Elsevier

Experimental Neurology

Volume 40, Issue 2, August 1973, Pages 491-504
Experimental Neurology

Pattern of dendritic branching in occipital cortex of rats reared in complex environments

https://doi.org/10.1016/0014-4886(73)90090-3Get rights and content

Abstract

The branching pattern of dendrites of neurons in occipital cortex was studied in rats reared in complex, social, or isolated environments. In stellate neurons and in small, medium-sized, and giant pyramidal neurons, when branching was analyzed in terms of the intersections between dendrites and concentric rings at 20-μm intervals from the cell body, roughly half of the variance was accounted for by the litter from which the subjects came, the experimental environments (up to 18% of the variance loaded on this factor alone), and their interaction. This analysis also indicated that the increased branching occurred within the same volume as that occupied by less highly arborized neurons in the deprived animals, supporting the notion that a specific “domain” exists for the neuron. When the number and length of segments of dendrites at each bifurcation away from the cell body were examined, the differences in numbers of branches were generally restricted to the basal portion of the pyramidal cell dendritic tree. Animals reared in complex environments tended to have many more basal branches beyond the third and fourth bifurcations. No consistent differences in branch length were seen in either pyramidal or stellate cells. The results suggest that the differences in dendritic branching seen after rearing in complex environments are a function of this complexity, rather than of visual deprivation, and indicate a mechanism whereby the effects of the early environment may be expressed in later behavior.

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      Many of the cardinal studies of EE examined the somatosensory cortices. EE consistently increases dendritic complexity (Greenough and Volkmar, 1973; Jung and Herms, 2012; Diamond et al., 1966; Leggio et al., 2005), synaptic plasticity (Briones et al., 2004; Turner and Greenough, 1985; Diamond et al., 1964), and neurotrophins (Torasdotter et al., 1998) in these areas. Similar effects have been noted in the hypothalamus, where EE increases dendritic complexity (Mitra and Sapolsky, 2012), and cerebellum, where EE increases BDNF (Angelucci et al., 2009).

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    This research was supported by National Institute of Mental Health Grant MH-19135-01, Public Health Service Grant FR-07030, National Science Foundation Grant GY-8744, and the University of Illinois Research Board. We thank J. McV. Hunt for his advice and encouragement and Carol Sue Carter for helpful comments on the manuscript.

    Dr. Volkmar's present address is: Stanford University Medical School, Stanford, CA 94305.

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