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Biomedical subjects

B G Cragg

Publications and source records attributed to B G Cragg.

At least 37 records · Page 2Linked to original sources
PubMed1979

The effect of destroying the whisker follicles in mice on the sensory nerve, the thalamocortical radiation and cortical barrel development.

Electrolytic destruction of whisker follicles in mice on the day of birth has been found to cause degeneration in the sensory nerve fibres supplying the follicles. The severity of the degeneration has been assessed in animals between 2 and 20 days old by counting the total number of myelinated fibres in the maxillary nerves on both normal and lesioned sides. The degeneration is apparent after 2 days and by 20 days the nerve on the lesioned side contains only 38% of the normal fibre content. This degeneration has also been shown to involve the trigeminal root, central to the ganglion. In addition, the lesioning procedure modifies the terminations of thalamocortical fibres in the barrel region of the sensory cortex. These terminations are normally in clusters, each corresponding to a barrel, but, after lesioning the follicles, the terminals appear to be evenly distributed in layer IV and cortical barrel structures no longer develop. In postnatal mice, electrolytic destruction of whisker follicles had less effect upon maxillary nerve fibres and cortical barrels. The number of myelinated axons surviving until day 20 increased progressively with later lesioning to reach nearly 80% of the control level when lesions were made on day 10. Cortical barrels became secure earlier than the maxillary nerve, for a normal number of cortical barrels was present at day 12 when follicles were destroyed on day 4. The implications of these results for the formation of cortical barrels is discussed.

Animals↗
PubMed1976

Ultrastructural features of human cerebral cortex.

Neuronal and glial elements have been examined in the temporal or frontal cortex of four brains with normal parenchyma. The identifying features recognized in animal brains have been found valid in human cortex for stellate and pyramidal neurons and their dendrites, spines, synapses, initial segments of axons, nodes of Ranvier and axon terminals; also for astrocytes, oligodendrocytes of various electron densities, pericytes, blood vessels and basement lamina, and for the relation of subarachnoid space to arterioles. However, most microglial cells have unexpectedly sparse and pale cytoplasm with few organelles, and the distribution of glial nuclear chromatin is not entirely in accordance with that described in animal brains. Fusiform neurons have been identified, and their cytoplasm resembles that of stellate cells. Peculiarities of human cortex include a nuclear inclusion that is present in stellate neurons only. Two neuronal cell-body profiles were myelinated, and a blood capillary was seen to penetrate a neuron. Somatic spines were found occasionally with or without synapses. Ribosomes can be present in axons, espicially at nodes of Ranvier, and a small portion of axon terminals contain a variety of dense bodies of which some are derived from mitochondria. Endoplasmic reticulum can occur in a compressed stack in neurons, and an unusual vesicular organelle has been seen in dendrites, axons and somata. Astrocytes as well as oligodendrocytes and occasional microglial cells act as satellites to neurons, and the exchange of a membrane-bound body between a neuron and asatellite glial cell is illustrated. Some dark pycnotic neurons were present, and it was remarkable that a closely apposed neuron could be entirely normal. These findings are compared with published descriptions of cortical ultrastructure in the brains of laboratory animals.

Animals↗
PubMed1975

The development of synapses in the visual system of the cat.

Synapses have been counted by electron microscopy and neurones by light microscopy through the depth of the visual cortex in a series of cats from 37 days gestation to adulthood. A few definite synapses are present as early as three weeks before birth, but there is then a latent period of four weeks before synapses increase rapidly in number 8-37 days after birth. The synapses occur just above and just below the cell plate at first, but in the adult cat they become evenly distributed in the depth of the cortex. The gradual separation of neurones by neuropil during development precedes a parallel increase in the density of synapses by about one week. The average number of synapses associated with one neurone rises to a peak of about 13,000 at seven weeks after birth. The densities of synapses and of neurones subsequently fall to slightly lower values in adult cats as the glial cells continue to develop. The timing of synaptic development in the visual cortex has been compared quantitatively with that in the L. G. N. and qualitatively with synaptogenesis in the retina. Synapses develop in the L. G. N. and cortex in a parallel fashion, and the L. G. N. precedes the cortex by a short interval of about two days. In the cell plate of the retina a few receptor synapses are present nine days before birth. Inner plexiform synapses are aslo present at this time, but ribbon-containing synapses do not appear until birth. Very few receptors possess outer segments with discs at birth, but five days later disc-bearing outer segments have developed. Thus synaptic development starts before afferent impulses can enter the visual system, but the main increase in synapses in the L. G. N. and cortex takes place four weeks after the start of synapse formation while the visual system is being used.

Age Factors↗
PubMed1975

The density of synapses and neurons in normal, mentally defective ageing human brains.

The densities of synapses and neurons were measured in 7 neurosurgical specimens of cerebral cortex, regarded as normal controls. The average result was 6 times 10-11 synapses/cm3, 15-6 times 10-6 neurons/cm3, and 38,000 synapses per neuron. Specimens of frontal and temporal cortex from 7 ageing brains (68 to 89 years) gave closely similar counts of neurons and synapses. Seven specimens from 3 severely retarded brains gave similar counts of neurons and slightly higher counts of synapses. A deficit of synaptic development is thus not a necessarre discussed.

Adolescent↗