Afferent and efferent connections of the striate and extrastriate visual cortex of the normal and reeler mouse

Abstract

In order to analyze the role of lamination in establishing the precisely ordered connectional pattern of the neocortex, we compared the afferent and efferent connections of the visual cortical areas in normal mice with those of the mutant mouse reeler (rl). The reeler mutation causes disruption of the laminar organization of the neocortex; all classes of neurons are present but are abnormally located. The corticocortical and thalamocortical connection os visual cortical areas 17, 18a, and 18b were determined in normal and reeler mice with injections of horseradish peroxidase (HRP) or HRP conjugated with wheat germ agglutinin (HRP-WGA). The diffusion of HRP-WGA is highly restricted due to the surface binding properties of the lectin; it was particularly effective in demonstrating retinotopically ordered connections. We found that the patterns of connections made the reeler mutant are indistinguishable from normal. Cortical loci in area 17 are reciprocally connected to homotopic locations in areas 18a and 18b. Area 17 is also reciprocally connected with dorsal lateral geniculate nucleus of the thalamus and projects to the superior colliculus. Areas 18a and 18b are reciprocally connected with each other and with the lateral posterior and lateral nuclei of the thalamus, respectively. In addition, we found evidence of reciprocal connections between the lateral posterior nucleus and area 17, and between the lateral nucleus and areas 17 and 18a. The results indicate the neurons in visual cortical areas of the reeler mutant mouse are capable of forming retinotopically organized corticocortical and thalamocortical connections in a pattern similar to that found in normal animals. Thus the genetic anomaly producing incorrect neuronal positioning during development of the reeler cortex does not seriously impede the pathway and target recognition mechanisms responsible for formation of functionally appropriate cortical connections.

Subcortical projections from ectopic neocortical neurons.

“…The present finding that ectopic neocortical neurons project to the spinal cord supports the conclusion based on observations of the neocortex of the reeler mutant mouse that neither a given migratory path nor a specific adult position is essential in establishing a particular subcortical projection (9,10,30,31). The present study extends this conclusion by demonstrating that the initial projection of corticospinal neurons is determined very early in their individual ontogeny, indeed, prior to migration.…”

Misplacement of Purkinje Cells during Postnatal Development in Bax Knock-Out Mice: A Novel Role for Programmed Cell Death in the Nervous System?

“…Similarly, migration defects of cortical neurons induced by ultrasonic exposure in embryonic rats does not result in marked PCD, and most of the misplaced neurons survive until adulthood in ectopic positions (Ang et al, 2006). Therefore, although a subset of misplaced neurons are eliminated by PCD, some misplaced neurons appear to adapt to their new environment, develop an appropriate neuronal phenotype (McConnell, 1995), and establish proper target connections (Caviness and Yorke, 1976;Simmons et al, 1982). Considering that target-derived neurotrophic signals are essential for the survival of neurons after forming provisional synaptic connections, it is possible, as first suggested by Jacobson (1991), that ectopically located neurons may be at a competitive disadvantage in this regard, resulting in an increased, but not inevitable, likelihood of PCD dependent on whether they establish appropriate efferent and afferent synaptic connections.…”

Cellular mechanisms of visual cortical plasticity: a game of cat and mouse.

“…Retinal ganglion cell axons representing this region project to eye-specific areas within the dorsal lateral geniculate nucleus (LGN) (M~tin et al 1983;Godement et al 1984). These geniculate cells project in turn to the lateral one-third of primary visual cortex, called the binocular zone (Dr~iger 1974(Dr~iger , 1975(Dr~iger , 1978Caviness 1975;Wagor et al 1980;Simmons et al 1982). Within this zone, nearly all neurons respond to stimuli presented to either eye, although contralateral eye inputs tend to drive most cells more strongly than do ipsilateral inputs ( Fig.…”