Involvement of Nitric Oxide in Ischemia-Evoked Taurine Release in the Mouse Hippocampus
The novel type of neurotransmitter/neuromodulator nitric oxide (NO) is linked to the activation of the N-methyl-D-aspartate (NMDA) class of glutamate receptors and has been shown to modify transmitter release in the brain1. The synaptically released glutamate activates postsynaptic NMDA receptors and depolarizes the cell, allowing Ca2+to enter through the receptor-linked ion channels, activating the Ca2+-dependent enzyme, NO synthase (NOS)2. The NO formed may either act intercellularly or diffuse out of the cell and act extracellularly at the soluble guanylyl cyclase, enhancing the formation of 3’,5’-cyclic guanosine monophosphate (cGMP)3. NO affects neurotransmitter transport in different brain areas, e.g., by evoking the release of monoamines, GABA5 and glutamate6. On the other hand, inhibitory effects have been observed in dopamine7, GABA8 and glutamate release9, indicating that the actions of NO are apparently complex.
KeywordsNitric Oxide Nitric Oxide Sodium Nitroprusside Hippocampal Slice Soluble Guanylyl Cyclase
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