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At least 685 records · Page 38Linked to original sources
PubMed1987

Neurons of the ventral lateral geniculate nucleus of the hereditary microphthalmic rat: a Golgi study.

Neurons of the lateral part of the ventral lateral geniculate nucleus in the microphthalmic rat were examined by the Golgi-Cox method. These neurons were divided into the same three types as normal neurons. However, the number of branches and the length of primary dendrites of these neurons were fewer and shorter, and the size of their perikarya was smaller, compared with normal cases.

Animals↗
PubMed1987

Uncrossed retinal projection to the medial terminal nucleus of the accessory optic system in the hereditary unilaterally microphthalmic rat.

The uncrossed optic projection to the medial terminal nucleus of the accessory optic system was studied in adult rats with hereditary unilateral microphthalmia. The vestigial eye of the mutant completely lacks the optic nerve. After injection of HRP into the remaining eye the ipsilateral labeled fibers of the accessory optic system via the superior fasciculus distinctly covered the three terminal nuclei. No ipsilateral inferior fasciculus of the accessory optic system was labeled. Aberrant expansion of the uncrossed superior fasciculus fibers was observed in the medial terminal nucleus.

Animals↗
PubMed1988

Little or no induction of hyperglycemia by 2-deoxy-D-glucose in hereditary blind microphthalmic rats.

Studies were made on whether hereditary microphthalmic rats (1), which are congenitally blind, showed a hyperglycemic response to intracerebroventricular injection of 2-deoxy-D-glucose (2DG) in their subjective light period. In contrast to previous findings in normal rats in which 2DG injection caused light-cycle dependent hyperglycemia (2) and bilateral lesion of the suprachiasmatic nucleus (SCN) completely abolished this hyperglycemia (3), 2DG injection caused no and only slight hyperglycemia in male and female rats with hereditary microphthalmia, respectively. Gross and histological examinations indicated that these rats had no optic nerve or retinohypothalamic tract and that their SCN had an abnormal structure. Locomotive activity recordings showed that all the blind rats had a free-running circadian activity rhythm. These findings suggest that the projection sites of the retinohypothalamic tract to the SCN are involved in the mechanism of the hyperglycemic response to 2DG, but that neural cells, which may be responsible for the generation of circadian rhythms, are not. We have reported that when adult rats were blinded by orbital enucleation, their hyperglycemic response to 2DG was suppressed temporarily 3-5 weeks after the operation, but that their plasma insulin level was basically higher and increased further after 2DG injection during this period (4). In congenitally blind rats, however, the basal plasma insulin level was not higher and the level did not change after 2DG treatment. This difference is discussed from the view point of the role of the premature SCN in regulation of the plasma insulin concentration.

Animals↗
PubMedDate not supplied

Persistent hyperplastic primary vitreous. A clinicopathologic study of 62 cases and review of the literature.

This is a clinicopathologic study of 62 cases of persistent hyperplastic primary vitreous (PHPV). The cases were divided into two main groups. Group 1 consisted of 55 unilateral cases not associated with any systemic abnormalities, including 36 eyes (58%) which were considered "pure cases" (Group 1A) and 19 (31%) which disclosed other ocular abnormalities in addition to PHPV (Group 1B). Group 2 consisted of 7 (11%) bilateral cases of PHPV accompanied by other ocular and systemic malformations. The most common presenting clinical signs are leukocoria, microphthalmia and cataract. The main histopathologic features of this condition are outlined, including those responsible for the disastrous results to the eye (retinal detachment, glaucoma, phthisis bulbi). Several clinical entities, usually mistaken for or associated with PHPV, such as retinoblastoma, congenital cataract, retinal dysplasia, trisomy 13 syndrome, and falciform retinal folds are discussed briefly.

Adolescent↗
PubMed1993

Mutations at the mouse microphthalmia locus are associated with defects in a gene encoding a novel basic-helix-loop-helix-zipper protein.

Mice with mutations at the microphthalmia (mi) locus have some or all of the following defects: loss of pigmentation, reduced eye size, failure of secondary bone resorption, reduced numbers of mast cells, and early onset of deafness. Using a transgenic insertional mutation at this locus, we have identified a gene whose expression is disrupted in transgenic animals. This gene encodes a novel member of the basic-helix-loop-helix-leucine zipper (bHLH-ZIP) protein family of transcription factors, is altered in mice carrying two independent mi alleles (mi and miws), and is expressed in the developing eye, ear, and skin, all anatomical sites affected by mi. The multiple spontaneous and induced mutations available at mi provide a unique biological resource for studying the role of a bHLH-ZIP protein in mammalian development.

Alleles↗
PubMed1985

Quantitative morphological changes in the superior colliculus and the parabigeminal nucleus in the bilaterally microphthalmic rat.

Quantitative morphological changes in the superior colliculus (SC) and the parabigeminal nucleus (PB) were studied in hereditary bilaterally microphthalmic rat, which lacks the optic nerve completely. Volumes of the retinorecipient superficial collicular layers of SC (SCS) to the central gray matter were decreased by 35% with respect to the normal. However, the cell density in SCS was increased as much as 150% of the normal. The stratum griseum superficiale was packed densely and irregularly with small-sized round nerve cells. The stratum opticum of the mutant rat appeared as a narrow band with few fiber components, but it contained some medium-sized polygonal neurons. No significant changes were found in the deeper layers of the microphthalmic SC. Bilaterally microphthalmic PB reduced both its volume and cellular density per unit area (about 30 and 75% of the normal, respectively). Furthermore, in contrast to the normal rat, the mutant PB could not be subdivided into the dorsal, middle and ventral subgroups.

Animals↗
PubMed1987

Organization of the dorsal lateral geniculate nucleus in a cat with congenital microphthalmia.

The effects of congenital monocular microphthalmia on the development of the lateral geniculate nucleus were examined in a 10-week-old cat. The left eye and optic nerve in this animal appear normal. The right eye is about 30% smaller in volume than the left and the optic nerve from this eye has a cross-sectional area that is only 15% that of the left. In addition, this nerve contains few, if any, large myelinated axons. Both lateral geniculate nuclei are abnormal and the abnormality differs rostrally and caudally. The caudal portion most closely resembles the normal nucleus. Retinal input from both eyes is segregated into cellular laminae that are separated from each other by cell sparse interlaminar zones. However, the input from the microphthalmic eye seems to be sparse and patchy and it does not support normal cell growth. All neurons, including glutamic acid decarboxylase-positive (GAD+) neurons, in laminae innervated by the small eye are reduced in size in a pattern similar to that seen following the removal of retinal input. In comparison, the rostral portion of the nucleus receives very little input from the microphthalmic eye. Instead the normal eye densely innervates nearly the entire nucleus. In this region, interlaminar zones fail to form but the input from the normal eye is able to support cell growth including the growth of GAD+ neurons.

Animals↗
PubMed1983

Optokinetic and spontaneous nystagmus in children with neurological disorders.

Binocular and monocular optokinetic nystagmus (OKN) was examined with EOG recordings in 26 visually impaired children with neurological disorders, aged 2.5 months to 15 years. Spontaneous and/or latent nystagmus, complicating the assessment of OKN, was seen in 73% of the children. Binocular OKN in 21 patients with positive visual functions was symmetrical in 5 cases, asymmetrical in 12 cases and could not be elicited in 4 patients. Monocular OKN was nearly always asymmetrical, with usually a superiority of the temporal-to-nasal (TN) components. Five blind children, 4 of them cortically blind, showed positive binocular and monocular OKN, suggesting that neural control of OKN in humans may be at least partly independent of the cortex. This, together with results from some of the sighted patients, indicates that in humans, cortical and subcortical contributions to OKN, and particularly to monocular nasal-to-temporal (NT) OKN, may be more complicated than had been thought.

Adolescent↗
PubMed1986

Neurons of the dorsal lateral geniculate nucleus of the hereditary microphthalmic rat: a Golgi study.

Neurons of the dorsal lateral geniculate nucleus (LGNd) in the microphthalmic rat were examined by the Golgi-Cox method. LGNd neurons in the microphthalmic rat were classified into the multipolar (I) and bipolar (II) types as in the normal rat. The multipolar type was further divided into two subclasses (Ia and Ib) on the basis of their dendritic patterns. The proximal portion of their primary dendrites was thinner than in normal LGNd neurons. The Ia cells had 6-7 primary dendrites extending radially, while the Ib cells had 3-4 primary dendrites spreading primarily parallel to the optic tract. Type II cells had two or three primary dendrites emerging from the cell bodies. In both types, primary dendrites were shorter in length or less branched than usual. These results suggested that LGNd neurons in the microphthalmic rat had smaller dendritic fields than those in the normal rat.

Animals↗
PubMed1987

Uncrossed retino-geniculate and retino-tectal projections in the hereditary unilaterally microphthalmic rats.

The dorsal lateral geniculate nucleus (CGLd) of the hereditary unilaterally microphthalmic rats showed a diminution of volume and an increase of neuronal density on the contralateral side of the vestigial eye without the optic nerve (about 60 and 160% of the normal, respectively; P less than 0.001). No significant changes were observed in the ipsilateral CGLd. Uncrossed retino-CGLd and -tectal projections were studied using the anterograde axonal transport of HRP in adult rats with the congenital unilateral microphthalmia. Aberrant expansions of the uncrossed retinal projection widely covered CGLd and the superficial layers of the superior colliculus (SCS). The distribution pattern of expanded uncrossed retinal pathway in the mutant was essentially similar to that of neonatally one-eyed rats.

Animals↗
PubMed1990

Bone surface structure in osteopetrotic grey lethal (gl/gl) and microphthalmic (mi/mi) mutant mice as revealed by scanning electron microscopy.

The surface structure of bone from two genetically distinct osteopetrotic strains of mice, grey lethal (gl) and microphthalmic (mi) has been examined by scanning electron microscopy. Although both conditions produce a classical osteopetrotic phenotype the means by which this is achieved is quite different. gl mice appear to retain woven bone and show no evidence of resorption: mi mice show evidence of imperfect remodelling. These results are in accordance with what is already known of osteoclast structure and function in these mutations.

Animals↗
PubMed1993

Reduced increase in plasma renin activity on water-deprivation in blind hereditary microphthalmic rats.

We compared the plasma renin activity (PRA) before and after 24-h water-deprivation in blind hereditary microphthalmic rats and Donryu rats. In the congenitally blind rats with a morphologically abnormal suprachiasmatic nucleus (SCN), hypovolemia induced significantly less elevation of the PRA and significantly more increase in the hematocrit value than in normal rats. The changes after water-deprivation in the blind rats were quite similar to those reported in rats with SCN lesions. However, the free-running circadian rhythms persisted in these blind rats, whereas those in rats with SCN lesions were completely eliminated. Thus, it is likely that SCN cells are involved in regulation of the PRA, and that if this is the case these cells are different from those containing the circadian pacemaker.

Animals↗
PubMed1994

Dysgenesis of melanocytes and cochlear dysfunction in mutant microphthalmia (mi) mice.

In order to evaluate the cytological homology of intermediate cells and melanocytes, and to investigate the function of melanocytes in the inner ear, hearing acuity and cochlear pathology were studied in three strains of mice, namely, wild type mice (+/+), albino mice without melanin (c2J/c2J), and microphthalmia mice with no melanocytes (mibw/mibw). Our histochemical data indicated that intermediate cells showed cytological characteristics almost identical to those of melanocytes and that disorders of melanin and/or melanocytes were reflected in the stria vascularis of each mouse. While c2J/c2J presented the same normal hearing acuity and normal structure of the stria vascularis as +/+, the hearing acuity of mibw/mibw mutants was severely impaired. Their stria vascularis was abnormally thin, lacking intermediate cells. According to these results, lack of melanin has little influence on hearing acuity; however, the absence of intermediate cells or melanocytes causes severe hearing loss, presumably due to a strial dysfunction.

Animals↗