Significantly reduced activities of glutamine synthetase (GS), which is predominantly present in glial cells, occur in the early stage of congenital hydrocephalic rat (LEW-HYR) brain development. GS activity is reported to be related to brain dysfunction. The effect of ventriculoperitoneal (VP) shunt on the suppression of GS activity was studied in the LEW-HYR. VP shunting improved the attenuation of GS activity in the LEW-HYR and the response of GS activity to methionine sulfoximine (a competitive GS inhibitor) treatment was similar to that seen in normal siblings. However, no enhancement of GS activity by hydrocortisone could be detected, although this enhancement occurs in the normal siblings. These results suggest that VP shunting is not completely effective in improving the suppression of brain GS activity in the LEW-HYR, since the suppression of GS activity in the LEW-HYR might be programmed genetically.

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http://dx.doi.org/10.2176/nmc.37.663DOI Listing

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In order to evaluate the appearance of brain bcl-2 during development of the hydrocephalus, we measured levels of bcl-2 mRNA in the cortex and cerebellum of congenital hydrocephalic rats (LEW-HYR) at 1 and 2 weeks after birth using the quantified reverse transcriptase-polymerase chain reaction (RT-PCR) with TaqMan fluorogenic detection system. Normal and hydrocephalic siblings were killed 7 and 14 days after birth, and their cortices and cerebella were homogenized with the Isogen-chloroform mixtured solution. By means of the RT-PCR with genetic analyzer, the sequence of bcl-2 mRNA detected in the LEW-HYR was identified to be the same as that of the registered rat brain (L14680).

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Significantly reduced activities of glutamine synthetase (GS), which is predominantly present in glial cells, occur in the early stage of congenital hydrocephalic rat (LEW-HYR) brain development. GS activity is reported to be related to brain dysfunction. The effect of ventriculoperitoneal (VP) shunt on the suppression of GS activity was studied in the LEW-HYR.

View Article and Find Full Text PDF

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