Neuroscience
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The ability of MK-801, a non-competitive N-methyl-D-aspartate receptor antagonist, to protect neurons in the cerebral cortex from injury induced by prolonged electrical stimulation was assessed in cats. Platinum disc electrodes 8.0 mm in diameter and with a surface area of 0.5 cm2 were implanted in the subdural space over the parietal cortex. Ten days after implantation of the electrodes, all animals received continuous stimulation for 7 h using charge-balanced, cathodic-first, controlled current pulses with a charge density of 20 microC/cm2 and a charge/phase of 10 microC/phase. ⋯ Thus prolonged electrical stimulation can be added to the list of neuropathologic conditions which involve glutamate-induced excitotoxic damage via the N-methyl-D-aspartate receptor. The results also support the hypothesis of neuronal hyperactivity as a principal cause of electrically-induced injury in the central nervous system. The implications for design of protocols for functional electrical stimulation are discussed.
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The present study investigated the effects of the presence of the serotonin uptake inhibitor citalopram in the perfusion medium on pharmacological manipulations which increased and decreased striatal serotonin release using in vivo microdialysis. A high performance liquid chromatography detection system equipped with a microbore column was used which reduced the detection limit to 0.5 fmol serotonin/5 microliters sample and enabled basal striatal serotonin release to be measured without the addition of a serotonin uptake inhibitor to the perfusion medium. Although serotonin uptake inhibitors have frequently been used to enhance the serotonin content of dialysate samples, the effects of the presence of serotonin uptake inhibitors on pharmacological manipulations which increased and decreased the release of serotonin have not yet been characterized. ⋯ In addition, citalopram dramatically prevented the four-fold increase in the release of serotonin produced by the systemic administration of the serotonin-releasing agent fenfluramine. The blockade of fenfluramine's effects by citalopram supports the hypothesis that transport of fenfluramine into serotonergic neurons is necessary to increase serotonin release. This study demonstrates that the use of an HPLC detection system equipped with a microbore column can reliably measure basal serotonin release using in vivo microdialysis.(ABSTRACT TRUNCATED AT 250 WORDS)