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W Bondareff

Publications and source records attributed to W Bondareff.

71 records · Page 4Linked to original sources
PubMed1968

Histochemical fluorescence after application of neurochemicals to caudate nucleus and septal area in vivo.

The movement of carbachol, norepinephrine, and dopamine from cannula sites in caudate nucleus and septal area of freely moving rats was traced by means of biogenic amine fluorescence. Fluorescent patterns seen after application of carbachol and norepinephrine to brain tissue did not appear to differ from controls. Three types of movement from the cannula site after administration of dopamine were observed. There was a spherical distribution approximately 2 millimeters in diameter. Fluorescence also followed axonal pathways in the orthodromic direction, suggesting that dopamine may have been transported by " axonal streaming " or by some other unknown mechanism in periaxonal spaces. Because fluorescence was present in both the ependymal lining and the choroid plexus, it was inferred that the cerebral ventricles were also involved in the movement of chemical. Any attempt to ascribe anatomical localization to behavioral effects resulting from chemical stimulation of the brain should take into account the widespread movement of chemicals after their local application to brain tissue.

Animals↗
PubMedDate not supplied

Decrease in the number of synapses in the senescent brain: a quantitative electron microscopic analysis of the dentate gyrus molecular layer in the rat.

Axo-dendritic synapses were counted in electron micrographs taken from the middle third of the dentate gyrus molecular layer of young adult and senescent Fischer 344 rats. A significant decrease in the number of synapses was found in senescent animals relative to young ones. This loss of synapses, which involved all the morphological varieties of axo-dendritic synaptic contacts in the dentate gyrus molecular layer, appeared to be unrelated to changes in dimensions of synapses, tissue volume or number of postsynaptic granule cells. It is proposed that the age-related loss of synaptic contacts might be attributed to a reduced capacity of senescent brains for synaptic regeneration and remodelling.

Aging↗
PubMedDate not supplied

Diminished axonal transport of glycoproteins in the senescent rat brain.

At various time intervals (10, 15, 20, 25, 30 min) after injection of 3H-fucose into the medial septal nucleus of young adult (3 months old) and senescent (25 months old) Fischer-344 rats, the specific activities of trichloroacetic acid-phosphotungstic acid (TCA-PTA) soluble and insoluble fractions were determined in the medial area of the septum and in three successive rostro-caudal sections of the hippocampal formation containing mainly the dentate gyrus, but also its hilus with fields CA4 and CA3c of the hippocampus. The rate of 3H-fucose incorporation into glycoproteins of the septum did not differ in young adult and senescent rats. Part of the TCA-PTA soluble and insoluble radioactive material was transported through the septo-hippocampal pathway to the dentate gyrus. This transport was inhibited by the injection of colchicine into the septum prior to 3H-fucose injection and was completely blocked by electrolytic lesion of the medial septal nucleus. The arrival time and the amount of the TCA-PTA soluble radioactive material transported to the dentate gyrus did not differ in young adult and senescent rats. However, the TCA-PTA insoluble labelled glycoprotein was transported to the dentate gyrus in a significantly smaller amount and during a longer period of time in the senescent animals. This age-related change may reflect a reduction in amount and/or in rate of axonal transport of glycoproteins in the septo-hippocampal pathway of senescent rats.

Aging↗
PubMedDate not supplied

Number of neurons in nucleus locus ceruleus in demented and non-demented patients: rapid estimation and correlated parameters.

The total number of neurons in nucleus locus ceruleus (nLC) was counted in 20 patients with dementia (19 with dementia of the Alzheimer type) and 10 non-demented patients with the assistance of an image analyzer. The average number of neurons in a single representative section of nLC through the site of maximal neuronal density was then determined in each case. Both the mean total neuronal count and the average number of neurons in single sections correlated significantly with age, severity of dementia and length of nLC. The mean total number of neurons for demented (5571.700 +/- 4151.073) and non-demented (12533.700 +/- 2336.320) subjects differed significantly. The mean number of neurons derived by averaging counts of single representative sections from demented subjects (67.9 +/- 31.19) correlated significantly with the total number of nLC neurons determined by Quantimet-assisted analysis and differed significantly from the mean number of neurons derived by averaging counts of single representative sections of non-demented subjects of comparable age (110.0 +/- 16.59). With both methods of estimating neuronal numbers, the number of surviving nLC neurons in demented patients fell into 2 distinct groups, with cut-off points at 5,000 neurons (mean total counts) and 67 neurons (average of single representative section counts). These findings provide clear evidence that samples of the nLC neuronal population derived from single section counts produce data of comparable utility to those obtained from more laborious total neuronal counts in the human locus ceruleus.

Aged↗
PubMedDate not supplied

Changes in the brain in aging and Alzheimer's disease assessed by neuronal counts.

Changes in the magnitude of neuronal loss, which represent the end point of neuronal degeneration, are controversial and of limited utility as a measure of functional decline in aging and Alzheimer's disease (AD). Changes in the size of neurons and organelles, in the distributions of dendritic and synaptic fields, and in the relationships between neurons and the transmitter substances they produce, may be more useful in that they estimate changes in neuronal function prior to neuronal loss. The quantitative assessment of metabolic change in individual neurons by measuring histochemical reactivity, or more directly measuring enzyme activity or the amounts of its products might more reliably reflect degenerative changes associated with aging or AD, prior to the loss of neurons.

Aging↗
PubMedDate not supplied

Neurofibrillary degeneration and neuronal loss in Alzheimer's disease.

Neuronal loss in Alzheimer's disease, especially in cerebral cortex and hippocampus, appears closely associated with the process of neurofibrillary degeneration. In certain noncortical nuclei neuronal loss appears not to depend upon the formation of neurofibrillary tangles. Neurofibrillary tangles and neurons were counted in the same populations of neurons in five brain regions. In the locus ceruleus and nucleus basalis, where tangles have a loose or globose structure, correlations with neuronal counts were not significant. In cerebral cortex and hippocampus, tangles have a more dense and often a flame-like appearance and their correlations with neuronal counts were significant. The relationships between tangles and noncortical neurons reported here suggest that the appearance of tangles does not necessarily herald the demise of a neuron in Alzheimer's disease. It can be reasonably anticipated that these relationships depend upon the clinical heterogeneity of Alzheimer's disease, regional differences in the brain and/or the macromolecular composition of neurofibrillary tangles.

Aged↗