The effect of magnetic field-exposure on the nervous system.
Item
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Title
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The effect of magnetic field-exposure on the nervous system.
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Identifier
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AAI3231949
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identifier
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3231949
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Creator
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Ahmed, Zaghloul.
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Contributor
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Adviser: Andrzej Wieraszko
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Date
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2006
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Language
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English
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Publisher
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City University of New York.
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Subject
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Biology, Neuroscience
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Abstract
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The influence of magnetic field exposure on the hippocampal-evoked potentials (PS), sciatic nerve compound action potentials (CAP), and animal behavior were studied. Two forms of magnetic field were mainly used: (1) the low intensity (15mT) low frequency (0.16Hz) so called pulsed magnetic field (PMF) and (2) repetitive trans-cranial magnetic stimulation (rTMS). The PMF induced effect was frequency dependent (tested only on CAP), and as its frequency varied from static to 0.5 Hz, respectively, its effect ranged from depression to amplification. The NMDA receptor antagonist did not block the PMFinduced amplification. However, PMF-induced epileptic field potential (EFP) and increased-spontaneous firing in the hippocampal slices were reduced by carbenoxolone (cbx), a gap junction blocker. When the absolute inhibition or facilitation of the second pulse was measured PPF and PPI were significantly increased. Expressed as a percentage of the initial pulse, there may not have been a change in the PPI or PPF. Antidromically evoked PS was increased in hippocampal slices following exposure to PMF and the PMF amplified sciatic nerve evoked CAP. Neither of the cbx, PKA and PKC inhibitors, nor the addition of free radical scavengers to the bath, had any effect on PMF-induced CAP amplification. In addition, PMF increased short-term depression (STD) significantly. Therefore, one interpretation of the data is that PMF shortened the recovery time of sodium channels from inactivation. It was also found that TEA, a potassium channel blocker, abolished the PMF effect on STD completely and reversed it to facilitation at longer inter-stimulus intervals. Elevated [K+] o blocked the PMF-induced CAP amplification, and potentiated the PMF effect on STD. The PMF reversed the action of TTX (10nM) and lidocaine (150muM), but not veratridine (100muM). Veratridine potentiated the effect of PMF on CAP2 inhibition but prevented the increase in CAP1. These results further showed, that PMF exposure changed the conformation of protein complexes of ion channels and transporters further modifying the ionic concentration surrounding the cell membrane and leading to long-term nervous system excitability. In behavioral experiments, PMF impaired the memory and learning processes of mice by inducing a masking effect that superseded the synaptic plasticity needed for these processes to take place. The rTMS had a similar effect at low frequencies (1 to 8 Hz) on memory and learning in mice. At a higher (15Hz) frequency, rTMS facilitated these processes when animals were tested immediately after application, but worsened when they were tested later. (Abstract shortened by UMI.).
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Type
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dissertation
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Source
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PQT Legacy CUNY.xlsx
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degree
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Ph.D.
