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G Horsburgh

Publications and source records attributed to G Horsburgh.

5 recordsLinked to original sources
PubMed1991

The effects of bilateral enucleation in the primate fetus on the parcellation of visual cortex.

Bilateral enucleation in the macaque fetus causes an areal reduction of an otherwise normal striate cortex. Here we show that in early operated animals this reduction is accompanied by a separation of striate and prostriate cortices which are normally contiguous. However this induced separation does not correspond to the areal reduction of striate cortex, indicating that extrinsic signals regulate either the proliferation and/or survival of striate cortical neurons.

Animals↗
PubMed1989

Maturation and connectivity of the visual cortex in monkey is altered by prenatal removal of retinal input.

In several species, the peripheral input from the eyes partly determines the pattern of interconnections between the visual areas of the two cerebral hemispheres through the fibre tract termed the corpus callosum. In the macaque monkey, the neurons projecting through the callosum are largely restricted to area 18 throughout ontogeny, whereas area 17 is characterized by few or no callosal projections. Here, we show that suppressing the peripheral input by prenatal removal of the eyes leads to a marked reduction in the extent of area 17, resulting in a large shift in the position of the histologically identifiable boundary between the two areas. Even so, the boundary continues to separate an area rich with callosal connections (area 18) from one poor in such projections (area 17), indicating there is no effect on the callosal connectivity of area 17. In contrast, in area 18, eye removal results in many more neurons with callosal projections than in normal animals. The results suggest that the factors that determine the parcellation of cortical areas also specify their connectivity.

Animals↗
PubMed1988

Small eye (Sey): a mouse model for the genetic analysis of craniofacial abnormalities.

Small eye (Sey) is a dominant mutation in the mouse affecting the embryonic development of the eyes and nose. In homozygous Sey/Sey embryos, the optic vesicles grow out but there is no lens induction and the nasal pits fail to develop. Scanning electron microscope studies of Sey/Sey embryos show that the maxillary processes develop normally and fuse with ridges of ectoderm in the frontonasal position. In Sey/+ heterozygotes, the vacuolated lens is smaller than normal, and there is folding of the margins of the optic cup and ingrowth of mesodermal cells. Evidence is presented that Sey is not allelic with Coloboma (Cm), another mutation affecting eye development on chromosome 2.

Animals↗
PubMed1986

Small eyes (Sey): a homozygous lethal mutation on chromosome 2 which affects the differentiation of both lens and nasal placodes in the mouse.

Small eyes (Sey) is a semidominant, homozygous lethal mutation in the mouse (Roberts, 1967). It is allelic with SeyH, a radiation-induced homozygous prenatal lethal which has been mapped on chromosome 2. The effect of the Sey mutation is apparently limited to the growth and differentiation of the presumptive lens and nasal placodes. Homozygous Sey/Sey embryos can be distinguished as early as 10.5 days post coitum (p.c.); the optic vesicles grow out, but the ectoderm does not give rise to a lens and nasal pits never form. Immunohistochemical studies show that the distribution of the extracellular matrix glycoprotein laminin is not significantly different in the cephalic region of Sey/Sey versus Sey/+ or +/+ embryos. Sey/Sey embryos develop to term but without eyes or nose, and die soon after birth. Further analysis of Sey/Sey embryos may throw light on the mechanisms underlying morphogenesis of craniofacial structures in mammals.

Animals↗