Sherren N, Pappas BA (2003) Dendritic dysgenesis in midline cortical regions following selective acetylcholine and dopamine lesions in neonatal rats. Neuroscience 2003 Abstracts 457.11. Society for Neuroscience, New Orleans, LA.
Summary: Both acetylcholine (ACh) and dopamine (DA) afferents reach their cortical targets during periods of synaptogenesis, and are perfectly positioned to influence the cytoarchitectural development of cortical neurons. Thus the behavioural outcomes of these lesions may be related to the development of appropriate dendritic morphology in neurons from cortical regions involved in cognition. Previous studies have either used non-specific lesion techniques or have not examined long-term effects. We lesioned rat pups at P7 with either 600 ng of the selective immunotoxin 192 IgG-saporin, or 150 ug of 6-hydroxydopamine preceded by desmethylimipramine, or both, and aged them to four months. One squad of rats was sacrificed for neurochemistry and another was prepared for morphological analysis using Golgi-Cox stain. The ACh lesion caused a 32% decrease in choline acetyltransferase activity in the frontal/cingulate cortex and a 72% reduction in retrosplenial cortex (RSC). This was associated with reductions in total dendritic length of the apical tree of layer V pyramidal cells in the medial prefrontal cortex (mPFC), the apical tree of layer III pyramidal cells in the anterior cingulate cortex (ACC), and the basal tree of layer III pyramidal cells in RSC. The DA lesion caused a 76% reduction in DA levels in frontal/cingulate cortex and no change in RSC levels. This was associated with reductions in total dendritic length of the basal and apical trees of layer V pyramidal cells in mPFC, and the basal tree of layer III pyramidal cells in ACC. No changes in layer III pyramidal cells were noted in RSC following the DA lesion. These data demonstrate that ascending ACh and DA afferents play a vital role in the cytoarchitectural development of the cortex. This is particularly important considering that hypofunction in these systems is a characteristic feature of neurodevelopmental disorders involving mental retardation, such as Rett and Down syndrome.
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