Effect of activity blockade on changes in vibrissae-related patterns in the rat's primary somatosensory cortex induced by serotonin depletion.
Depletion of cortical serotonin (5-HT) during development results in a decrease in the size of the patches of thalamocortical afferents representing the mystacial vibrissae in lamina IV 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 present experiments directly tested the role that modulation of activity may play in the morphologic changes observed after reducing cortical 5-HT concentrations. Serotonin was depleted from the cortex by systemic administration of 5,7-dihydroxytryptamine (5,7-DHT, 100 mg/kg) on the day of birth in animals that also had either tetrodotoxin (TTX)-impregnated or control implants placed unilaterally over the developing SI on this day. Other rat pups were treated with TTX-impregnated or control implants alone. Administration of 5,7-DHT reduced cortical serotonin levels and this effect was not significantly modified by the presence of either control or TTX-impregnated cortical 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 the animals treated with both 5,7-DHT and TTX-impregnated implants. Treatment 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 area of the part of SI devoted to the representation of the long mystacial vibrissae. These results suggest that the effects of 5-HT depletion on the size of the cortical patches representing the long vibrissae are independent of activity that can be blocked by administration of TTX.
Rhoades
R W
RW
Department of Anatomy and Neurobiology, Medical College of Ohio, Toledo 43614-5804, USA. rrhoades@gemini.mco.edu
Chiaia
N L
NL
Lane
R D
RD
Bennett-Clarke
C A
CA
D015116:5,7-Dihydroxytryptamine / Q000633:toxicity*; D000200:Action Potentials / Q000187:drug effects; D000344:Afferent Pathways / Q000187:drug effects / Q000648:ultrastructure; D000818:Animals; D000831:Animals, Newborn; D002799:Cholinergic Fibers / Q000187:drug effects / Q000648:ultrastructure; D004343:Drug Implants; D051381:Rats; D012701:Serotonin / Q000172:deficiency* / Q000502:physiology; D015222:Sodium Channels / Q000187:drug effects; D013003:Somatosensory Cortex / Q000187:drug effects* / Q000254:growth & development / Q000648:ultrastructure; D013779:Tetrodotoxin / Q000008:administration & dosage / Q000494:pharmacology; D013788:Thalamus / Q000648:ultrastructure; D014738:Vibrissae / Q000294:innervation*
D004343:Drug Implants; D015222:Sodium Channels; C023790:tetrodotoxin-binding protein; D015116:5,7-Dihydroxytryptamine; D012701:Serotonin; D013779:Tetrodotoxin