Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Binge-like ethanol exposure on postnatal day (PN) 4 induces a concentration dependent loss of Purkinje cells in the rat cerebellum. The mechanism of this ethanol-induced Purkinje cell vulnerability is not presently understood. Nevertheless, the specific timing of this vulnerability leads us to consider the neurotrophin system crucial to the regulation of neuronal development. Differentiation, maturation, and survival of Purkinje cells are shown to involve an intimate interaction between brain-derived nerve growth factor (BDNF) and neurotrophin-3 (NT3) acting primarily through their specific tyrosine-kinase (Trk) receptors. We believe that the specific ethanol vulnerability, and the timing of this vulnerability result from alterations in the BDNF-NT3 interplay. We hypothesize that disruption of TrkB and/or TrkC mediated neurotrophin communication is, in part, responsible for the ethanol-induced loss of Purkinje cells during development. The current study was undertaken to define the impact of ethanol exposure at the onset of ethanol vulnerability on the relative concentrations of mRNA encoding the neurotrophic factor receptors TrkB and TrkC. The reverse transcriptase (RT) polymerase chain reaction (PCR) amplification technique was used to identify the relative expression levels of mRNA specific to these receptors as well as the truncated TrkB receptor isoforms. We identify a specific decrease in overall TrkB receptor mRNA expression that is primarily a function of the TrkB-T2 receptor isoform. Concurrent decreases in mRNA specific to BDNF were also identified. No significant alterations to the expression of TrkC mRNA were found indicating that ethanol-exposure appears to act selectively on the BDNF communication system.
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PMID:Early postnatal ethanol exposure selectively decreases BDNF and truncated TrkB-T2 receptor mRNA expression in the rat cerebellum. 1153 37

Noise, ototoxic substances and various genetic factors are common causes of profound hearing loss. Cochlear implants can often restore hearing in these cases, but only if a sufficient number of responsive auditory nerve fibers remain. Over time, these nerve fibers degenerate in the damaged ear, and it is therefore important to establish factors that control neuronal survival and maintain neural excitability. Recent studies show that neuregulins and their receptors are important for survival and proper targeting of neurons in the developing inner ear. A role for neuregulins as maintainers of the neuronal population in the mature inner ear was therefore hypothesized. Here, this hypothesis was directly tested by chronic local application of substances that block neuregulin receptors. Using auditory brainstem response measurements, we demonstrate that such receptor block leads to a progressive hearing impairment that develops over the course of weeks. This impairment occurs despite a normal number of auditory neurons and preserved outer hair cell function. Real-time quantitative reverse transcriptase-polymerase chain reaction shows alterations in neurotrophin-3 expression, suggesting that this growth factor participates in regulating cochlear sensitivity. The present work demonstrates the critical importance of neuregulin/erbB signaling in long-term functional regulation in the mature guinea pig hearing organ.
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PMID:Signaling through erbB receptors is a critical functional regulator in the mature cochlea. 2067 12

We evaluated the feasibility of external epineurial splinting as a way of alleviating tension caused by sutures in the reconstruction of peripheral nerve injuries, utilizing Wistar rat median nerve injury on 40 animals, in four experimental groups with 10 animals on each surgical setting. The nerve regeneration outcomes of four surgical procedures were compared: 1) primary end-to-end sutures (EES); 2) alleviated tension sutures (ATS) with a removal of 7 mm nerve segment, namely external epineurial splinting, utilizing a polypropylene mesh as a protective scaffold; 3) sutures under tension with a 7 mm gap between nerve stumps; and 4) sham (C) (n = 10 animals). Regeneration of the median nerve postneurorrhaphy was followed by means of functional evaluations, including time to first day of finger flexion recovery, and grasp strength; quantification of atrophy of the flexor pronator muscle group; and mRNA expression of nerve growth factor and neurotrophin-3 by polymerase chain reaction-reverse transcriptase. Similar, significant median nerve regeneration was observed in the EES-treated and ATS-treated groups, relative to controls. The EES and ATS surgical procedures methods demonstrated important similar results considering functional and molecular biology analysis of the median nerve injury.
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PMID:The mesh repair: tension free alternative on dealing with nerve gaps-experimental results. 2226 3


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