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In some central systems, excitatory postsynaptic potential (EPSP) amplitude increases substantially during repetitive synaptic stimulation ("frequency potentiation"), as does the probability of spike generation. An apparently analogous phenomenon at the neuromuscular junction ("frequency facilitation") depends on residual Ca2+ in nerve terminals. However,(More)
There is increasing evidence that experimental interventions that alter adrenal corticosteroid plasma concentrations can modulate aging changes in the rodent hippocampus. However, there still is very little evidence that elevation of endogenous corticosteroid levels within physiological ranges, such as occurs during chronic stress, can accelerate(More)
Animal models of neuronal injury can be used to explore mechanisms that regulate the expression of genes coding for cytoskeletal proteins and transmitter-related markers. In the present study, in situ hybridization was used to measure levels of messenger ribonucleic acid (mRNA) encoding each of the neurofilament subunits and beta-tubulin in spinal motor(More)
Synaptic vesicles were quantified 20 min after the induction of long-term potentiation (LTP) in the Schaffer-commissural system of the hippocampus. With LTP, significant increases were found in vesicles attached to the active zone membrane, and in the percentage of vesicles adjacent to the active zone. In addition, as others have reported, overall vesicle(More)
Lesions of the fimbria-fornix (FF) have been reported to cause retrograde changes in neurons of the medial septal nucleus (MSN). To analyze the nature and time course of these events, we investigated changes in cytoskeletal elements (phosphorylated and non-phosphorylated neurofilament (NF) proteins) and transmitter-related enzymes (choline acetyltransferase(More)
Cholinergic neurons in the basal forebrain magnocellular complex (BFMC) respond to nerve growth factor (NGF) during development and in adult life, and it has been suggested that the administration of NGF might ameliorate some of the abnormalities that occur in neurological disorders associated with degeneration of this population of neurons. A prerequisite(More)
The present study tested aspects of a novel etiological/pathogenetic hypothesis of Alzheimer's disease (AD), which proposes that alterations in endocrine regulation of peripheral calcium/phosphate (Ca/PO4) homeostasis (e.g., by glucocorticoids, vitamin D, etc.) induce and/or reflect altered calcium homeostasis and neurotoxicity in brain neurons. Two key(More)
Experimental lesions have been widely used to induce neuronal degeneration and to test the ability to trophic molecules to prevent lesion-induced alterations, but these studies have not demonstrated unequivocally that afflicted neurons die as a result of these manipulations. The documentation of neuronal death in the above-described models and the time when(More)
Technical complexities associated with studies of defined synapses in the mammalian CNS have made it difficult to determine whether CNS synaptic vesicles respond to repetitive monosynaptic activation in the same ways as do PNS vesicles. Moreover, even in the PNS, the specific ultrastructural correlates of short-term synaptic potentiation are not well(More)
The pathologic diagnosis of Alzheimer's disease (AD) rests upon the identification of senile plaques and neurofibrillary tangles (NFT) in brain tissue. Methods for staining these structures vary in their sensitivity. Six different silver stains and immunocytochemistry for the beta-amyloid (A beta) peptide were compared for sensitivity in staining of plaques(More)