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note
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All animal care was in accordance with institutional guidelines. A total of 25 fetuses (E56, n = 22; E42, n = 3) were studied from pregnant cats in our breeding colony of known gestational age. Anesthesia, sterile surgical techniques, and minipump implantations were according to (22). After infusion of either 300 μM TTX or vehicle (300 μM sodium citrate buffer) between E42 and E56, the fetuses were delivered by cesarean section and were transcardially perfused (3). Fetuses are always studied as littermate pairs (TTX-treated compared with vehicle-treated) because TTX diffuses throughout the entire forebrain and midbrain bilaterally (9), and therefore it is not possible to compare hemispheres in the same animal.
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Crystals of Dil (D-282, Molecular Probes, Eugene, OR) were placed into either the subplate or cortical plate of visual cortex to label LGN neurons that project there or into the LGN itself to visualize the axonal projection from LGN to cortex. In the same animals, crystals of DiD (D-7757, Molecular Probes) were also placed into the region of auditory cortex to label LGN axons that might extend collaterals into this region on their way back to visual cortex. After 3 months for dye diffusion, brains were sectioned horizontally on a vibratome at 100 μm, and retrogradely labeled LGN neurons were counted. Because the number of retrogradely labeled neurons is directly proportional to the size of the dye injection site, great care was taken to make similar dye injection sizes for each TTX-and vehicle-treated littermate pair (n = 11 matched littermate pairs studied). The variations in total neuron number seen in Fig. 1, C and D, reflect differing size injections, and therefore comparisons can only made between matched littermate pairs.
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Infusion of vehicle did not have an apparent effect on the magnitude of the LGN projection to visual cortex; the number of retrogradely labeled LGN neurons was within 10% (± 2% SEM, n = 3 unmanipulated and 3 vehicle-treated; P < 0.005) of untreated littermate controls matched for similar injection sizes.
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Previous studies have demonstrated that intracranial minipump infusions of TTX produce concentrations that are sufficient to block sodium-dependent action potentials bilaterally throughout the entire forebrain and midbrain at E42 to E56 (22) and result in the failure of retinal ganglion axons to segregate into eye-specific layers in the LGN (17, 23). However, many other aspects of development proceed normally: Cell migration and cell division within the cortex are unimpaired, the brain grows to normal size during the treatment period and its gross histological organization is indistinguishable from normal (23), and the somatic and dendritic development of retinal ganglion cells and LGN neurons is normal [(22); M. Dalva, A. Ghosh, C. J. Shatz, J. Neurosci. 14, 3588 (1994)]. Moreover, the development of cortical pyramidal cell dendrites, radial glial cells, and the overall appearance and thickness of the cortical plate is indistinguishable from normal (12).
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TTX infusions were begun at E42, after large numbers of MGN axons had already invaded the auditory cortical plate [A. Ghosh and C. J. Shatz, Development 117, 1031 (1993)].
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3) in identical cortical locations were analyzed for topographic precision (n = 4 pairs) (Fig. 3). The location of individual labeled LGN neurons with respect to the borders of the LGN was marked on digitized images of sections. The mediolateral distribution of marked neurons within a single section was plotted in 100-μm bin widths (NIH Image version 1.61). This procedure was repeated for every LGN section. The distributions for all sections were added together, and the peak num-ber of retrogradely labeled neurons was determined. Finally, the percentage of total mediolateral width of LGN covered by labeled neurons at half-peak was derived and plotted in Fig. 3B.
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The peak in the number of retrogradely labeled neurons was located near the center of LGN in vehicle-treated animals (within 250 to 300 μm of the center of LGN), consistent with dye placements within the corresponding locations in visual cortex. However, in TTX-treated animals, the peak was located further medially in two cases and further laterally in one case (550 to 350 μm away from the center) than in vehicle-treated control littermates, even though the Dil injections were similarly placed in cortex, suggesting that there is more variability in the overall topography of the geniculocortical projection after TTX treatment.
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The normal increase between E42 and E56 in the number of LGN neurons projecting to visual cortex, as determined by retrograde labeling with Dil injections, is about 30-fold (n = 3 untreated animals at E42 and 3 vehicle-treated animals at E56).
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It is conceivable that TTX somehow disrupts cortical differentiation, which in turn affects LGN axon targeting and ingrowth. Although this disruption is possible, we note that many aspects of cortical development can proceed normally after similar TTX treatments; see (9).
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note
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We thank A. Raymond and D. Escontrias for help with the fetal surgeries. Supported by NIH grant EY02838 (C.J.S.) and National Research Service Award EY06491 (S.M.C.). S.M.C. is an Associate and C.J.S. is an Investigator of the Howard Hughes Medical Institute.
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