Biomedical subjects

R R Sturrock

Publications and source records attributed to R R Sturrock.

At least 37 records · Page 2Linked to original sources

PubMed1990

A comparison of quantitative histological changes in different regions of the ageing mouse cerebellum.

The number of Purkinje cells per mm and the number of granule cells per mm3 were estimated in the lobus simplex of mice aged 6, 15, 22, 25, 28 and 31 months. The results were compared with similar estimations already carried out in the spinocerebellum and nodulus of the same cerebella. All regions showed a decrease of approximately 30% in Purkinje cell number between 6 and 31 months of age with the decrease occurring between 15 and 31 months. At each age examined the number of Purkinje cells per mm was similar in the spino- and pontocerebellum but significantly smaller in the nodulus. Granule cell density was identical in all parts of the cerebellum at all ages. Molecular layer thickness varied significantly with age in all cerebellar regions but this may be an artefactual variation. Granule layer thickness did not vary with age in either the nodulus or spinocerebellum but there was a significant variation in granule layer thickness, in the pontocerebellum due to a substantial decrease in thickness between 28 and 31 months of age. This might be the result of a loss of granule cells in this region which is not apparent in other parts of the cerebellum.

Aging↗

PubMed1990

An electron microscopic study of the leptomeninx and associated cells of the aged mouse.

The ultrastructure of the leptomeninx was examined in mice aged 25, 28 and 31 months. Apart from occasional lipofuscin granules there were no obvious age related changes in the ultrastructure of leptomeningeal cells. Granular pial cells usually contained large honeycomb bodies and were a prominent feature of the ageing leptomeninx but in contrast leptomeningeal macrophages showed no evidence of phagocytic activity suggesting that cell death or degeneration was not a feature of cells of the leptomeninx even in extremely old mice.

Aging↗

PubMed1990

An ultrastructural study of development of the leptomeninx of the rabbit spinal cord.

Development of the rabbit spinal cord leptomeninges was examined in embryos and fetuses aged 12 to 30 d post-conception. In the early stages of development all mesenchymal cells surrounding the neural tube were structurally similar, resembling immature fibroblasts. At 16 d post-conception cells adjacent to the glia limitans showed little structural change, apart from an increase in the amount of rough endoplasmic reticulum, but cells in the presumptive arachnoid became packed with glycogen. By E22 glycogen was present in pial cells but never in the amounts found in the arachnoid. As development proceeded the amount of glycogen in the leptomeninges declined. Pial collagen increased both in amount and in fibre diameter with age.

Animals↗

PubMed1989

Stability of neuron and glial number in the parabigeminal nucleus of the ageing mouse.

The number of neurons and glia in the albino mouse parabigeminal nucleus remains constant between 6 and 31 months of age. The presence of a small number of mitotic and pyknotic cells in the parabigeminal nucleus indicates a slow turnover of the glial population throughout life. Examination of the superior colliculus showed that degenerating neurons were present from 6 months of age and neurons appeared to be much more sparsely scattered in the superficial layers of aged mice than in young adults. The stability of the neuron number in the parabigeminal nucleus may be due to the reciprocal innervation of neurons of the superior colliculi and parabigeminal nuclei protecting each other from transneuronal degeneration which might otherwise occur as a consequence of loss of retinal ganglion cells. Alternatively, since each neuron in the parabigeminal nucleus probably synapses with many tectal neurons, the loss of only some of its target neurons would probably not lead to transneuronal degeneration.

Aging↗

PubMed1989

A quantitative histological study of the anterodorsal thalamic nucleus and the lateral mammillary nucleus of ageing mice.

The number of neurons and neuroglia in the anterodorsal nucleus of the thalamus and in the lateral mammillary nucleus of the ASH/TO strain mouse was estimated at 6, 25, 28 and 31 months of age. There was no significant variation in neuron number in either nucleus with age but there was a statistically significant increase (approximately 20%) in the number of neuroglia in the anterodorsal nucleus between 28 and 31 months of age which raised the glia to neuron ratio from 0.59 to 0.72. There was no change in neuroglial number in the ageing lateral mammillary nucleus. Neurons in both nuclei lost Nissl substance. This was first evident at 28 months in the anterodorsal nucleus and at 31 months in the lateral mammillary nucleus. Lipofuscin accumulation was common in the perikarya of anterodorsal nuclear neurons from 25 months onwards but was very rare in neurons of the lateral mammillary nucleus even at 31 months.

Aging↗

PubMed1989

Loss of neurons from the external cuneate nucleus of the ageing mouse brain.

The number of neurons in the ASH/TO mouse external cuneate nucleus was examined at 6, 15, 22, 25, 28 and 31 months of age. There is a highly significant decrease in the number of neurons between 6 and 31 months of age. Neuron loss begins at 15 months when degenerating neurons are first found in the nucleus and becomes more rapid with increasing age. It is suggested that neuronal loss is due to anterograde transneuronal degeneration following a loss of primary proprioceptive neurons, first from the spinal roots and later from the brainstem.

Aging↗

PubMed1989

Loss of neurons from the intracerebellar nuclei of the ageing mouse.

The intracerebellar nuclei of the ASH/TO mouse brain were examined at 6, 22, 25, 28 and 31 months of age using quantitative histological techniques. Neuron number remained constant between 6 and 22 months of age but there was a statistically significant (P less than 0.01) decrease in neuronal number between 22 and 31 months of age with neuron number declining from 6970 +/- 690 at 22 months to 4140 +/- 246 at 31 months of age. Neuronal nuclear diameter remained constant between 6 and 25 months of age but increased from 10.6 +/- 0.6 microns at 25 months to 12.2 +/- 0.3 microns at 31 months of age. Whether this was due to an actual increase in nuclear diameter or to a proportionately greater loss of small neurons is not known.

Aging↗

PubMed1989

An ultrastructural study of the development of the leptomeninx of the mouse spinal cord.

The ultrastructure of the mouse spinal cord leptomeninx was studied from 11 days post-conception to 5 days post natum. At all ages the cells investing the developing cord resembled immature fibroblasts. The most characteristic feature was the rough endoplasmic reticulum, filled with an amorphous ground substance and frequently branched. At first other cytoplasmic organelles were sparse apart from numerous free ribosomes. During development mitochondria became more numerous. From E11 presumptive leptomeningeal processes were joined by tight junctions and the endothelial cells of leptomeningeal vessels were united by zonulae occludentes. Collagen fibrils were found from E11 and in prenatal mice were of small diameter, although the quantity of collagen increased with age. In the postnatal mice collagen was of larger diameter with the characteristic banded appearance.

Animals↗

PubMed1989

Age related changes in neuron number in the mouse lateral vestibular nucleus.

The number of large neurons in the lateral vestibular nucleus of the mouse brain decreases in number after 25 months of age, from 488 at 25 months to 298 at 31 months. The number of small neurons in the nucleus remains constant up to 31 months of age. Large neurons accumulate lipofuscin from 25 months and their mean nuclear diameter increases significantly between 25 and 28 months of age. Small neurons contain very little lipofuscin even at 31 months of age and their mean nuclear diameter remains constant between 6 and 31 months. The difference in response of the two types of neurons to ageing may be due to their connections. Large neurons project to spinal motor neurons which decline in number with age and they receive projections from Purkinje cells in the anterior lobe of the cerebellum which also decline in number with age. Small neurons mainly project to the oculogyric nuclei in at least one of which (the abducens) there is no loss of neurons up to 31 months of age.

Aging↗

PubMed1989

Stability of neuron and glial number in the abducens nerve nucleus of the ageing mouse brain.

The number of neurons and glia in the mouse abducens nerve nucleus was estimated at 6, 25, 28 and 31 months of age. There was no significant variation in either the number of neurons (mean 118) or glia (mean 168) or in the glia to neuron ratio (mean 1.42) with age. Mean neuronal and glial nuclear diameters also remained constant and there was no obvious loss of Nissl substance and only a minimal accumulation of lipofuscin in neuronal perikarya with age. The apparent lack of age-related changes in neurons of the abducens nucleus could be a consequence of the high degree of motor activity in the extrinsic eye muscles during both the waking and sleeping states.

Abducens Nerve↗

PubMed1989

Age related changes in Purkinje cell number in the cerebellar nodulus of the mouse.

The cortex of the cerebellar nodulus of mice aged 6, 15, 22, 25, 28 and 31 months was examined in parasagittal sections using quantitative histological techniques. The number of Purkinje cells per mm declined from 11.2 +/- 0.8 or 6 months to 7.0 +/- 0.6 at 31 months. Granule cell density remained constant (2.58 x 10(6) per mm3) between 6 and 31 months of age. The granule cell to Purkinje cell ratio increased from 119 +/- 7 at 6 months of age to 173 +/- 7 at 31 months of age. The change in Purkinje cell number began between 15 and 22 months of age. These results do not differ significantly from those of a similar study of quantitative histological changes in the anterior lobes of the same cerebella. This suggests that loss of Purkinje cells occurs in a similar fashion throughout the cerebellum despite differences in afferent and efferent connections in different regions.

Aging↗

PubMed1989

Changes in neuron number in the cerebellar cortex of the ageing mouse.

The cerebellar cortex of mice aged 6, 15, 22, 25, 28 and 31 months was examined in parasagittal sections using quantitative histological techniques. The number Purkinje cells per mm declined from 13.0 +/- 0.2 at 6 months to 9.1 +/- 0.8 at 31 months. Granule cell density remained constant (2.63 x 10(6) per mm3) between 6 and 31 months of age. The granule cell to Purkinje cell ratio increased from 132.4 +/- 4.2 at 6 months of age to 184.2 +/- 6.9 at 31 months of age. The stellate and basket cell density declined from 83.8 +/- 8.1 per 10(6) mm at 6 months to 58.4 +/- 5.7 at 31 months. The stellate and basket cell to Purkinje cell ratio remained constant at 5.0 +/- 0.1 from 6 to 31 months of age whilst the granule cell to stellate and basket cell ratio increased from 25.5 +/- 0.6 at 6 months to 35.1 +/- 0.6 at 31 months of age. Since granule cell number does not increase in the adult the increase in the granule cell to Purkinje cell and granule cell to stellate and basket cell ratios must be due to loss of Purkinje cells and stellate and basket cells with increasing age. The correlation between Purkinje cell and stellate and basket cell loss is statistically significant (P less than 0.01).

Aging↗

PubMed1988

Fluorescent granular perithelial cells in the meninges and optic nerve of the human embryo.

Cells containing small dense granules were present in the meninges surrounding the human embryonic optic nerve from 8 weeks post-conception. Typical fluorescent granular perithelial cells (FGP) containing large dense granules were present in the meninges by 12 weeks post-conception and in the large perivascular space around large vessels within the optic nerve by 14-15 weeks post-conception. The time of appearance of these cells in the CNS seems to be related to the stage of vascularization rather than to the stage of CNS development.

Cytoplasmic Granules↗

PubMed1988

The beta astrocyte: its possible role as a central nervous system phagocyte.

Phagocytic cells in the normal ageing mouse brain have the structural characteristics of the cells described by Reyners et al. (1982) as beta astrocytes and are quite different from microglial cells. Like the beta astrocyte (Reyners et al. 1986) they remain mitotically active even in extreme old age. Phagocytic cells in the immature mouse central nervous system contain glycogen but no microfilaments and may be immature beta astrocytes. A re-examination of the literature indicates that many phagocytes previously unidentified or considered to be microglial cells are probably beta astrocytes.

Aging↗

PubMed1988

An electron microscopic study of macrophages in the meninges of the human embryonic optic nerve.

Macrophages were found in the meningeal sheath of the human optic nerve at all ages from 8 to 18 weeks post-conception. At 8 weeks the majority of macrophages contained few cytoplasmic organelles or vacuoles, but even at this age a small number of cells packed with small dense bodies were present. With increasing age the number of organelles increased and some vacuolated macrophages were present. The morphology of macrophages largely depended on the part of the meninges in which they were situated. Those lying in the subarachnoid space or loose outer layers of the dura were irregularly shaped and often vacuolated, whereas those lying in the tightly packed layer of arachnoid at its junction with the dura were elongated and contained few, if any, vacuoles. A few meningeal macrophages were observed apparently migrating along the fibrous septa which carry blood vessels into the substance of the nerve. The main structural differences between meningeal macrophages and optic nerve microglia (Sturrock, 1984) were the presence in the latter of numerous small vacuoles and long strands of endoplasmic reticulum. These structural differences may be the result of microglia being actively engaged in phagocytosis of the large number of degenerating axons which are present in the optic nerve between 8 and 10 weeks post-conception.

Gestational Age↗

PubMed1988

Loss of neurons from the motor nucleus of the facial nerve in the ageing mouse brain.

The number of neurons and neuronal nuclear diameter was estimated in the motor nucleus of the mouse facial nerve at 6, 25, 28 and 31 months of age. Neuronal number decreased significantly (P less than 0.01) from 2010 +/- 58 to 1699 +/- 42 and neuronal diameter (P less than 0.001) increased significantly (P less than 0.001) from 11.6 +/- 0.1 microns to 14.2 +/- 0.2 microns between 25 and 28 months of age. Facial motor neurons lost Nissl substance between 6 and 25 months of age and also showed an accumulation of lipofuscin at 28 and 31 months. A small number of degenerating neurons was present in the motor nucleus of the facial nerve at 28 and 31 months.

Aging↗

PubMed1988

Loss of neurons from the retrofacial nucleus of the mouse in extreme old age.

The retrofacial nucleus, a general visceral efferent component of the vagal nuclei, was examined using quantitative histological techniques in young adult (6 months) and elderly (25, 28 and 31 months) mice. Neuron number remained constant between 6 months (206 +/- 2) and 25 months (209 +/- 4) and thereafter declined rapidly at 28 (181 +/- 11) and 31 months (157 +/- 4). Neuronal nuclear diameter (mean 11.0 microns) did not vary significantly with age. Neurons of the retrofacial nucleus lost Nissl substance with age and lipofuscin accumulation was marked in the perikaryon and dendrites.

Aging↗

PubMed1988

Variations in the structure of the jugular foramen of the human skull.

The jugular foramina were examined in 156 skulls. In 69% of cases the right was larger than the left and in 23% the left was larger, with the remainder being of equal size. An obvious dome caused by a superior jugular bulb was present bilaterally in 54%, on the right only in 30%, on the left only in 6% and was absent bilaterally in 10%. Of the 312 jugular foramina examined there was no evidence of an enlargement due to a superior jugular bulb in 28%.

Anatomy, Comparative↗