title: Sensitive period for lesion-induced reorganization of intracortical projections within the vibrissae representation of rat's primary somatosensory cortex.
abstract: Previous experiments from this laboratory demonstrated that intracortical connections in lamina IV of the rat primary somatosensory cortex (SI) are most dense outside the patches of cytochrome oxidase (CO) staining that correspond to the mystacial vibrissae. This pattern of intracortical connections becomes apparent on postnatal day 4 (P-4), at least 2 days after the appearance of the vibrissae-related pattern of thalamocortical afferents. Transection of the infraorbital nerve (ION) on the day of birth (P-0) disrupts both the CO and intracortical projection patterns. This series of experiments was undertaken to determine whether the patterning of either thalamocortical afferents or intracortical projections defines the end of the period over which peripheral damage can alter intracortical projections in lamina IV of SI. The infraorbital nerve (ION) was transected in different cohorts of rats on P-1 through P-5, and animals were allowed to survive > or =45 days, at which time biotinylated dextran amine (BDA) injections were made into the SI. After 7 days, animals were killed, and alternate cortical sections were processed for the demonstration of BDA or CO. Transection of the ION on P-1 or P-2 altered the patterning of both CO and intracortical connections in the SI. In contrast, cutting the ION on P-3 left the pattern of CO densities in the SI intact, but significantly altered the patterning of intracortical connections. Transection of the nerve on P-5 resulted in qualitatively and quantitatively normal patterns of both CO densities and BDA-labelled intracortical projections. These results indicate that the establishment of a stable barrel pattern in layer IV of the SI is not sufficient for normal adult patterning of intracortical projections in this lamina. However, once the mature pattern of intracortical projections in layer IV is established, ION lesions can no longer alter it.
authors.affiliation: Department of Anatomy and Neurobiology, Medical College of Ohio, Toledo 43699-0008, USA. rrhoades@gemini.mco.edu
authors.forename: R W
authors.initials: RW
authors.lastname: Rhoades
authors.forename: V
authors.initials: V
authors.lastname: Strang
authors.forename: C A
authors.initials: CA
authors.lastname: Bennett-Clarke
authors.forename: H P
authors.initials: HP
authors.lastname: Killackey
authors.forename: N L
authors.initials: NL
authors.lastname: Chiaia
mesh_terms: D000375:Aging / Q000502:physiology; D000818:Animals; D001710:Biotin / Q000031:analogs & derivatives; D003911:Dextrans; D005456:Fluorescent Dyes; D009416:Nerve Regeneration / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D009915:Orbit / Q000294:innervation / Q000502:physiology; D051381:Rats; D013003:Somatosensory Cortex / Q000254:growth & development* / Q000473:pathology / Q000502:physiology; D014276:Trigeminal Nerve / Q000254:growth & development* / Q000502:physiology; D014738:Vibrissae / Q000294:innervation*
chemical_list: D003911:Dextrans; D005456:Fluorescent Dyes; C076397:biotinylated dextran amine; D001710:Biotin