Gene/Protein Disease Symptom Drug Enzyme Compound
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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

These studies were performed to determine the developmental expression pattern of neurotrophic factor (NTF: nerve growth factor (betaNGF), brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), ciliary neurotrophic factor (CNTF), neurotrophin-3 (NT-3) and NT-4 mRNA and NGF, NT-3 and NT-4 protein in the urinary bladder of the postnatal Wistar rat. It was hypothesized that NTFs may contribute to the development of the spinobulbospinal micturition reflex that represents the adult micturition pattern. Changes in NTF mRNA or protein expression in the urinary bladder at the time of development of the mature micturition reflex (postnatal days (P) 16-18) may suggest an involvement of target-derived NTFs in this maturation process. Developmental ages, prior to (P5, P10, P15) or following (P20, P30, adult P90) the development of the spinobulbospinal micturition reflex were selected and the urinary bladder was analyzed for levels of neurotrophic factor mRNA or protein. Results from ribonuclease protection assays demonstrated a similar developmental pattern among each neurotrophic factor examined. Neurotrophic factor mRNA levels increased by P10 and reach a maximum by P15. Subsequently, NTF mRNA levels declined to adult levels that were less than the earliest postnatal time examined (P5). NTF mRNA expression was significantly (p</=0.05-0.001) greater at P10, P15, P20 and P40 (NT-4 mRNA) compared to adult levels for each NTF examined except GDNF mRNA. In general, NGF, NT-3 and NT-4 urinary bladder protein levels in early postnatal development, as determined by ELISA, were similar when compared to the corresponding mRNA expression. Differences in the correlation between NT-3 and NT-4 mRNA and protein expression were demonstrated in the adult urinary bladder where significantly (p</=0. 001) greater levels of protein were revealed despite relatively low abundance of NT-3 and NT-4 mRNA. The developmental expression pattern (maximum expression at the second to third postnatal week) of NTFs in the urinary bladder is consistent with a potential role in the development of the spinobulbospinal reflex. Relatively high expression of NT-3 and NT-4 protein in the adult urinary bladder suggests a potential importance of these factors in the adult lower urinary tract.
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PMID:Developmental expression of urinary bladder neurotrophic factor mRNA and protein in the neonatal rat. 1067 71

Hypothyroidism has devastating consequences on brain development. While the mechanisms that mediate these effects are not known, several lines of evidence suggest that a reduction in insulin-like growth factor-I (IGF-I) expression and/or action has a role. To assess whether reduced IGF-I expression and/or actions mediates the brain pathology of congenital hypothyroidism, we induced hypothyroidism by treating pregnant mice and lactating dams with 0. 1% propylthiouracil (PTU) in drinking water. Control and PTU-treated pups were sacrificed on postnatal day (P) 7, 10 and 14, and IGF-I mRNA expression was assessed in the cerebral cortex and cerebellum by ribonuclease protection assay. To control for mRNA loading, the signal of IGF-I protected bands was normalized to those for cyclophillin. IGF-I mRNA expression in hypothyroid animals was decreased significantly in cortex at P10 and P14 (42 and 60%, respectively). In the cerebellum, IGF-I mRNA expression was down-regulated at all ages studied, but the decrease was only statistically significant at P7 (31% decreased). We conclude that hypothyroidism alters IGF-I expression in the developing brain. Furthermore, we speculate that IGF-I plays a role in mediating some thyroid hormone actions during brain development.
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PMID:Effects of hypothyroidism on insulin-like growth factor-I expression during brain development in mice. 1102 43

The capacity of the central nervous system for axonal growth decreases as the age of the animal at the time of injury increases. Changes in the expression of neurotrophic factors within embryonic and early postnatal spinal cord suggest that a lack of trophic support contributes to this restrictive growth environment. We examined neurotrophic factor gene profiles by ribonuclease protection assay in normal neonate and normal adult spinal cord and in neonate and adult spinal cord after injury. Our results show that in the normal developing spinal cord between postnatal days 3 (P3) and P10, compared to the normal adult spinal cord, there are higher levels of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), and glial-derived neurotrophic factor (GDNF) mRNA expression and a lower level of ciliary neurotrophic factor (CNTF) mRNA expression. Between P10 and P17, there is a significant decrease in the expression of NGF, BDNF, NT-3, and GDNF mRNA and a contrasting steady and significant increase in the level of CNTF mRNA expression. These findings show that there is a critical shift in neurotrophic factor expression in normal developing spinal cord between P10 and P17. In neonate spinal cord after injury, there is a significantly higher level of BDNF mRNA expression and a significantly lower level of CNTF mRNA expression compared to those observed in the adult spinal cord after injury. These findings suggest that high levels of BDNF mRNA expression and low levels of CNTF mRNA expression play important roles in axonal regrowth in early postnatal spinal cord after injury.
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PMID:Differences in neurotrophic factor gene expression profiles between neonate and adult rat spinal cord after injury. 1135 54