ISSN:
1432-1106
Keywords:
Thalamic lesions
;
Kainic acid
;
HRP
;
Callosal connections
;
Laminar density
;
Rat
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary The patterns of callosal interconnections between the visual cortices of rats display considerable plasticity in response to various neonatal manipulations. In the present study, many neurones in the principal visual thalamic relay nuclei, the dorsal lateral geniculate nucleus (DLG) and to a lesser extent those in the lateral posterior nucleus (LP) were destroyed by injections of the neurotoxin — kainic acid — on the first day of postnatal life. Four weeks later, as demonstrated with the anterograde and retrograde transport of the enzyme horseradish peroxidase (HRP) injected into the occipital lobe of one hemisphere, callosally projecting neurones and terminals were distributed more widely in the retinotopically organized areas 17, 18a and 18b of the visual cortex ipsilateral to the lesioned visual thalamus than in unoperated control animals of the same age. By contrast, in the visual cortex contralateral to the lesioned visual thalamus the areal distribution of callosally projecting neurones and terminals was similar to that of the controls, that is, largely but not exclusively restricted to the common border of areas 17 and 18a. Both in unoperated and operated animals, cells in lamina V of several cytoarchitectonically defined areas that are not retinotopically organized (area 8 in the frontal lobe, area 29d in the retrosplenial limbic cortex and perirhinal areas 35/13 in the temporal lobe) also project to contralateral visual cortices. In areas 8 and 29d, the total numbers, laminar distributions and densities of labelled callosal cells both ipsilateral and contralateral to the kainate-injected visual thalamus were similar to those in the controls. However, in the temporal lobe, the areal distribution of the labelled callosal neurones was more extensive than that in the controls and labelled cells in areas 35/13 of the cortex contralateral to the kainate-lesioned visual thalamus merged with those in the neighbouring areas 20 and 36. By contrast, the areal distribution of associational neurones in area 18a and in nonretinotopically organized areas projecting to area 17 were very similar in controls and in operated animals (neonatal kainate lesion of the visual thalamus, neonatal section of the corpus callosum or both procedures combined). However, in operated animals, the labelled associational neurones projecting from the supragranular laminae (II/III) of area 18a to area 17 constituted a higher proportion of all cells than did those in the unoperated control animals. Thus, overall the number of associational neurones projecting from area 18a to area 17 was slightly increased by the experimental manipulations performed. The implications of these results concerning the mechanism(s) underlying the developmental changes in the distribution of commissural and associational neurones projecting to the rat's visual cortex are discussed.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00231769
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