Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.26.9 (ribonuclease)
 6,589 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of neonatal nicotine exposure on the development of nicotinic acetylcholine receptor (nAChR) alpha2, alpha3, alpha4, alpha7, and beta2 subunit mRNAs and the number of nAChR isoforms in rat brain were studied. The mRNA levels for nAChR subunits were measured by ribonuclease protection assay, and the number of nAChR isoforms was measured with (-)-[3H]nicotine, [3H]epibatidine, and alpha-[3H]bungarotoxin ([3H]alpha-Bgt). Pups were divided into two groups: One group received (-)-nicotine treatment (0.1 mg/kg s.c. free base twice per day) during postnatal day (P)1 to P21 and the other during P8 to P16. The period from P8 to P16 was chosen due to persistent changes that occur in brain nAChRs and in the behavior of adult mice that received (-)-nicotine treatment during P10 to P16. (-)-Nicotine exposure from P1 to P21 significantly up-regulated the number of [3H]epibatidine and high-affinity (-)-[3H]nicotine binding sites in most of the brain regions studied but did not influence the number of [3H]alpha-Bgt binding sites. This effect was a transient one: The up-regulated binding sites returned to control level 1 week after withdrawal from nicotine. (-)-Nicotine exposure during P8 to P16 resulted in a significant and long-lasting increase in the number of nAChR isoforms labeled by (-)-[3H]nicotine, but not by [3H]epibatidine, in the cortex, hippocampus, and striatum of adult rat. This treatment converted the low-affinity binding sites of (-)-nicotine into a high-affinity state revealed by the competition studies of (-)-[3H]nicotine/(-)-nicotine. No changes in the mRNA levels of the subunits studied were observed following nicotine treatment during these two periods. These results suggest that the second postnatal week is a critical period during which nicotine treatment can induce permanent effects on the nAChRs in rat brain. The underlying mechanisms involved in the up-regulation of the number of nAChRs observed in this study are posttranscriptional.
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PMID:Nicotine exposure during a critical period of development leads to persistent changes in nicotinic acetylcholine receptors of adult rat brain. 945 71

Interactions between neurotrophic factors and neurotransmitters participate in the formation and maintenance of appropriate connections, as well as in neurodegenerative processes. Here we have measured changes in the developmental expression pattern of BDNF and NT-3 in the striatum, cortex, and substantia nigra induced by intrastriatal injection of the N-methyl-d-aspartate glutamate receptor agonist quinolinic acid (QUIN). Animals were injected at different postnatal ages, and BDNF and NT-3 mRNA levels were determined 6 h after lesion using a ribonuclease protection assay. Our results show a biphasic increase in BDNF mRNA levels in striatum and in the ipsilateral cortex at postnatal day (P)5 and P21. In contrast, although NT-3 expression did not change in the striatum, it was down-regulated in the ipsilateral cortex at P5 and P30. Intrastriatal QUIN injection did not induce changes in either BDNF or NT-3 expression in the ipsilateral substantia nigra. These findings show that neurotrophin expression is developmentally regulated after excitotoxic injury, which suggests that this endogenous response may be involved in different neuronal maturation and vulnerability during development.
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PMID:Developmental regulation of BDNF and NT-3 expression by quinolinic acid in the striatum and its main connections. 1096 90

Although brain injury induced by undernutrition during early life is well described, the mechanisms that mediate the effects of undernutrition on brain development are not known. IGF-I plays an important role in the stimulation of postnatal somatic and brain growth. We have shown that IGF-I overexpression in brain ameliorates the effects of undernutrition on early postnatal brain growth, and thus, we postulated that alterations in IGF-I expression or action mediate the pathogenesis of malnutrition-induced brain injury. To begin to address this issue we evaluated the influence of undernutrition on brain IGF-I expression during early postnatal development in mice. Undernutrition was induced in mice by separating half of the pups in each litter from their lactating dams for a defined period each day. Pups were killed at postnatal day (P) 7, P14, P21, and P28. The changes in IGF-I mRNA were quantified by ribonuclease protection assay. At P7 IGF-I mRNA abundance in undernourished animals was increased in cerebral cortex (223% of controls), but decreased in diencephalon (36% of controls). At P14, IGF-I mRNA abundance was increased in diencephalon (230% of controls). Although there were no other statistically significant alterations of IGF-I mRNA in undernourished mice, IGF-I abundance in the cerebral cortex appeared increased at P14 (142% of controls), and in cerebellum it was consistently but modestly decreased (78 and 59% of controls) from P7 to P21, respectively. We conclude that nutrition regulates murine brain IGF-I expression in a developmentally specific fashion that is dependent on the region of expression. Importantly, the influence of undernutrition on IGF-I expression is markedly different in the brain than in liver, where nutritional deficiency profoundly decreases IGF-I expression. We speculate that the relative preservation of or increases in regional brain IGF-I expression explain, at least in part, the well-known finding that undernutrition during early postnatal development has less marked growth-retarding effects on the brain than it does on the soma.
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PMID:Nutritional regulation of IGF-I expression during brain development in mice. 1115 13