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Biomedical subjects

B J Crain

Publications and source records attributed to B J Crain.

At least 73 records · Page 4Linked to original sources
PubMed1988

The laminar distribution of neuritic plaques in the fascia dentata of patients with Alzheimer's disease.

Neuritic plaques are prominent in the fascia dentata of the hippocampus and are often linearly oriented in stratum moleculare. Since the afferents to this region are also organized in a laminar pattern, the present study focused on the relative number and laminar distribution of plaques in this region to shed light on the genesis of the neuritic plaques. Examination of 19 brains from patients with Alzheimer's disease showed approximately the same number of plaques in the stratum moleculare of the fascia dentata and in CA1 (Sommer's sector) of the hippocampus, even though the area of the latter is much greater. Laminar analysis of plaque location showed that the plaques were centered on a band between 26% and 40% of the way between the border of stratum granulosum and the outer edge of stratum moleculare. The mean location was 35% of the way through the layer at the intersection of the inner and middle thirds. Plaques appear in approximately the same location, but in lesser numbers, in non-demented patients. The significance of this localization is discussed in terms of the normal anatomy of the fascia dentata and its possible reorganization in Alzheimer's disease. The predictability of plaque formation in this region could be useful in defining the pathogenesis of the neuritic plaque.

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PubMed1988

Selective neuronal death after transient forebrain ischemia in the Mongolian gerbil: a silver impregnation study.

An important feature of ischemic brain damage is the exceptional vulnerability of specific neuronal populations and the relative resistance of others. Silver impregnation was used to delineate the extent and time-course of neuronal degeneration produced by 5 min of complete forebrain ischemia in the Mongolian gerbil. Lesions were confined to four brain regions: (1) hippocampal areas CA1, CA2-CA3a and CA4; (2) the dorsomedial portion of the lateral septal nucleus; (3) the dorsolateral portion of the striatum; and (4) the somatosensory neocortex. The ischemic lesion evolved with time in all four regions, but at different rates. Somatic argyrophilia developed rapidly in the striatum and hippocampal area CA4 (maximal in 24 h or less), at intermediate rates in the somatosensory neocortex, hippocampal areas CA1a and CA2-CA3a and the lateral septal nucleus (maximal in 2 days), and slowly in hippocampal area CA1b (maximal in 3 days). These results emphasize that the extent and rate of neuronal degeneration can vary even within a presumably homogeneous neuronal population, as evidenced by the different results in areas CA1a and CA1b. Similar results were obtained from analysis of brain sections stained with Cresyl Violet, hematoxylin-eosin or hematoxylin-eosin/Luxol Fast Blue. Terminal-like silver granules were observed in the projection fields of degenerated neurons. They also appeared, however, in the perforant path terminal zone of the hippocampal dentate molecular layer 1-2 days after transient ischemia and in stratum oriens and stratum radiatum of area CA1b prior to somatic degeneration. These granular deposits could not be clearly related to the degeneration of neuronal somata. Novel findings of this study include the degeneration of some dentate basket cells and lateral septal neurons and the appearance of terminal-like argyrophilia in the hippocampal formation without any obvious relation to somatic degeneration. Some of our results lend support to the hypothesis that ischemic neuronal cell death constitutes an excitotoxic process. Other results, however, suggest that the selective vulnerability of neurons to transient ischemia must involve factors beyond excitotoxicity.

Animals↗
PubMed1987

An in vitro autoradiographic analysis of mu and delta opioid binding in the hippocampal formation of kindled rats.

Recent studies have shown that opioid peptide levels are altered in hippocampal formation of kindled animals. We therefore studied the distributions of mu and delta opioid binding sites in hippocampal formation of kindled and control rats using quantitative in vitro autoradiography. Animals received daily stimulations of the amygdala until they experienced 3 class 5 seizures. Paired control animals underwent implantation of electrodes but were not stimulated. Mu binding sites were labeled with 125I-FK-33824. Twenty-four hours after the last kindled seizure, mu binding was decreased by 32% in stratum pyramidale of CA1 and stratum radiatum of CA2 and by 17-27% throughout most of the rest of CA1, CA2, and CA3. Few, if any, differences were seen between kindled and control animals at 7 or 28 days after the last kindled seizure. Delta binding sites were labeled with 125I-[D-Ala2,D-Leu5]enkephalin in the presence of the morphiceptin analog PL-032. Twenty-four hours after the last kindled seizure, delta binding was decreased only in stratum moleculare of the dentate gyrus. Seven days after the last kindled seizure, delta binding was decreased by 11-17% throughout CA1, CA3, and the dentate gyrus. At 28 days after the last seizure, however, no differences were found between kindled and control animals. Since the decreases in mu and delta opioid binding are transient, they are unlikely to be the molecular basis of the permanent kindling phenomenon. Rather, these changes in opioid binding may represent responses to repeated seizures.

Animals↗
PubMed1986

Quantitative autoradiographic analysis of mu and delta opioid binding sites in the rat hippocampal formation.

The distributions of mu and delta opioid binding sites were studied in rat hippocampal formation by using quantitative in vitro autoradiography. Mu binding sites, labeled with 125I-FK-33824, showed a highly organized laminar distribution. Binding was greatest at the foot of the obliterated hippocampal fissure in stratum lacunosum-moleculare of CA3. Stratum pyramidale and stratum lacunosum-moleculare of CA2 and stratum pyramidale of CA3 were next highest in mu binding, followed by stratum oriens and stratum radiatum of CA2, stratum oriens of CA3, and stratum pyramidale of CA1. The distribution of delta binding sites, labeled with 125I-D-ala2-D-leu5-enkephalin in the presence of the unlabeled mu receptor ligand PL-032, was similar to the distribution of mu binding in that binding within each region was greatest in a band centered over stratum pyramidale and in stratum lacunosum-moleculare. Over all, delta binding was greatest in CA2 followed by CA3 and then CA1. Compared to mu binding, delta binding was relatively enriched in stratum moleculare of the dentate gyrus. These laminar distributions correlate reasonably well with the distribution of enkephalin immuno-reactivity in hippocampal formation, although binding was surprisingly low in stratum lucidum, an area rich in dynorphin and enkephalin immunoreactivity.

Animals↗
PubMed1986

Spinal cord infarction following intraaortic balloon support.

Infarction of the lumbar and sacral spinal cord was demonstrated at autopsy of a 72-year-old man in whom acute paraplegia developed following coronary artery bypass grafting and atrial septal defect repair with intraoperative insertion of an intraaortic balloon. Autopsy findings showed that infarcts of the spinal cord and other key organs were caused by critical occlusion of small arterioles by cholesterol emboli. These emboli apparently arose as a result of the fragmentation of atheromatous plaques within the aorta during use of the intraaortic balloon pump with subsequent embolization and occlusion of small blood vessels.

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PubMed1985

Autoradiographic localization of benzomorphan binding sites in rat brain.

The benzomorphan subpopulation of opiate binding sites was labeled by [3H]diprenorphine in the presence of unlabeled ligands selected to quench mu and delta opiate binding sites. The distribution of benzomorphan binding sites was then localized autoradiographically. Areas particularly enriched in these sites were nucleus solitarius, nucleus ambiguus, substantia gelantinosa of the trigeminal nerve, the habenula, and the medial nucleus of the amygdala. Within hippocampal formation, binding was relatively enhanced in the pyramidal and granule cell layers. Within the basal ganglia, binding was greatest in the dorsomedial caudate nucleus and least in the globus pallidus. No 'patches' of increased binding were present in the striatum. The interstitial nucleus of the stria terminalis and the medial preoptic nucleus also showed significant binding. This distribution differs from the distributions of mu, delta and kappa opiate binding and is quite similar to the distribution of beta-endorphin immunoreactivity. These observations support the hypothesis, based on biochemical studies in brain membranes, that benzomorphan binding sites may represent the ligand recognition sites of putative epsilon receptors.

Animals↗
PubMed1985

The kindling model of epilepsy: a critical review.

Kindling is an animal model of epilepsy induced by electrical stimulation of the brain. This model has attracted the interest of many neuroscientists, in part because it involves a robust, permanent modification of brain function. This report will describe the kindling phenomenon and critically review current understanding of the underlying mechanisms. The review will carefully consider whether this model accurately reflects analogous processes in humans. The review will consider some hypotheses inspired by the kindling studies which may be relevant to human epilepsy.

Acetylcholine↗
PubMed1983

Cunninghamella: a newly recognized cause of rhinocerebral mucormycosis.

Cunninghamella, a zygomycete in the order Mucorales, is an extremely rare cause of human infection. Of the five reported cases of human disease caused by this fungus, none involved rhinocerebral infection. Here, the authors document what appears to be the first case of rhinocerebral mucormycosis caused by Cunninghamella bertholletiae in an elderly man who had diabetes with sideroblastic anemia and hemochromatosis. The disease was rapidly fatal. The mycology and classification of this organism are presented, and the previous case reports in the literature are reviewed.

Aged↗
PubMed1981

The normal organization of the lateral posterior nucleus in the golden hamster and its reorganization after neonatal superior colliculus lesions.

We have studied the normal organization of the hamster lateral posterior nucleus and its reorganization after neonatal superior colliculus lesions. First, we divided the lateral posterior nucleus into rostrolateral, rostromedial and caudal subdivisions and determined the normal distributions of terminals contributed to each division by the ipsilateral and contralateral superior colliculi, the ipsilateral posterior neocortex and the contralateral retina. Since the rostrolateral subdivision receives most of the projections from the ipsilateral superior colliculus, our studies concentrated on this region. The rostrolateral subdivision contains synaptic clusters formed primarily by medium-sized M-terminals synapsing around a central dendrite. Electron microscopic observations showed that the majority of M-terminals are from the ipsilateral colliculus, although a few are contributed by the contralateral colliculus and retina. Therefore, after an ipsilateral neonatal colliculus lesion the synaptic clusters must develop in the absence of their major input. The next step was to examine the distributions of the remaining afferents to the rostrolateral subdivision in adult animals which had received ipsilateral neonatal colliculus lesions. In the cases, the normally restricted projection fields of the contralateral colliculus and the retina expand until they share a border in the rostrolateral subdivision. In contrast the cortical projection, which normally extends throughout the lateral posterior nucleus, is reduced in the region containing retinal terminals. At the ultrastructural level, we found morphologically normal synaptic clusters and showed the M-terminals now occupying the clusters are contributed by the remaining colliculus and the retina. The results suggested that the afferents to the lateral posterior nucleus normally compete for synaptic space and that this competition continues after a neonatal colliculus lesion. In our final experiments, we performed various combinations of neonatal lesions (bilateral superior colliculus, superior colliculus and retina, superior colliculus and cortex) and found that the remaining afferent expand their terminal fields still further in the absence of two inputs.

Animals↗
PubMed1981

Retinoblastoma as a possible primary intracranial tumor.

A 10-month-old infant with a small, unilateral, peripheral retinal lesion also had a large, well-encapsulated, suprasellar retinoblastoma. The primary vs. the metastatic nature of the intracranial tumor is considered. It is postulated that primary intracranial tumors may arise within areas of the central nervous system embryologically related to the retina in patients with the genetic form of retinoblastoma.

Brain Neoplasms↗
PubMed1980

The normal organization of the lateral posterior nucleus of the golden hamster.

As a first step in analyzing the influence of various afferent projections on the development of the hamster lateral posterior nucleus, its normal organization was studied using both light and electron microscopic techniques. Rostrolateral, rostromedial, and caudal subdivisions were identified. The rostrolateral subdivision receives dense projections from the ipsilateral superior colliculus and posterior neocortex, as well as sparser, more restricted projections from the contralateral colliculus and retina. The ipsilateral colliculus is by far the major source of medium-sized (M)terminals with round vesicles. These terminals synapse around the shafts of large central dendrites to form distinctive synaptic clusters. The contralateral colliculus and retina contribute a few M-terminals to the clusters. In contrast, axons from the posterior neocortex form very large (RL-)terminals with round vesicles from the posterior neocortex form very large (RL)terminals with round vesicles which synapse onto numerous appendages of single proximal dendrite, are surrounded by glial lamellae, and rarely participate in the clusters. Axons from all four sources also form small (RS)terminals with round vesicles which synapse on the shafts of small dendrites. Finally, F-terminals with flat or pleomorphic vesicles form symmetric synaptic contacts both within and outside the clusters. The only identified projection to the rostromedial subdivision is from the ipsilateral posterior neocortex, which contributes RL- and RS-terminals. F-terminals are also found, but neither M-terminals nor synaptic clusters are present. The caudal subdivision also receives RL- and RS-terminals from the ipsilateral posterior neocortex. Small inputs from the ipsilateral and contralateral colliculi are present, but their axons form only RS-terminals. No M-terminals or synaptic clusters are found. These results indicate that a large neonatal superior colliculus lesion would eliminate the vast majority of the M-terminals in the synaptic clusters of the ipsilateral lateral posterior nucleus. In subsequent studies (Crain and Hall, '80 a,b,c), we will examine how the remaining inputs from the retina, contralateral superior colliculus, and posterior neocortex contribute to the synaptic organization when it develops after such a lesion.

Animals↗
PubMed1980

The organization of the lateral posterior nucleus of the golden hamster after neonatal superior colliculus lesions.

The reorganization of the adult hamster's lateral posterior nucleus after neonatal superior colliculus lesions was studied using primarily light and electron microscopic degeneration techniques. Two types of experiments were conducted. First, the distributions of the remaining afferents from the contralateral superior colliculus, the cotralateral retina, and the ipsilateral posterior neocortex were determined using the Fink-Heimer ('67) technique. Normally the projections from the contralateral superior colliculus and retina are sparse and restricted to small areas in the rostrolateral subdivision. After neonatal lesions of the ipsilateral colliculus, however, these two minor projections greatly increase in density and expand to share a common border. In contrast, the normal projection from the posterior neocortex is dense throughout the rostrolateral subdivision. After a neonatal colliculus lesion, however, this projection is greatly decreased in the region occupied by the optic tract terminals. Second, the ultrastructural organizatin of the rostrolateral subdivision was studied in adult animals whhich had received neonatal colliculus lesions. Normally, this region is characterized by synaptic clusters in which numerous medium-sized terminals (M-terminals), almost all from the ipsilateral colliculus, synapse around the shaft of a large central dendrite. The contralateral colliculus and retina normally contribute only a few M-terminals. After a neonatal colliculus lesion, typical clusters still form, but now the expanded projections from the contralateral colliculus and retina contribute numerous M-terminals. The cortex does not contribute M-terminals in either normal or experimental animals. These results suggest that the afferents to the rostrolateral subdivision normally compete for synaptic space. The various factors that might be involved in determining the outcome of such competition are discussed.

Animals↗
PubMed1980

The organization of afferents to the lateral posterior nucleus in the golden hamster after different combinations of neonatal lesions.

After a neonatal lesion of the ipsilateral superior colliculus, the projections to the lateral posterior nucleus from the contralateral superior colliculus and retina expand their terminal fields until they share a common border. In the first experiment described in this paper, we removed both superior colliculi at birth and used the Fink-Heimer method to show that the optic tract projection could expand even further and enter the region which would have been occupied by the terminals of the crossed colliculus projection. Similarly, in the second experiment, we showed that the crossed collicular projection could be increased even more if the contralateral eye as well as the ipsilateral colliculus was removed at birth. Another result of a neonatal superior colliculus lesion is that the projection from the optic tract shares a border with the posterior neocortical projection. In the third experiment, we removed both the ipsilateral superior colliculus and the posterior neocortex at birth and demonstrated that the optic tract projection expanded more than after an ipsilateral colliculus lesion alone. Our results support the hypotheses that the projections from the ipsilateral and contralateral superior colliculi and the retina compete for synaptic space in the lateral posterior nucleus, and that a similar competition between the retinal and cortical projections may also occur.

Animals↗
PubMedDate not supplied

Correlation between function and structure in "epileptic" human hippocampal tissue maintained in vitro.

Intracellular and extracellular recordings were obtained from the CA1 region and gyrus dentatus of human hippocampi that had been surgically removed for treatment of intractable seizures. Pathologic diagnoses were obtained, and electrophysiologic results were correlated with degree of principal cell loss (sclerosis) in the regions studied. Extracellular field potentials were absent or smaller in amplitude, with abnormal characteristics, in sclerotic regions. In all regions, regardless of the degree of sclerosis, individual pyramidal or granule cells could be penetrated. These neurons showed apparently normal electrophysiologic characteristics and intact excitatory synaptic input. No signs of hyperexcitability were observed.

Adolescent↗
PubMedDate not supplied

Adult onset Niemann-Pick disease type C presenting with dementia and absent organomegaly.

A 39-year-old female presented to the Bryan Memory Disorders Clinic at Duke University with a 7-year history of an atypical progressive dementia, mildly impaired vertical gaze, dysarthria and mild ataxia. There was no evidence of organomegaly by clinical examination or by radionuclide liver/spleen scan. Brain biopsy disclosed a neuronal storage disorder characterized by ballooned neurons filled with oligo-lamellar cytosomes and lipid droplets. Cultured skin fibroblasts had diminished sphingomyelinase activity and impaired cholesterol esterification, although peripheral leukocyte sphingomyelinase activity was normal. Two years after biopsy, follow-up examination revealed marked progression of vertical gaze paralysis and ataxia. This case expands the clinical spectrum of Niemann-Pick disease type C by presenting in adulthood with subtle neurologic abnormalities; no visceromegaly and profound dementia.

Adult↗
PubMedDate not supplied

Lobar atrophy without Pick bodies.

Four patients from the Kathleen Price Bryan Brain Bank with clinical Pick's syndrome are presented. Thorough neurological evaluation revealed no evidence of a movement disorder. The brains showed marked knife-blade type atrophy of the frontal and temporal lobes with relative sparing of the superior temporal gyrus and parietal and occipital lobes. There was marked caudate atrophy in all four. Histologically there was severe neuronal loss and gemistocytic astrocytosis in the involved areas with marked myelin pallor in the deep white matter and subcortical gliosis. There was sometimes marked spongiform change in cortical layer 2. There was severe neuronal loss and gliosis of the caudate nucleus. The gross and microscopic features were characteristic of Pick's disease except that careful search failed to uncover either Pick's bodies or Pick's cells. Review of the literature revealed that fronto-temporal cortical and caudate atrophy with clinical features of Pick's disease has received many different names including Pick's disease type C, Pick's disease type II, progressive subcortical gliosis, presenile glial dystrophy, long duration Creutzfeldt-Jakob disease, frontal lobe degeneration, dysphasic dementia, and dementia lacking distinctive histologic features. Nevertheless, the morphologic findings in the present cases so closely resemble Pick's disease that they may well represent endstage Pick's disease. In our experience, such cases account for a significant proportion of non-Alzheimer disease dementia.

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