Brain research
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The purpose of this study was to determine the optimal stimulation site and parameters that result in the greatest changes in cutaneous blood flow during dorsal column stimulation (DCS). Laser Doppler flowmetry was used to assess cutaneous blood flow changes in both rat hindpaws during DCS with a unipolar ball electrode. We found that stimulating the dorsal column at the L2 spinal segment at 0.6 mA at either 25 or 50 Hz with a pulse duration of 0.2 ms resulted in the largest cutaneous blood flow increases in the rat hindpaw. In addition, the DCS response appeared to be limited primarily to the hindpaw ipsilateral to the site of DCS.
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The physiological model for glutamate receptor mediated excitotoxicity entails elevation of intraneuronal calcium levels. Excessive activation of the NMDA receptor leads to excitotoxicity by prolonged calcium influx via its calcium channel. The purpose of this research was to examine the mechanism of non-NMDA glutamate receptor mediated excitotoxicity. ⋯ AMPA receptors appear to result in excitotoxic damage via glutamate release. Glutamate opens NMDA receptor calcium channels which increases intraneuronal calcium levels. Kainate receptors probably mediate excitotoxicity via direct calcium conductance with glutamate release being important in the CA1 area and neocortex.
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Two experiments were performed to investigate the relationship between the expression of sodium appetite and the appearance of Fos-like immunoreactivity (Fos-IR) in the brain of rats. In the first experiment, rats were depleted of sodium by treatment with furosemide 24 h prior to sacrifice and without access to either food or sodium solution. Some rats had access to distilled water, and others had no fluids available during the 24 h. ⋯ Both Fos-IR and fluid intake were antagonized by administration of losartan, an angiotensin II type 1 receptor antagonist. Thus, only the circumventricular organs of the lamina terminalis showed Fos-IR during each natriorexigenic regimen in these studies. These data support the view that Ang II of both central and peripheral origin activates the SFO and/or peri-OVLT region and contributes to sodium appetite.