Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P00492 (hypoxanthine-guanine phosphoribosyltransferase)
 2,385 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats treated as neonates with 6-hydroxydopamine are proposed to model the dopamine deficiency associated with Lesch-Nyhan syndrome (LNS). To understand the neurobiological basis of specific behaviors in LNS, investigations were undertaken in these neonatally lesioned rats. Several new findings resulted from these studies. The first was that D1-dopamine receptors are essential for the action of D2-dopamine receptors, a phenomenon called "coupling" of receptor function. Another finding was that D1-dopamine receptors must be repeatedly stimulated before maximal behavioral sensitivity can be observed. This has been referred to as "priming" of D1-dopamine receptor responsiveness. This priming action by repeated administration of a D1-dopamine agonist was antagonized by NMDA antagonists indicating a potential role of glutamate in this sensitization. Ongoing work suggests that DARPP-32 is not involved in priming of D1-dopamine receptor responsiveness. However, we have observed an accumulation of GFAP in brain following repeated administration of a D1-dopamine agonist. In addition, immunoblots employing an antibody to phospho-DARPP-32 revealed a protein present in lesioned rats that was not present in control rats. Studies in these lesioned rats are expected to continue to contribute to our basic understanding of adaptive changes caused by lesioning of dopaminergic neurons during development.
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PMID:Neonatal destruction of dopaminergic neurons. 809 Mar 54

Reference genes are often used to normalize expression of data from real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR), and only a validation of their stability during a given experimental paradigm leads to reliable interpretations. The present study was thus designed to validate potential reference genes in a mouse model of mesiotemporal lobe epilepsy (MTLE) with focal seizures after unilateral intrahippocampal injection of kainate (KA). Ipsilateral and contralateral hippocampi were removed during nonconvulsive status epilepticus (5 hr), epileptogenesis (7 days), and the chronic period of recurrent focal seizures (21 days). Naive animals were equally studied. The stability of eight potential reference genes (hypoxanthine phosphoribosyltransferase, Hprt1; peptidylprolyl isomerase A, Ppia; TATA box binding protein, Tbp; beta-actin, Actb; acidic ribosomal phosphoprotein P0, Arbp; glyceraldehyde-3-phosphate dehydrogenase, Gapdh; ribosomal RNA 18S, 18S rRNA; and glucuronidase beta, Gusb) were determined using geNorm and NormFinder software. The first five (Hprt1, Ppia, Tbp, Actb, and Arbp) were found to be stable across the different phases of the disease and appeared adequate for normalizing RT-qPCR data in this model. This was in contrast to the other three (18S rRNA, Gapdh, and Gusb), which showed unstable expressions and should be avoided. The analysis of KA-induced changes in the expression of glial fibrillary acidic protein (Gfap) gene resulted in various relative expressions or even a completely different pattern when unstable reference genes were used. These results highlight the absolute need to validate the reference genes for a correct interpretation of mRNA quantification.
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PMID:Selection of reference genes for real-time quantitative reverse transcription-polymerase chain reaction in hippocampal structure in a murine model of temporal lobe epilepsy with focal seizures. 1993 10