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Toshio Terashima - One of the best experts on this subject based on the ideXlab platform.
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Postnatal Development of the Corticospinal Tract in the Reeler Mouse.
The Kobe journal of medical sciences, 2015Co-Authors: Tomohiro Namikawa, Satoshi Kikkawa, Go Inokuchi, Toshio TerashimaAbstract:Corticospinal tract (CST) neurons are dislocated in the motor cortex of Reelin-deficient Mouse, Reeler. In the present study, we examined whether postnatal axonal growth arising from these dislocated CST neurons are normal or not with use of anterograde tracer, DiI and retrograde tracer, HRP. A single injection of DiI into the motor cortex of the normal and Reeler mice was made during postnatal period and 8-24 hours later, the animals were sacrificed to examine DiI-labeled CST axons at the lower medulla and spinal cord. Both in the normal and Reeler mice, CST axons arrived at the pyramidal decussation and entered into the contralateral spinal cord around on postnatal day (P) 0.5, and descend in the ventral area of the contralateral dorsal funiculus at C2 level on P2, at C8 level on P3, at the mid-thoracic level on P4, and at the upper lumbar level on P8. The similar results were also demonstrated by the retrograde labeling of CST neurons with injection of HRP into the C1 level or upper lumbar enlargement. Next, we examined CaMKIIα expression in the CST axons of the adult normal and Reeler mice. CaMKIIα-immunopositive fibers were recognized throughout the CST pathway from the internal capsule to the dorsal funiculus of the spinal cord both in the normal and Reeler mice. The present study has demonstrated that ectopic location of cell bodies of Reeler CST neurons do not affect postnatal development of CST axons in the spinal cord.
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Subcortically and callosally projecting neurons are distinct neuronal pools in the motor cortex of the Reeler Mouse.
The Kobe journal of medical sciences, 2012Co-Authors: Hideaki Imai, Satoshi Kikkawa, Yu Katsuyama, Tatsuro Yamamoto, Toshio TerashimaAbstract:Subcortically projecting neurons and callosally projecting ones are distinct neuronal pools in the cerebral cortex of the rodents. However, cortical efferent neurons are known to project multiple targets transiently by plural collateral axons. These plural axons are eliminated during prenatal and postnatal development. In the cerebral cortex of the Reelin-deficient Mouse, Reeler, which is caused by mutation of the reelin gene, cortical efferent neurons are ectopically distributed. However, it is still unknown whether cortical efferent neurons in the Reeler Mouse lose surplus collateral axons or maintain them during developmental periods. If surplus collaterals of malpositioned cortical neurons are not eliminated, neurons projecting subcortically may project their axons to the contralateral hemisphere. To test this plausible hypothesis, we made double injections of two fluorescent dyes, Fast Blue and Diamidino yellow dihydrochloride into two of three regions, i.e., upper cervical cord, ventral lateral thalamic nucleus, and contralateral motor cortex of the normal and Reeler mice, to label corticospinal, corticothalamic and callosal commissure neurons in the motor cortex, retrogradely. No double labeled neurons were identified in the motor cortex of the normal and Reeler mice, although the distribution patterns of these cortical efferent neurons were completely different between normal and Reeler mice. These findings strongly suggest that collateral elimination of cortical efferent neurons during developing periods are not affected in this mutant Mouse.
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Developmental anatomy of Reeler mutant Mouse.
Development growth & differentiation, 2009Co-Authors: Yu Katsuyama, Toshio TerashimaAbstract:The Reeler Mouse is one of the most famous spontaneously occurring mutants in the research field of neuroscience, and this mutant has been used as a model animal to understand mammalian brain development. The classical observations emphasized that laminar structures of the Reeler brain are highly disrupted. Molecular cloning of Reelin, the gene responsible for Reeler mutant provided insights into biochemistry of Reelin signal, and some models had been proposed to explain the function of Reelin signal in brain development. However, recent reports of Reeler found that non-laminated structures in the central nervous system are also affected by the mutation, making function of Reelin signal more controversial. In this review, we summarized reported morphological and histological abnormalities throughout the central nervous system of the Reeler comparing to those of the normal Mouse. Based on this overview of the Reeler abnormalities, we discuss possible function of Reelin signal in the neuronal migration and other morphological events in Mouse development.
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unusual patch matrix organization in the retrosplenial cortex of the Reeler Mouse and shaking rat kawasaki
Cerebral Cortex, 2008Co-Authors: Toshio Terashima, Noritaka Ichinohe, Adrian Knight, Masaharu Ogawa, Toshio Ohshima, Katsuhiko Mikoshiba, Yoshihiro Yoshihara, Kathleen S RocklandAbstract:The rat granular retrosplenial cortex (GRS) is a simplified cortex, with distinct stratification and, in the uppermost layers, distinct modularity. Thalamic and cortical inputs are segregated by layers and in layer 1 colocalize, respectively, with apical dendritic bundles originating from neurons in layers 2 or 5. To further investigate this organization, we turned to reelin-deficient Reeler Mouse and Shaking rat Kawasaki. We found that the disrupted lamination, evident in Nissl stains in these rodents, is in fact a patch-matrix mosaic of segregated afferents and dendrites. Patches consist of thalamocortical connections, visualized by vesicular glutamate transporter 2 (VGluT2) or AChE. The surrounding matrix consists of corticocortical terminations, visualized by VGluT1 or zinc. Dendrites concentrate in the matrix or patches, depending on whether they are OCAM positive (matrix) or negative (patches). In wild-type rodents and, presumably, mutants, OCAM + structures originate from layer 5 neurons. By double labeling for dendrites (filled by Lucifer yellow in fixed slice) and OCAM immunofluorescence, we ascertained 2 populations in Reeler: dendritic branches either preferred (putative layer 5 neurons) or avoided (putative supragranular neurons) the OCAM + matrix. We conclude that input-target relationships are largely preserved in the mutant GRS and that dendrite-dendrite interactions involving OCAM influence the formation of the mosaic configuration.
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Unusual Patch–Matrix Organization in the Retrosplenial Cortex of the Reeler Mouse and Shaking Rat Kawasaki
Cerebral cortex (New York N.Y. : 1991), 2007Co-Authors: Noritaka Ichinohe, Toshio Terashima, Adrian Knight, Masaharu Ogawa, Toshio Ohshima, Katsuhiko Mikoshiba, Yoshihiro Yoshihara, Kathleen S RocklandAbstract:The rat granular retrosplenial cortex (GRS) is a simplified cortex, with distinct stratification and, in the uppermost layers, distinct modularity. Thalamic and cortical inputs are segregated by layers and in layer 1 colocalize, respectively, with apical dendritic bundles originating from neurons in layers 2 or 5. To further investigate this organization, we turned to reelin-deficient Reeler Mouse and Shaking rat Kawasaki. We found that the disrupted lamination, evident in Nissl stains in these rodents, is in fact a patch-matrix mosaic of segregated afferents and dendrites. Patches consist of thalamocortical connections, visualized by vesicular glutamate transporter 2 (VGluT2) or AChE. The surrounding matrix consists of corticocortical terminations, visualized by VGluT1 or zinc. Dendrites concentrate in the matrix or patches, depending on whether they are OCAM positive (matrix) or negative (patches). In wild-type rodents and, presumably, mutants, OCAM + structures originate from layer 5 neurons. By double labeling for dendrites (filled by Lucifer yellow in fixed slice) and OCAM immunofluorescence, we ascertained 2 populations in Reeler: dendritic branches either preferred (putative layer 5 neurons) or avoided (putative supragranular neurons) the OCAM + matrix. We conclude that input-target relationships are largely preserved in the mutant GRS and that dendrite-dendrite interactions involving OCAM influence the formation of the mosaic configuration.
Katsuhiko Mikoshiba - One of the best experts on this subject based on the ideXlab platform.
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unusual patch matrix organization in the retrosplenial cortex of the Reeler Mouse and shaking rat kawasaki
Cerebral Cortex, 2008Co-Authors: Toshio Terashima, Noritaka Ichinohe, Adrian Knight, Masaharu Ogawa, Toshio Ohshima, Katsuhiko Mikoshiba, Yoshihiro Yoshihara, Kathleen S RocklandAbstract:The rat granular retrosplenial cortex (GRS) is a simplified cortex, with distinct stratification and, in the uppermost layers, distinct modularity. Thalamic and cortical inputs are segregated by layers and in layer 1 colocalize, respectively, with apical dendritic bundles originating from neurons in layers 2 or 5. To further investigate this organization, we turned to reelin-deficient Reeler Mouse and Shaking rat Kawasaki. We found that the disrupted lamination, evident in Nissl stains in these rodents, is in fact a patch-matrix mosaic of segregated afferents and dendrites. Patches consist of thalamocortical connections, visualized by vesicular glutamate transporter 2 (VGluT2) or AChE. The surrounding matrix consists of corticocortical terminations, visualized by VGluT1 or zinc. Dendrites concentrate in the matrix or patches, depending on whether they are OCAM positive (matrix) or negative (patches). In wild-type rodents and, presumably, mutants, OCAM + structures originate from layer 5 neurons. By double labeling for dendrites (filled by Lucifer yellow in fixed slice) and OCAM immunofluorescence, we ascertained 2 populations in Reeler: dendritic branches either preferred (putative layer 5 neurons) or avoided (putative supragranular neurons) the OCAM + matrix. We conclude that input-target relationships are largely preserved in the mutant GRS and that dendrite-dendrite interactions involving OCAM influence the formation of the mosaic configuration.
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Unusual Patch–Matrix Organization in the Retrosplenial Cortex of the Reeler Mouse and Shaking Rat Kawasaki
Cerebral cortex (New York N.Y. : 1991), 2007Co-Authors: Noritaka Ichinohe, Toshio Terashima, Adrian Knight, Masaharu Ogawa, Toshio Ohshima, Katsuhiko Mikoshiba, Yoshihiro Yoshihara, Kathleen S RocklandAbstract:The rat granular retrosplenial cortex (GRS) is a simplified cortex, with distinct stratification and, in the uppermost layers, distinct modularity. Thalamic and cortical inputs are segregated by layers and in layer 1 colocalize, respectively, with apical dendritic bundles originating from neurons in layers 2 or 5. To further investigate this organization, we turned to reelin-deficient Reeler Mouse and Shaking rat Kawasaki. We found that the disrupted lamination, evident in Nissl stains in these rodents, is in fact a patch-matrix mosaic of segregated afferents and dendrites. Patches consist of thalamocortical connections, visualized by vesicular glutamate transporter 2 (VGluT2) or AChE. The surrounding matrix consists of corticocortical terminations, visualized by VGluT1 or zinc. Dendrites concentrate in the matrix or patches, depending on whether they are OCAM positive (matrix) or negative (patches). In wild-type rodents and, presumably, mutants, OCAM + structures originate from layer 5 neurons. By double labeling for dendrites (filled by Lucifer yellow in fixed slice) and OCAM immunofluorescence, we ascertained 2 populations in Reeler: dendritic branches either preferred (putative layer 5 neurons) or avoided (putative supragranular neurons) the OCAM + matrix. We conclude that input-target relationships are largely preserved in the mutant GRS and that dendrite-dendrite interactions involving OCAM influence the formation of the mosaic configuration.
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Callosal commissural neurons of Dab1 deficient mutant Mouse, yotari.
Neuroscience research, 2001Co-Authors: Takeya Aoki, T Setsu, Katsuhiko Mikoshiba, Haruo Okado, Yoshifumi Watanabe, Toshio TerashimaAbstract:The yotari Mouse is an autosomal recessive mutant Mouse, caused by mutation of disabled homolog 1 (Dab1) gene. The mutant Mouse is recognized by unstable gait and tremor and by early deaths around at the time of weaning. The cytoarchitectures of cerebeller and cerebral cortices and hippocampal formation of the yotari Mouse are abnormal. These malformations strikingly resemble those of Reeler Mouse. In the present study we examined the callosal commissural (CC) neurons of yotari, Reeler and normal mice with the injection of recombinant adenovirus into the frontal area 1 (Fr1) to find some possible phenotypes specific for the yotari Mouse. The distribution pattern of CC neurons of the yotari was similar to that of the Reeler: retrogradely labeled CC neurons were seen throughout all depths of the contralateral Fr1. However, the present statistical analysis revealed that the difference of the mean intracortical position of the CC neurons between the yotari and the Reeler is significantly different (Student's t-test), suggesting that the phenotype of the yotari is clearly different from that of the Reeler.
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The disabled 1 gene is disrupted by a replacement with L1 fragment in yotari mice.
Brain research. Molecular brain research, 2000Co-Authors: Toshio Kojima, Kazunori Nakajima, Katsuhiko MikoshibaAbstract:The yotari autosomal recessive mutant Mouse has a phenotype that is almost identical to that of the Reeler Mouse. We reported in our previous study that the yotari Mouse expresses a mutated form of disabled 1 (Dab1) mRNA resulting in no Dab1 protein. In this study, we demonstrate that the yotari mutation is caused by a replacement of gene sequence with a long interspersed nuclear element (L1) fragment. The nucleotides of two complete exons and part of an additional exon of Dab1 were eliminated as well as three introns by this substitution. The substituted L1 fragment contains 962 nucleotides and is highly homologous to the members of the T(F) subfamily of L1. It is truncated at both the 5' and 3' ends and contains two blocks in a head-to-head arrangement. Based on the DNA sequences around the replacement we developed a screening method that enables us to distinguish wild type, yotari, and heterozygous mice. This method should greatly contribute to analyses of the early anatomical and physiological consequences of the yotari mutation.
Sahebarao P. Mahadik - One of the best experts on this subject based on the ideXlab platform.
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increased truncated trkb receptor expression and decreased bdnf trkb signaling in the frontal cortex of Reeler Mouse model of schizophrenia
Schizophrenia Research, 2008Co-Authors: Anilkumar Pillai, Sahebarao P. MahadikAbstract:Abstract Heterozygous Reeler Mouse has been used as an animal model for schizophrenia based on several neuropathological and behavioral abnormalities homologous to schizophrenia. Since some of these abnormalities are primarily associated with altered BDNF signaling we investigated BDNF signaling in the frontal cortex of Reeler mice in order to shed some light on the neuropathology and treatment of schizophrenia. BDNF, TrkB receptor isoforms (full-length and truncated), reelin, GAD67, GAD65, p75NTR, and NRH-2 levels were measured in the frontal cortex samples from Reeler (B6C3Fe a/a-Relnrl/+) and wild-type (WT) mice. BDNF protein levels were significantly higher in Reeler compared to WT. The protein levels of full-length TrkB were not altered in Reeler mice, but both mRNA and protein levels of truncated TrkB were significantly higher. Protein analysis showed that TrkB activity, as indicated by the levels of tyrosine-phosphorylated TrkB, was lower in Reeler mice. We did not find any significant change in the levels of p75NTR and NRH-2, regulatory proteins of TrkB signaling, in the Reeler mice. Furthermore, we found significant reduction in reelin and GAD67 expressions, but not GAD65 expression in Reeler compared to WT mice. In summary, molecular processes associated with defective BDNF signaling in Reeler mice provide new therapeutic targets for neuroprotective pharmacotherapy for schizophrenia.
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Increased truncated TrkB receptor expression and decreased BDNF/TrkB signaling in the frontal cortex of Reeler Mouse model of schizophrenia☆
Schizophrenia Research, 2008Co-Authors: Anilkumar Pillai, Sahebarao P. MahadikAbstract:Abstract Heterozygous Reeler Mouse has been used as an animal model for schizophrenia based on several neuropathological and behavioral abnormalities homologous to schizophrenia. Since some of these abnormalities are primarily associated with altered BDNF signaling we investigated BDNF signaling in the frontal cortex of Reeler mice in order to shed some light on the neuropathology and treatment of schizophrenia. BDNF, TrkB receptor isoforms (full-length and truncated), reelin, GAD67, GAD65, p75NTR, and NRH-2 levels were measured in the frontal cortex samples from Reeler (B6C3Fe a/a-Relnrl/+) and wild-type (WT) mice. BDNF protein levels were significantly higher in Reeler compared to WT. The protein levels of full-length TrkB were not altered in Reeler mice, but both mRNA and protein levels of truncated TrkB were significantly higher. Protein analysis showed that TrkB activity, as indicated by the levels of tyrosine-phosphorylated TrkB, was lower in Reeler mice. We did not find any significant change in the levels of p75NTR and NRH-2, regulatory proteins of TrkB signaling, in the Reeler mice. Furthermore, we found significant reduction in reelin and GAD67 expressions, but not GAD65 expression in Reeler compared to WT mice. In summary, molecular processes associated with defective BDNF signaling in Reeler mice provide new therapeutic targets for neuroprotective pharmacotherapy for schizophrenia.
Noritaka Ichinohe - One of the best experts on this subject based on the ideXlab platform.
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unusual patch matrix organization in the retrosplenial cortex of the Reeler Mouse and shaking rat kawasaki
Cerebral Cortex, 2008Co-Authors: Toshio Terashima, Noritaka Ichinohe, Adrian Knight, Masaharu Ogawa, Toshio Ohshima, Katsuhiko Mikoshiba, Yoshihiro Yoshihara, Kathleen S RocklandAbstract:The rat granular retrosplenial cortex (GRS) is a simplified cortex, with distinct stratification and, in the uppermost layers, distinct modularity. Thalamic and cortical inputs are segregated by layers and in layer 1 colocalize, respectively, with apical dendritic bundles originating from neurons in layers 2 or 5. To further investigate this organization, we turned to reelin-deficient Reeler Mouse and Shaking rat Kawasaki. We found that the disrupted lamination, evident in Nissl stains in these rodents, is in fact a patch-matrix mosaic of segregated afferents and dendrites. Patches consist of thalamocortical connections, visualized by vesicular glutamate transporter 2 (VGluT2) or AChE. The surrounding matrix consists of corticocortical terminations, visualized by VGluT1 or zinc. Dendrites concentrate in the matrix or patches, depending on whether they are OCAM positive (matrix) or negative (patches). In wild-type rodents and, presumably, mutants, OCAM + structures originate from layer 5 neurons. By double labeling for dendrites (filled by Lucifer yellow in fixed slice) and OCAM immunofluorescence, we ascertained 2 populations in Reeler: dendritic branches either preferred (putative layer 5 neurons) or avoided (putative supragranular neurons) the OCAM + matrix. We conclude that input-target relationships are largely preserved in the mutant GRS and that dendrite-dendrite interactions involving OCAM influence the formation of the mosaic configuration.
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Unusual Patch–Matrix Organization in the Retrosplenial Cortex of the Reeler Mouse and Shaking Rat Kawasaki
Cerebral cortex (New York N.Y. : 1991), 2007Co-Authors: Noritaka Ichinohe, Toshio Terashima, Adrian Knight, Masaharu Ogawa, Toshio Ohshima, Katsuhiko Mikoshiba, Yoshihiro Yoshihara, Kathleen S RocklandAbstract:The rat granular retrosplenial cortex (GRS) is a simplified cortex, with distinct stratification and, in the uppermost layers, distinct modularity. Thalamic and cortical inputs are segregated by layers and in layer 1 colocalize, respectively, with apical dendritic bundles originating from neurons in layers 2 or 5. To further investigate this organization, we turned to reelin-deficient Reeler Mouse and Shaking rat Kawasaki. We found that the disrupted lamination, evident in Nissl stains in these rodents, is in fact a patch-matrix mosaic of segregated afferents and dendrites. Patches consist of thalamocortical connections, visualized by vesicular glutamate transporter 2 (VGluT2) or AChE. The surrounding matrix consists of corticocortical terminations, visualized by VGluT1 or zinc. Dendrites concentrate in the matrix or patches, depending on whether they are OCAM positive (matrix) or negative (patches). In wild-type rodents and, presumably, mutants, OCAM + structures originate from layer 5 neurons. By double labeling for dendrites (filled by Lucifer yellow in fixed slice) and OCAM immunofluorescence, we ascertained 2 populations in Reeler: dendritic branches either preferred (putative layer 5 neurons) or avoided (putative supragranular neurons) the OCAM + matrix. We conclude that input-target relationships are largely preserved in the mutant GRS and that dendrite-dendrite interactions involving OCAM influence the formation of the mosaic configuration.
Kathleen S Rockland - One of the best experts on this subject based on the ideXlab platform.
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unusual patch matrix organization in the retrosplenial cortex of the Reeler Mouse and shaking rat kawasaki
Cerebral Cortex, 2008Co-Authors: Toshio Terashima, Noritaka Ichinohe, Adrian Knight, Masaharu Ogawa, Toshio Ohshima, Katsuhiko Mikoshiba, Yoshihiro Yoshihara, Kathleen S RocklandAbstract:The rat granular retrosplenial cortex (GRS) is a simplified cortex, with distinct stratification and, in the uppermost layers, distinct modularity. Thalamic and cortical inputs are segregated by layers and in layer 1 colocalize, respectively, with apical dendritic bundles originating from neurons in layers 2 or 5. To further investigate this organization, we turned to reelin-deficient Reeler Mouse and Shaking rat Kawasaki. We found that the disrupted lamination, evident in Nissl stains in these rodents, is in fact a patch-matrix mosaic of segregated afferents and dendrites. Patches consist of thalamocortical connections, visualized by vesicular glutamate transporter 2 (VGluT2) or AChE. The surrounding matrix consists of corticocortical terminations, visualized by VGluT1 or zinc. Dendrites concentrate in the matrix or patches, depending on whether they are OCAM positive (matrix) or negative (patches). In wild-type rodents and, presumably, mutants, OCAM + structures originate from layer 5 neurons. By double labeling for dendrites (filled by Lucifer yellow in fixed slice) and OCAM immunofluorescence, we ascertained 2 populations in Reeler: dendritic branches either preferred (putative layer 5 neurons) or avoided (putative supragranular neurons) the OCAM + matrix. We conclude that input-target relationships are largely preserved in the mutant GRS and that dendrite-dendrite interactions involving OCAM influence the formation of the mosaic configuration.
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Unusual Patch–Matrix Organization in the Retrosplenial Cortex of the Reeler Mouse and Shaking Rat Kawasaki
Cerebral cortex (New York N.Y. : 1991), 2007Co-Authors: Noritaka Ichinohe, Toshio Terashima, Adrian Knight, Masaharu Ogawa, Toshio Ohshima, Katsuhiko Mikoshiba, Yoshihiro Yoshihara, Kathleen S RocklandAbstract:The rat granular retrosplenial cortex (GRS) is a simplified cortex, with distinct stratification and, in the uppermost layers, distinct modularity. Thalamic and cortical inputs are segregated by layers and in layer 1 colocalize, respectively, with apical dendritic bundles originating from neurons in layers 2 or 5. To further investigate this organization, we turned to reelin-deficient Reeler Mouse and Shaking rat Kawasaki. We found that the disrupted lamination, evident in Nissl stains in these rodents, is in fact a patch-matrix mosaic of segregated afferents and dendrites. Patches consist of thalamocortical connections, visualized by vesicular glutamate transporter 2 (VGluT2) or AChE. The surrounding matrix consists of corticocortical terminations, visualized by VGluT1 or zinc. Dendrites concentrate in the matrix or patches, depending on whether they are OCAM positive (matrix) or negative (patches). In wild-type rodents and, presumably, mutants, OCAM + structures originate from layer 5 neurons. By double labeling for dendrites (filled by Lucifer yellow in fixed slice) and OCAM immunofluorescence, we ascertained 2 populations in Reeler: dendritic branches either preferred (putative layer 5 neurons) or avoided (putative supragranular neurons) the OCAM + matrix. We conclude that input-target relationships are largely preserved in the mutant GRS and that dendrite-dendrite interactions involving OCAM influence the formation of the mosaic configuration.