Journal: The Journal of Neuroscience

Article Title: The Lack of Emx2 Causes Impairment of Reelin Signaling and Defects of Neuronal Migration in the Developing Cerebral Cortex

doi: 10.1523/JNEUROSCI.20-03-01109.2000

Figure Lengend Snippet: Neuron-specific class III β-tubulin andOct6 mRNA in the telencephalon of wild-type andEmx2−/− late gestation embryos.a, b, Distribution of Oct6mRNA in the telencephalon of E16.0 wild-type (a) and Emx2−/− (b) embryos; frontal sections, slightly caudal to the level of the foramen of Monro. Medial is to the right. In both cases, the RNA is in the developing striatum, as well as in the pallium. In the cerebral cortex, the signal is detectable throughout the transitional field. It gives rise to an very intense band in the outer part of this layer, just underneath the subplate (a,b). In the outer lateral cortical plate of the wild-type cortex, an additional thin Oct6 band can be found, possibly corresponding to the first neurons belonging to the prospective layer V, which overcame the subplate and settled at their final radial level (a, white arrowheads). No trace of this additional signal can be detected at corresponding locations in the Emx2−/− brain (b). c–f, Distribution of the neuron-specific class III β-tubulin on middle frontal sections of dorsal telencephalon in wild-type (c) andEmx2−/− (d) embryos, revealed by the monoclonal antibody TuJ1. In eand f, magnifications of boxed areas ofc and d are represented, respectively. In normal embryos, immunoreactivity is detectable throughout the entire width of the cortical wall, except the ventricular and the inner subventricular zones (c, e). InEmx2−/− animals, several scattered TuJ1-positive cells can be found in the ventricular zone, and numerous clustered immunoreactive cells lie around the border between subventicular and intermediate zones (d,f). CP, Cortical plate;HI, hippocampus; IZ, intermediate zone;MZ, marginal zone; SP, subplate;ST, striatum; SVZ, subventricular zone;TF, transitional field; VZ, ventricular zone. Scale bar, 100 μm.

Article Snippet: The following primary antibodies were used: α-BrdU, mouse monoclonal (Becton Dickinson, Mountain View, CA), 1:100; α-calretinin, rabbit polyclonal (Swant), 1:100; α-EMX1, rabbit polyclonal ( Briata et al., 1996 ), 1:400; α-neuron-specific class III β-tubulin, mouse monoclonal (clone TuJ1; BabCo, Richmond, CA), 1:100; α-microtubule-associated protein 2 (MAP2), mouse monoclonal (clone AP20; Boehringer Mannheim, Indianapolis, IN) 1:100; and α-RC2, monoclonal, 1:1 ( Misson et al., 1988 ).

Techniques:

Journal: The Journal of Neuroscience

Article Title: The Lack of Emx2 Causes Impairment of Reelin Signaling and Defects of Neuronal Migration in the Developing Cerebral Cortex

doi: 10.1523/JNEUROSCI.20-03-01109.2000

Figure Lengend Snippet: Radial distribution of RC2 and MAP2 in the neocortex of E16–E16.5 wild-type,Emx2−/−, andReln−/− embryos. a–f, Radial glia in E16.5 wild-type (a),Emx2−/− (b), and Reln−/− (c) embryos, stained by the monoclonal α-RC2 antibody, rostral neocortex, frontal sections. In c, d, ande, there are magnifications of boxedareas in a, b, and c, respectively. In the normal cortex, the thick labeled glial bundles, which ascend from the ventricular toward the marginal zone, undergo a sudden reduction in their size at the level of the subplate (a); in the cortical plate, they are regularly arranged and separated by relatively narrow interspaces (d, arrowheads). InEmx2−/− embryos, thick glial bundles ascend from the ventricular zone and enter the cortical plate; they are separated by wider interspaces (e, arrowheads) and do not undergo any appreciable reduction in width, while crossing the cortical plate (b, e). Similar distribution of RC2 can be seen in Reln−/− mutants (c). In these animals, the glial bundles cross the entire cerebral wall and reach, still thick, the marginal layer commonly termed superplate (c); relatively large interspaces are detectable among them, underneath the superplate (f, arrowheads).g–l, Distribution of neuron-specific MAP2 immunoreactivity on frontal sections through rostral telencephalons of E16.0 wild-type (g),Emx2−/−(h), andReln−/− (i) embryos; inj, k, and l, there are magnifications of the boxed areas of g,h, and i, respectively. In the case of wild-type animals, cortical plate neurons are prevalently fusiform and tightly clustered in a palisade-like structure; the marginal zone, less cellularized, displays intense α-MAP2 immunoreactivity, possibly associated with terminal harborizations of cortical plate neurons apical dendrites (j). InEmx2−/− embryos, the cortical plate neurons appear more rounded and loosely distributed, and the marginal zone is more irregularly shaped (k). All of that is somehow reminiscent of what can be seen in theReln−/− neocortex at the level of the poorly laminated, broad layer replacing cortical plate and transitional field, as well as in the overlying superplate (l). CP, Cortical plate;MZ, marginal zone; SbP, subplate;SpP, superplate; TF, transitional field;VZ, ventricular zone. Scale bar, 100 μm.

Article Snippet: The following primary antibodies were used: α-BrdU, mouse monoclonal (Becton Dickinson, Mountain View, CA), 1:100; α-calretinin, rabbit polyclonal (Swant), 1:100; α-EMX1, rabbit polyclonal ( Briata et al., 1996 ), 1:400; α-neuron-specific class III β-tubulin, mouse monoclonal (clone TuJ1; BabCo, Richmond, CA), 1:100; α-microtubule-associated protein 2 (MAP2), mouse monoclonal (clone AP20; Boehringer Mannheim, Indianapolis, IN) 1:100; and α-RC2, monoclonal, 1:1 ( Misson et al., 1988 ).

Techniques: Staining, Labeling