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Unilateral intrahippocampal microinjection of the nitric oxide (NO) donor, sodium nitroprusside (33 nmol in 1 microliter), in the rat resulted in a marked degeneration of the ipsilateral hippocampal formation characterised by a virtual absence of pyramidal cells and dentate granule cells. Damage was not observed contralateral to the injection site. Quinolinic acid (100 nmol in 1 microliter) also produced neuronal damage within the ipsilateral hippocampus although the lesion was considerably smaller and more discrete than that caused by sodium nitroprusside. Injection of equimolar amounts of potassium ferricyanide failed to mimic the neurotoxic effects of sodium nitroprusside suggesting that NO is responsible specifically for the neuronal damage observed. |
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