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Articles 91 - 97 of 97

Full-Text Articles in Neurology

Lead Activation Of A Developmentally Regulated Calcium Channel In Rat Hippocampal Nerve Terminals, Troy E. Rhodes Jul 1996

Lead Activation Of A Developmentally Regulated Calcium Channel In Rat Hippocampal Nerve Terminals, Troy E. Rhodes

Theses and Dissertations in Biomedical Sciences

Low level lead (Pb2+) exposure may produce lasting deficits in learning and memory by altering calcium (Ca2+) dependent processes. Isolated presynaptic nerve terminals from rat hippocampus were loaded with the intracellular (Ca2+) indicator Fura-2. The changes in cytoplasmic free calcium ([Ca2+]i) were measured by stopped-flow fluorescence spectroscopy following depolarization with elevated potassium on a millisecond time scale (Lentzner et al., 1992). Depolarization promoted a rapid increase in Ca2+i which occured in two kinetically distinguishable phases: a fast component, representing the activity of rapidly inactivating Ca2+ channels (τ …


Neuronal Toxicity Of Humoral Factors From Patients With Diabetic Neuropathy And Mechanism Of Neuronal Death On Cultured Adrenergic Neurons: Studies Of Autoimmune Pathogenesis In Diabetic Neuropathy, Dong Liu Jul 1996

Neuronal Toxicity Of Humoral Factors From Patients With Diabetic Neuropathy And Mechanism Of Neuronal Death On Cultured Adrenergic Neurons: Studies Of Autoimmune Pathogenesis In Diabetic Neuropathy, Dong Liu

Theses and Dissertations in Biomedical Sciences

Diabetic neuropathy is an extremely common medical problem because of the high frequency of diabetes and its complications. Diabetic neuropathy consists of not one, but many patterns of nerve injury, each potentially with its own discrete pathogenic mechanisms. Evidence is accumulating that indicates autoimmunity plays a role in diabetic peripheral neuropathy. However, the significance of immunopathogenesis of diabetic neuropathy is as yet unclear.

Using the N1E-115 mouse neuroblastoma cell line (NB) as a model of the adrenergic autonomic neuron, we found that sera of IDDM patients with neuropathy inhibit growth and differentiation of adrenergic neurons in culture (Pittenger et al, …


Identification And Characterization Of Mitochondrial Dna Variants In Alzheimer's Disease, Natasha Singh Hamblet Jul 1995

Identification And Characterization Of Mitochondrial Dna Variants In Alzheimer's Disease, Natasha Singh Hamblet

Theses and Dissertations in Biomedical Sciences

Alzheimer's Disease (AD) is a complex neurodegenerative disorder that affects a significant portion of the human population regardless of ethnicity or gender. A mitochondrial hypothesis of AD has been proposed based on a number of studies which establish altered oxidative phosphorylation (OXPHOS) and ATP synthesis in AD tissue. ATP demand is most prevalent in the brain; damage to OXPHOS could severely impair brain metabolism, thereby leading to a decline in cognitive function. Four out of five complexes in the OXPHOS pathway are partly encoded by mitochondrial DNA (mtDNA); thus, this may be a crucial site of lesions that alter brain …


An Analysis Of Mitochondrial Dna In Rett Syndrome And Other Neurodegenerative Disorders, Catherine Erickson Burgess Jan 1994

An Analysis Of Mitochondrial Dna In Rett Syndrome And Other Neurodegenerative Disorders, Catherine Erickson Burgess

Theses and Dissertations in Biomedical Sciences

Mitochondrial dysfunction resulting from mutations on mitochondrial DNA (mtDNA) is being recognized in a growing spectrum of diseases. These diseases, resulting from single base mutations, large deletions, or insertions, have been largely neuromuscular in origin. However, as an understanding of the effects of mtDNA mutations progresses, attention is now focusing on neurodegenerative diseases. Rett Syndrome (RS), a progressive neurodegenerative disease with predominantly female cases, demonstrates morphologic mitochondrial changes, mitochondrial enzyme deficiencies and maternal inheritance (characteristic of mtDNA diseases). No investigation of mtDNA involvement has been previously conducted and, to date, no biological marker exists for this disorder.

Our preliminary studies …


Transplantation Of The Mammalian Pineal Gland: Studies Of Survival, Revascularization, Reinnervation And Recovery Of Function, Wutian Wu Oct 1991

Transplantation Of The Mammalian Pineal Gland: Studies Of Survival, Revascularization, Reinnervation And Recovery Of Function, Wutian Wu

Theses and Dissertations in Biomedical Sciences

The survival, revascularization, reinnervation, and recovery of function of transplanted newborn rat pineal glands were studied following grafting into four different locations in pinealectomized rats. These locations were the third cerebral ventricle, in situ (where the pineal gland is normally located), the renal capsule, and the anterior chamber of the eye.

Pinealocytes in the grafts maintained high metabolic activity as evidenced by the presence of euchromatic nuclei, prominent nucleoli, infolded nuclear envelopes, numerous mitochondria and Golgi apparati, and relatively abundant endoplasmic reticulum and ribosomes. In addition, morphological correlates of two putative secretory processes were observed in the grafts. The first …


The Role Of Gaba In Reproductive Neuroendocrine Systems, Robert Carter Mcree Oct 1991

The Role Of Gaba In Reproductive Neuroendocrine Systems, Robert Carter Mcree

Theses and Dissertations in Biomedical Sciences

Local gamma-amino butyric acid (GABA) neurons in the hypothalamus can modulate the luteinizing hormone releasing hormone (LHRH) pulse generating system.

Two animal models (intact and ovariectomized rats) were used to determine the nature of modulation of LHRH release by GABA. The experiment determined the release of LHRH, serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) during two hormonal states with each model. In the intact rat the proestrus and estrus states were examined, and in the ovariectomized rat in-vitro release was determined with (OVX2) and without (OVX) estradiol treatment.

In-vivo experiments studied the effect of stimulation of GABA receptors …


Morphological And Physiological Examination Of A Demyelinating And Remyelinating Lesion, Paul Anson Felts Apr 1990

Morphological And Physiological Examination Of A Demyelinating And Remyelinating Lesion, Paul Anson Felts

Theses and Dissertations in Biomedical Sciences

Multiple sclerosis causes demyelination of central nerve fibers, and it is this pathology which results in most of the symptoms of the disease. The repair of the fibers by remyelination has been advanced as a potential symptomatic therapy, but at present the conduction properties of remyelinated central fibers are not well understood. In this study the conduction properties of Schwannian or oligodendrocyte remyelinated central nerve fibers have been determined. In addition, the status of the blood-brain barrier has been examined in lesions characterized by Schwann cell remyelination. These lesions chronically lack astrocytes, a cell believed to be involved in the …