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Biomedical subjects

T P Powell

Publications and source records attributed to T P Powell.

At least 37 records · Page 2Linked to original sources

Changes in the size of cells in the monocular segment of the primate lateral geniculate nucleus during normal development and following visual deprivation.

Cell areas have been measured in the monocular segment of the lateral geniculate nucleus in a series of 18 normal rhesus monkeys and in 27 following monocular or binocular lid closure or monocular enucleation. Cells in the parvocellular monocular segment shrank by 16% during the later period of normal development, between about 3 and 18 months of age, in contrasts to cells in the binocular segment which did not. Monocular closure at birth caused hypertrophy of cells in the undeprived monocular segment whereas long-term closure started later caused shrinkage of both deprived and undeprived parvocellular cells additional to that occurring during normal development. In both these instances cells in the monocular segment related to the undeprived eye are undergoing changes indicating some form of binocular interactions even in the monocular segment, but these interactions are considerably weaker than in the binocular part of the nucleus. Enucleation caused marked transneuronal degeneration of cells in the contralateral monocular segment of both infant and adult monkeys.

Animals↗

Anterograde vs. retrograde degeneration of the nucleus basalis medialis in Alzheimer's disease.

The evidence that degeneration in the basal forebrain cholinergic nuclei in Alzheimer's disease is a secondary phenomenon is reviewed. Experimental retrograde degeneration in these nuclei shares some common features with the degeneration actually observed in the disease, and can occur without direct damage to the cholinergic axons within the cortex. The neuroanatomical distribution of the pathological changes typical of Alzheimer's disease in the neocortex suggests a progression of the disease process, from the medial temporal cortex and amygdala out into the parieto-temporal association areas. Neurochemical evidence also points to the early and severe involvement of the amygdala in the disease. The close reciprocal relationship between the amygdala and the basal nucleus may underly the degeneration seen in the basal nucleus in Alzheimer's disease.

Alzheimer Disease↗

Hypertrophy of cholinergic neurones of the basal nucleus in the rat following damage of the contralateral nucleus.

The effect of damage of the basal nucleus of one side on the size of immunohistochemically identified cholinergic cells in the contralateral nucleus has been studied in rats. Following stereotaxic injections of kainic acid into the nucleus of one side, the choline acetyltransferase (ChAT)-containing neurones in the contralateral basal nucleus are significantly larger (mean +19%) than those in normal animals. This hypertrophy is of comparable magnitude to that seen following damage of the contralateral cortex (mean +21%) and appears to persist indefinitely.

Animals↗

Hypertrophy of motor neurons in the oculomotor nucleus of the rat following removal of the contralateral extraocular muscles.

Motor neurons of the oculomotor nucleus of the rat were identified immunohistochemically using a monoclonal antibody against choline acetyltransferase (ChAT). The number and size of the cell bodies were examined following removal of the extraocular muscles on one side. 35 days postoperatively, motor neurons of the oculomotor nucleus ipsilateral to the muscle removal are undiminished in number and are of normal size when compared with littermate control animals. Cholinergic cells in the contralateral nucleus are significantly larger than normal (+23%). This hypertrophy appears to persist at least until 300 days after operation, the longest survival time examined.

Animals↗

The organization of the corticocortical projection of area 5 upon area 7 in the parietal lobe of the monkey.

The distribution of labelled cells and of extracellular granules in the cortex of area 5 of the parietal lobe of the monkey has been studied after injections of horseradish peroxidase into area 7. Area 5 is related only to area 7b (PF) and not to area 7a (PG). The corticocortical connections between area 5 and 7b are reciprocal and well organized so that the same representations in each area are interconnected. No corticocortical fibres pass between areas 7a (PG) and 7b (PF).

Animals↗

The relationship between the auditory cortex and the claustrum in the cat.

The relationship between the primary auditory cortex and the claustrum has been re-examined in the cat with axoplasmic flow and axonal degeneration methods. Labelled cells are found in a restricted part of the claustrum after injections of HRP or HRP-WGA in the primary auditory cortex, but they are relatively few in number and are palely stained. The number of labelled cells and their depth of staining are greatest at 72 h (the longest survival time used here), and this survival period an occasional labelled cell is also present in the claustrum of the contralateral hemisphere. No labelled cells are seen after 24 h. After small lesions in the primary auditory cortex, fibre and terminal degeneration are present in the part of the claustrum where labelled cells are seen with axoplasmic flow techniques. It is concluded that there are reciprocal connections between the primary auditory cortex and the claustrum, but the rate of axoplasmic flow is unusually slow.

Animals↗

The cortex of the primary auditory area in Alzheimer's disease.

The cortex of the superior temporal gyrus has been examined in two brains with Alzheimer's disease. Numerous neurofibrillary tangles and neuritic plaques that are characteristic of the disease, were present in area 38 in the anterior part of the gyrus and in area 22 more posteriorly but the primary auditory cortex, area 41, was virtually unaffected by these pathological changes. This relatively minor involvement of the primary auditory cortex, like that of the primary somatic and visual areas, again emphasises the uniqueness of the olfactory system in being severely degenerate. The findings are considered to support the suggestion that the distribution of the pathological changes in Alzheimer's disease has an anatomical basis due to spread of the disease process along certain well-defined sets of cortical fibre connections.

Alzheimer Disease↗

The effect of visual deprivation upon the basal dendrites of Meynert cells in the striate cortex of the monkey.

The basal dendrites of Meynert cells in the striate cortex have been studied with the Golgi method in the brains of monkeys that had been reared for varying periods with the eyelids closed over one eye. The lengths and arrangement of the dendrites were compared with those in normal brains. In the visually deprived brain almost half of the cells had basal dendrites that were apparently normal with the dendritic fields in the form of an ellipse and the long axes parallel to the direction of the ocular dominance bands. The other cells had dendritic fields that have rarely been seen in normal material and two distinct types could be recognized. The 'lop-sided' cell had an ellipsoidal dendritic field with the major axis parallel to the ocular dominance bands, but the extents of the dendrites along the minor axis were very asymmetric; the ratio of the means of the long and short arms of the minor axis of the 'lop-sided' cell is 2.3:1 compared with 1.1:1 in normal brains. The 'perpendicular' type of cell also had an ellipsoidal dendritic field but the relation of the major and minor axes to the direction of the ocular dominance bands was the reverse of the normal cell, with the long axis of the ellipse being aligned perpendicular to the bands. 'Lop-sided' cells formed approximately 18% of the total of Meynert cells studied and the 'perpendicular' 32%. The proportion of the cells with abnormal basal dendritic fields, and particularly the 'perpendicular', increased with longer durations of eyelid closure. It is suggested that the alterations in the dendritic fields of the 'lop-sided' and 'perpendicular' cells may be correlated with the changes in width of the ocular dominance bands that are known to occur after monocular eyelid suture.

Age Factors↗

Hypertrophy of cholinergic neurones of the rat basal nucleus following section of the corpus callosum.

The effect of division of the corpus callosum on immunohistochemically identified cholinergic neurones of the basal nucleus has been examined in rats. Following callosal section the cholinergic cell bodies on both sides are significantly larger (25%) than those in normal animals. This hypertrophy persists for at least 62 days after operation, the longest survival time examined. It is greatest when the animal is operated on in infancy, but it occurs at all ages examined. The enlargement is similar to that seen in the cells of the same nucleus on one side following contralateral cortical damage.

Animals↗

The callosal connexions of the primary somatic sensory cortex in the monkey.

The callosal connexions of the primary somatic sensory cortex, SI, of the monkey have been studied with axonal degeneration methods after the placement of lesions of varying size in the cortex of one hemisphere and after section of the corpus callosum. For the correlation of the distribution of the degeneration with the cytoarchitectonic subdivisions of SI and with their boundaries, planar reconstructions of the extents of the subdivisions and of area 5 were made. The extent of area 5 is surprisingly large, being about the same as SI, and area 3a can be recognized as a distinct subdivision along the entire medio-lateral extent of SI. The callosal fibres end in narrow, irregular bands aligned in the medio-lateral dimension and there are accentuations at the boundaries of the cytoarchitectural subdivisions. In the representations of the trunk and face, the bands of degeneration are present across the entire antero-posterior extent of SI and with increases at the boundaries, while in the limb regions the degeneration becomes restricted to the boundaries. It is suggested that the callosal connexions of the somatic sensory cortex, like those in the visual and auditory areas, are connecting those parts of the cortex in the two hemispheres that are concurrently activated by a peripheral stimulus. The parts of SI that are devoid of callosal connexions are related to the distal limbs. The callosal connexions are homo- and heterotopical; an architectonic subdivision within the callosally connected regions projects to the same and other architectonic subdivisions at the same medio-lateral level in the opposite hemisphere; the cortex containing the representation of the caudal trunk near the post-central dimple is connected with the same region in the other hemisphere and with that of the separate representation of the caudal trunk in the posterior part of the cingulate sulcus, while the representation of the occipital region at the post-central dimple is connected both with the homotopical site in the other hemisphere and with the other representation of this part of the periphery at the level of the lower end of the intraparietal sulcus.

Animals↗

The ipsilateral cortico-cortical connexions between the cytoarchitectonic subdivisions of the primary somatic sensory cortex in the monkey.

The ipsilateral cortico-cortical connexions passing between the architectonic subdivisions of the primary somatic sensory cortex, S1, of the monkey have been studied with axonal degeneration methods after the placement of small lesions. All architectonic subdivisions except area 3a, and all the topographic representations, have been involved by the lesions. The degeneration of local intracortical fibres has the same features that have been described in other cortical areas: dense terminal degeneration for about 200 micron immediately around the lesion and moderate degeneration extending for a few millimetres with that in layers I, IV and the deep part of V being the most marked and reaching furthest; the degeneration extends further in the antero-posterior than in the medio-lateral dimension, and further posteriorly than anteriorly. The arrangement of the intercortical fibre connexions varies with the architectonic subdivision and with the topographic representation, and as in other sensory areas these fibres may be considered as either feed-forward or feed-back. The feed-forward projections are heavy, terminate in all layers of the cortex but mainly in layer IV and the deep part of layer III, whereas the feed-back connexions are lighter and end in layers I, II, the superficial part of layer III and in layers V and VI. In the antero-posterior dimension, feed-forward fibres from area 3b go to areas 3a, 1 and 2; area 1 sends feed-forward connexions to areas 3a and 2 and feed-back to area 3b; area 2 sends a feed-forward projection to area 3a and feed-back to areas 3b and 1; all areas also send fibres to area 5. A lesion in one of the architectonic subdivisions in the trunk and face representations results in degeneration throughout the antero-posterior extent of S1, but after damage within an architectonic area in the distal limb regions, there are foci of degeneration in the middle of the antero-posterior extents of the other areas but with little or none at the boundaries. The cortico-cortical fibres also extend medially or laterally for a few millimetres, in bands a few hundred micron wide. After damage of the trunk, occiput or proximal limb representations, the degenerating fibres pass predominantly along the boundaries; the separate representations of the caudal trunk, at the postcentral dimple and cingulate sulcus, are connected by continuous bands along the boundaries of area 3a and at the 2/5 boundary, and those of the occiput region at the levels of the postcentral dimple and lower end of the intraparietal sulcus are similarly linked.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

The projection of the primary somatic sensory cortex upon area 5 in the monkey.

The projection of the cortex of the primary somatic sensory area (S1) upon area 5 in the rhesus monkey has been studied with axonal degeneration methods. There is little or no overlap between the major topographic representations in area 5 but there is both convergence and divergence within a representation; the degeneration after a small lesion in a representation in SI virtually fills the representation in area 5 and there is extensive overlap of the degeneration after two lesions in widely separated parts of the representation in S1. The representation of the arm in area 5 is surprisingly large, that of the face is relatively smaller than in S1 and the trunk and leg are about the same as in S1. Lesions in the trunk and face representations result in terminal degeneration throughout the antero-posterior extent of area 5, but after damage of the limb representations the degeneration in area 5 is concentrated into 3 medio-laterally disposed bands. Of the cytoarchitectonic subdivisions of S1, area 2 projects most heavily upon area 5 and area 3b the least, and there is a reversal in the antero-posterior dimension with more posterior parts of S1 projecting to more anterior parts of area 5. The corticocortical fibres from S1 end in layers III and IV of area 5, and while the degeneration in layer IV is continuous it is in distinct 'prongs' in layer III.

Animals↗

Sizes of neurons in the primate lateral geniculate nucleus during normal development.

Measurements of cell area have been made in the lateral geniculate nuclei (LGNs) of 18 normal rhesus monkeys aged from 8 days to fully adult. There is much less variability between individual animals than had been thought from measurements of undeprived cells in experimental animals following visual deprivation. It is therefore possible to make reliable comparisons of cell size between different animals. There is no change in size of cells in the parvocellular laminae between 8 days of age and adulthood, although cells in the magnocellular laminae grow a little. In the primate, unlike the cat, the period of maximum sensitivity to visual deprivation does not correspond to a period of rapid cell growth in the LGN.

Age Factors↗

Effects of monocular closure at different ages on deprived and undeprived cells in the primate lateral geniculate nucleus.

This study has examined the effects of monocular visual deprivation on cells in the lateral geniculate nucleus of the primate by comparing the sizes of cells in deprived and undeprived LGN laminae of experimental rhesus monkeys with those of cells in the corresponding laminae of normal animals. A number of conclusions may be drawn from this comparison: monocular visual deprivation has major effects on cells in the undeprived LGN laminae and these vary with age at closure; the initial effect of monocular closure from birth is to cause marked hypertrophy of undeprived parvocellular cells with little shrinkage of the deprived parvocellular cells, whereas late monocular closure (after 2 months of age) causes marked shrinkage of both undeprived and deprived parvocellular cells; following monocular closure at birth, the LGN abnormality continues to evolve until at least 3 months of age, with a marked parallel shrinkage affecting both deprived and undeprived parvocellular cells. The initial hypertrophy of the undeprived cells is reversed and the deprived cells become smaller than normal; cells in the monkey LGN are sensitive to visual deprivation until about 1 year of age, much later than previously thought. Visual experience, however, modifies this sensitivity so that the effects of monocular visual deprivation are both qualitatively and quantitatively different at different ages; there are important differences between the susceptibility of cells in the magnocellular and parvocellular laminae to visual deprivation; and actual shrinkage of cells to markedly below normal size occurs and the smaller size is not simply failure of growth.

Age Factors↗

Effect of reopening an eye after a period of monocular deprivation on sizes of neurons in the primate lateral geniculate nucleus.

Following monocular closure shortly after birth the deprived eye of 4 rhesus monkeys was reopened at different times. Following long-term recovery, cells in the undeprived laminae of the lateral geniculate nucleus of these animals were of normal size and those in the deprived laminae were markedly shrunken. Comparisons with animals monocularly deprived for similar periods indicate, however, that in 3 of these animals the undeprived parvocellular cells would have been markedly hypertrophied at the time of reopening the deprived eye, and in two of the animals, little shrinkage of the deprived parvocellular cells would have occurred by this time. Both undeprived and deprived parvocellular cells have therefore undergone marked shrinkage after the deprived eye had been reopened. The parallel shrinkage of deprived and undeprived parvocellular cells which occurs following closure at birth thus appears to be a consequence of the initial abnormalities produced by monocular closure rather than a direct result of the continuing lack of visual input to one eye.

Animals↗

Anatomical correlates of the distribution of the pathological changes in the neocortex in Alzheimer disease.

The numbers and distribution of the neurofibrillary tangles and neuritic plaques have been determined in several areas of the neocortex in brains affected by various degrees of severity of Alzheimer disease. The homotypical cortex of the "association" areas of the temporal, parietal, and frontal lobes are severely involved, whereas the motor, somatic sensory, and primary visual areas are virtually unaffected. The neurofibrillary tangles are mainly in the supra- and infragranular layers, particularly in layers III and V. In all areas except area 18 in the occipital lobe, there are approximately twice as many tangles in layer V as in layer III. The tangles are arranged in definite clusters, and those in the supra- and infragranular layers are in register. The neuritic plaques occur in all layers but predominantly affect layers II and III and do not show clustering. These data on the severity of the pathological involvement in different areas of the neocortex and the laminar distribution and the clustering of the tangles support the suggestion that the pathological changes in Alzheimer disease affect regions that are interconnected by well-defined groups of connections and that the disease process may extend along the connecting fibers. The invariable and severe involvement of the olfactory areas of the brain in this disease is in striking contrast to the minimal changes in the somatic sensory and primary visual areas and raises the possibility that the olfactory pathway may be initially involved.

Aged↗