Rw. Rhoades et al., Effect of activity blockade on changes in vibrissae-related patterns in the rat's primary somatosensory cortex induced by serotonin depletion, J COMP NEUR, 402(2), 1998, pp. 276-283
Depletion of cortical serotonin (5-HT) during development results in a decr
ease in the size of the patches of thalamocortical afferents representing t
he mystacial vibrissae in lamina TV of the primary somatosensory cortex (SI
). We previously suggested that this change may be due to a reduction in 5-
HT-induced suppression of thalamocortical activity in these animals. The pr
esent experiments directly tested the role that modulation of activity may
play in the morphologic changes observed after reducing cortical 5-HT conce
ntrations. Serotonin was depleted from the cortex by systemic administratio
n of 5,7-dihydroxytryptamine (5,7-DHT, 100 mg/kg) on the day of birth in an
imals that also had either tetrodotoxin (TTX)-impregnated or control implan
ts placed unilaterally over the developing SI on this day. Other rat pups w
ere treated with TTX-impregnated or control implants alone. Administration
of 5,7-DHT reduced cortical serotonin levels and this effect was not signif
icantly modified by the presence of either control or TTX-impregnated corti
cal implants. Administration of 5,7-DHT reduced the cross-sectional area of
the cortical patches, demonstrated by acetylcholinesterase, corresponding
to the vibrissae by 19.9% (P < 0.05). A similar reduction was observed in t
he animals treated with both 5,7-DHT and TTX-impregnated implants. Treatmen
t with TTX-impregnated implants alone resulted in a 3.1% increase in patch
size (P > 0.05). None of the treatments significantly altered the overall a
rea of the part of SI devoted to the representation of the long mystacial v
ibrissae. These results suggest that the effects of 5-HT depletion on the s
ize of the cortical patches representing the long vibrissae are independent
of activity that can be blocked by administration of TTX. J. Comp. Neurol.
402:276-283, 1998. (C) 1998 Wiley-Liss, Inc.