. After deafferentation the edges of the rec
eptive field often could not be defined accurately. Spontaneous activi
ty in 31% (n = 47) of the neurons from deprived cortex could be modula
ted by manipulations of the body but these changes were sufficiently s
low and ill-defined that they were not classified as a receptive field
. In some cases, manipulation of the body gradually reduced the discha
rge rate. This slow decline in activity was different from the abrupt
inhibition of spontaneous activity elicited by somatic simuli in anoth
er class of cells (n = 18). In other cases the manipulation produced a
gradual increase in the discharge rate. After deafferentation antidro
mically 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 ventropost
erior thalamus increased from 2.7 ms to 4.6 ms. The lost forelimb rece
ptive fields were rarely replaced by inputs from adjacent body parts o
ver the two-week duration of this study. Most responses to somatic sti
muli obtained from cortical neurons in the deafferented cortex were cl
early abnormal.