Mouse Netrin-G1a Antibody

Detection of Mouse Netrin-G1a by Immunohistochemistry Transient expression of Cyp26b1 in the PFC does not occur in the absence of thalamus–cortex interactions in Gbx2 mutant mice. A–F, Thalamus–PFC disconnection in Gbx2 mutant mice. A, B, Immunostaining for NetrinG1 at E16.5. In control mice, NetrinG1-labeled thalamocortical axons are visible in coronal sections of frontal cortex. Arrowhead in A shows the medial PFC, where robust labeling is detected. In contrast, NetrinG1 labeling is barely detectable in the frontal cortex of Gbx2 mutant mice, including the medial PFC (B, arrowhead). Scale bar, 200 µm. C–F, DiI labeling at P14. C, D, DiI placement in medial PFC retrogradely labels medial thalamic nuclei in the control brains. E, F, In Gbx2 mutants, the label is severely reduced, indicating the deficiency of both thalamocortical and corticothalamic projections. G–J, Expression of ROR beta and Lmo4 is qualitatively normal in the PFC of Gbx2 mutant mice at P8. G, I, The expression of ROR beta in layer 4 is comparable between control (G) and Gbx2 mutant (cko) mice (I, arrows). H, J, Laminar expression patterns of Lmo4 also appear unchanged in Gbx2 mutants. Scale bar, 1 mm. K–Z, Transient expression of Cyp26b1 in the PFC does not occur in the absence of thalamus–cortex interactions in Gbx2 mutant mice. K–T, in situ hybridization of frontal sections through PFC at various postnatal stages with a Cyp26b1 probe. K–O, In control mice (K–O), Cyp26b1 expression starts at P2 in medial (K, arrowhead) and ventral (K, single arrow) PFC, and continues until P14 (M). N, O, At P21, expression in medial PFC is reduced (N) and is no longer detectable at P35 (O). K–O, In addition to medial and ventral PFC, Cyp26b1 is also expressed in lateral frontal cortex, including the motor and somatosensory areas (double arrows) and agranular insula (double arrowheads). P–T, In Gbx2 mutant mice, the expression of Cyp26b1 is not induced in medial or ventral PFC at P2 as well as at later stages, although ventral PFC does not appear to be affected at P14 and later. P–T, Expression in more superficial layer of lateral cortex (double arrows and double arrowheads) is not affected in Gbx2 mutant mice. U, X, Expression of the layer 6 marker Syt6 is not affected in Gbx2 mutant mice. V, Y, Expression of Aldh1a3 in layer 2 of medial PFC and anterior cingulate cortex (arrow) is not affected in Gbx2 mutant mice. Scale bar, 1 mm. W, Z, Summary schematic for this figure. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/30868103), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse Netrin-G1a by Immunocytochemistry/ Immunofluorescence Normal induction of Cyp26b1 in PFC in mice expressing tetanus toxin light chain in thalamocortical axons. A–D, Immunostaining for VAMP2 on frontal sections of somatosensory cortex at E16.5 control (A, B) and mutant mice with ectopic expression of TeNT in thalamic neurons (C, D). TeNT expression leads to the deletion of VAMP2, specifically in thalamocortical axons at E16.5. Thalamocortical axons are shown by NetrinG1 staining (B, D, green). In control brains, both thalamocortical (bracket, A–D) and corticofugal (asterisk, A–D) axons express VAMP2, whereas in TeNT-expressing mice, VAMP2 staining is specifically diminished in thalamocortical axons (C, D, bracket). Scale bar, 500 μm. E, F, Deletion of VAMP2 in thalamocortical axons results in the lack of the characteristic pattern of ROR beta expression in the barrel field of primary somatosensory cortex at P8 (arrow), similar to the defect found in Gbx2 mutant mice (Vue et al., 2013). G–J, Immunostaining for VAMP2 on frontal sections of prefrontal cortex at P0 control (G, H) and mutant mice with ectopic expression of TeNT in thalamic neurons (I, J). Similar to the somatosensory cortex, VAMP2 staining in thalamocortical axons is diminished in TeNT-expressing mice (I, J, bracket). Scale bar, 200 μm. K, L, Expression of Cyp26b1 in medial (arrowhead) and ventral PFC is intact in TeNT-expressing mice (L), similar to control (K), at P8. Scale bars: G, H, I, J, 200 μm; E, F, K, L, 1 mm. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/30868103), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse Netrin-G1a by Immunohistochemistry Transient expression of Cyp26b1 in the PFC does not occur in the absence of thalamus–cortex interactions in Gbx2 mutant mice. A–F, Thalamus–PFC disconnection in Gbx2 mutant mice. A, B, Immunostaining for NetrinG1 at E16.5. In control mice, NetrinG1-labeled thalamocortical axons are visible in coronal sections of frontal cortex. Arrowhead in A shows the medial PFC, where robust labeling is detected. In contrast, NetrinG1 labeling is barely detectable in the frontal cortex of Gbx2 mutant mice, including the medial PFC (B, arrowhead). Scale bar, 200 µm. C–F, DiI labeling at P14. C, D, DiI placement in medial PFC retrogradely labels medial thalamic nuclei in the control brains. E, F, In Gbx2 mutants, the label is severely reduced, indicating the deficiency of both thalamocortical and corticothalamic projections. G–J, Expression of ROR beta and Lmo4 is qualitatively normal in the PFC of Gbx2 mutant mice at P8. G, I, The expression of ROR beta in layer 4 is comparable between control (G) and Gbx2 mutant (cko) mice (I, arrows). H, J, Laminar expression patterns of Lmo4 also appear unchanged in Gbx2 mutants. Scale bar, 1 mm. K–Z, Transient expression of Cyp26b1 in the PFC does not occur in the absence of thalamus–cortex interactions in Gbx2 mutant mice. K–T, in situ hybridization of frontal sections through PFC at various postnatal stages with a Cyp26b1 probe. K–O, In control mice (K–O), Cyp26b1 expression starts at P2 in medial (K, arrowhead) and ventral (K, single arrow) PFC, and continues until P14 (M). N, O, At P21, expression in medial PFC is reduced (N) and is no longer detectable at P35 (O). K–O, In addition to medial and ventral PFC, Cyp26b1 is also expressed in lateral frontal cortex, including the motor and somatosensory areas (double arrows) and agranular insula (double arrowheads). P–T, In Gbx2 mutant mice, the expression of Cyp26b1 is not induced in medial or ventral PFC at P2 as well as at later stages, although ventral PFC does not appear to be affected at P14 and later. P–T, Expression in more superficial layer of lateral cortex (double arrows and double arrowheads) is not affected in Gbx2 mutant mice. U, X, Expression of the layer 6 marker Syt6 is not affected in Gbx2 mutant mice. V, Y, Expression of Aldh1a3 in layer 2 of medial PFC and anterior cingulate cortex (arrow) is not affected in Gbx2 mutant mice. Scale bar, 1 mm. W, Z, Summary schematic for this figure. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/30868103), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse Netrin-G1a by Immunohistochemistry Transient expression of Cyp26b1 in the PFC does not occur in the absence of thalamus–cortex interactions in Gbx2 mutant mice. A–F, Thalamus–PFC disconnection in Gbx2 mutant mice. A, B, Immunostaining for NetrinG1 at E16.5. In control mice, NetrinG1-labeled thalamocortical axons are visible in coronal sections of frontal cortex. Arrowhead in A shows the medial PFC, where robust labeling is detected. In contrast, NetrinG1 labeling is barely detectable in the frontal cortex of Gbx2 mutant mice, including the medial PFC (B, arrowhead). Scale bar, 200 µm. C–F, DiI labeling at P14. C, D, DiI placement in medial PFC retrogradely labels medial thalamic nuclei in the control brains. E, F, In Gbx2 mutants, the label is severely reduced, indicating the deficiency of both thalamocortical and corticothalamic projections. G–J, Expression of ROR beta and Lmo4 is qualitatively normal in the PFC of Gbx2 mutant mice at P8. G, I, The expression of ROR beta in layer 4 is comparable between control (G) and Gbx2 mutant (cko) mice (I, arrows). H, J, Laminar expression patterns of Lmo4 also appear unchanged in Gbx2 mutants. Scale bar, 1 mm. K–Z, Transient expression of Cyp26b1 in the PFC does not occur in the absence of thalamus–cortex interactions in Gbx2 mutant mice. K–T, in situ hybridization of frontal sections through PFC at various postnatal stages with a Cyp26b1 probe. K–O, In control mice (K–O), Cyp26b1 expression starts at P2 in medial (K, arrowhead) and ventral (K, single arrow) PFC, and continues until P14 (M). N, O, At P21, expression in medial PFC is reduced (N) and is no longer detectable at P35 (O). K–O, In addition to medial and ventral PFC, Cyp26b1 is also expressed in lateral frontal cortex, including the motor and somatosensory areas (double arrows) and agranular insula (double arrowheads). P–T, In Gbx2 mutant mice, the expression of Cyp26b1 is not induced in medial or ventral PFC at P2 as well as at later stages, although ventral PFC does not appear to be affected at P14 and later. P–T, Expression in more superficial layer of lateral cortex (double arrows and double arrowheads) is not affected in Gbx2 mutant mice. U, X, Expression of the layer 6 marker Syt6 is not affected in Gbx2 mutant mice. V, Y, Expression of Aldh1a3 in layer 2 of medial PFC and anterior cingulate cortex (arrow) is not affected in Gbx2 mutant mice. Scale bar, 1 mm. W, Z, Summary schematic for this figure. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/30868103), licensed under a CC-BY license. Not internally tested by R&D Systems.