Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.99.3 (diaphorase)
 5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to systematically investigate differences in gene expression between sleep and waking, mRNA differential display was used to examine mRNAs from the cerebral cortex of rats who had been spontaneously asleep, spontaneously awake, or sleep deprived for a period of 3 h. It was found that, while the vast majority of transcripts were expressed at the same level among these three conditions, the expression of a subset of mRNAs was modulated by sleep and waking. Half of these transcripts had known sequences in databases. RNAs expressed at higher levels during waking included those for the transcription factors c-fos, NGFI-A, and rlf, as well as three transcripts encoded by the mitochondrial genome, those for subunit I of cytochrome c oxidase, subunit 2 of NADH dehydrogenase, and 12S rRNA. As shown by in situ hybridization, the level of RNAs encoded by the mitochondrial genome was uniformly higher during waking in many cortical regions and in several extracortical structures. By contrast, mRNA levels corresponding to two mitochondrial protein subunits encoded by the nuclear genome were unchanged. This finding suggests the hypothesis that an increase in the level of mitochondrial RNAs may represent a rapid regulatory response of neural tissue to adapt to the increased metabolic demand of waking with respect to sleep.
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PMID:Differences in gene expression between sleep and waking as revealed by mRNA differential display. 960 59

Nitric oxide (NO) is a molecular messenger involved in several events of synaptic plasticity in the central nervous system. Ca2+ influx through the N-methyl-D-aspartate receptor (NMDAR) triggers the synthesis of NO by activating the enzyme neuronal nitric oxide synthase (nNOS) in postsynaptic densities. Therefore, NMDAR and nNOS are part of the intricate scenario of postsynaptic densities. In the present study, we hypothesized that the intracellular distribution of nNOS in the neurons of superior colliculus (SC) superficial layers is an NMDAR activity-dependent process. We used osmotic minipumps to promote chronic blockade of the receptors with the pharmacological agent MK-801 in the SC of 7 adult rats. The effective blockade of NMDAR was assessed by changes in the protein level of the immediate early gene NGFI-A, which is a well-known NMDAR activity-dependent expressing transcription factor. Upon chronic infusion of MK-801, a decrease of 47% in the number of cells expressing NGFI-A was observed in the SC of treated animals. Additionally, the filled dendritic extent by the histochemical product of nicotinamide adenine di-nucleotide phosphate diaphorase was reduced by 45% when compared to the contralateral SC of the same animals and by 64% when compared to the SC of control animals. We conclude that the proper intracellular localization of nNOS in the retinorecipient layers of SC depends on NMDAR activation. These results are consistent with the view that the participation of NO in the physiological and plastic events of the central nervous system might be closely related to an NMDAR activity-dependent function.
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PMID:NMDA receptor blockade alters the intracellular distribution of neuronal nitric oxide synthase in the superficial layers of the rat superior colliculus. 1927 47