Literature DB >> 9762705

Ribonuclease improves the state of hippocampal sections in the post-ischemic period.

I E Kudryashov1, I V Kudryashova, V V Raevskii.   

Abstract

Living hippocampal slices from Wistar rats were used to study the dynamics of changes in population electrical responses in field CA1 to electrical stimulation of Shaffer collaterals during the development of ischemia (imposed by exclusion of oxygen and glucose from the perfusion solution). These studies showed that during ischemia, addition of ribonuclease (a blocker of protein synthesis) to the perfusion solution resulted in a significantly smaller increase in the latent period of the response and slowed the onset of the reduction in the amplitude of the evoked potential, and promoted faster recovery of the response after the ischemia session ended. It is suggested that the reduction in protein synthesis due to ribonuclease preserved energy reserves in the nerve tissue, which in turn promoted more complete recovery of neuron function in the post-ischemic period.

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Year:  1998        PMID: 9762705     DOI: 10.1007/bf02464788

Source DB:  PubMed          Journal:  Neurosci Behav Physiol        ISSN: 0097-0549


  47 in total

1.  Single glutamate channels in CA1 pyramidal neurones after transient ischaemia.

Authors:  H Tsubokawa; K Oguro; H P Robinson; T Masuzawa; N Kawai
Journal:  Neuroreport       Date:  1995-02-15       Impact factor: 1.837

2.  Protein synthesis and energy metabolism in hippocampal slices during extended (24 hours) recovery following different periods of ischemia.

Authors:  B Djuricic; R Berger; W Paschen
Journal:  Metab Brain Dis       Date:  1994-12       Impact factor: 3.584

3.  Temporal profiles of accumulation of amyloid beta/A4 protein precursor in the gerbil after graded ischemic stress.

Authors:  H Tomimoto; H Wakita; I Akiguchi; S Nakamura; J Kimura
Journal:  J Cereb Blood Flow Metab       Date:  1994-07       Impact factor: 6.200

4.  Hippocampal slices: glutamate overflow and cellular damage from ischemia are reduced by sodium-channel blockade.

Authors:  C P Taylor; S P Burke; M L Weber
Journal:  J Neurosci Methods       Date:  1995-06       Impact factor: 2.390

5.  PAF antagonist, BN52021, inhibits [3H]D-aspartate release after ischaemia in vitro.

Authors:  B Zabøocka; K Domańska-Janik
Journal:  Neuroreport       Date:  1994-12-30       Impact factor: 1.837

6.  Cycloheximide and actinomycin D block the toxic effect of glutamic acid on PC12 cells.

Authors:  R Serghini; P Froissard; B Sola; D Duval
Journal:  Neuroreport       Date:  1994-12-30       Impact factor: 1.837

7.  Induction of heat shock protein 70 and glial fibrillary acidic protein in the postischemic gerbil hippocampus.

Authors:  T Araki; H Kato; X H Liu; K Kogure; Y Itoyama
Journal:  Metab Brain Dis       Date:  1994-12       Impact factor: 3.584

8.  A selective N-type Ca(2+)-channel blocker prevents CA1 injury 24 h following severe forebrain ischemia and reduces infarction following focal ischemia.

Authors:  A M Buchan; S Z Gertler; H Li; D Xue; Z G Huang; K E Chaundy; K Barnes; H J Lesiuk
Journal:  J Cereb Blood Flow Metab       Date:  1994-11       Impact factor: 6.200

9.  Effect of the non-NMDA receptor antagonist GYKI 52466 on the microdialysate and tissue concentrations of amino acids following transient forebrain ischaemia.

Authors:  B Arvin; D Lekieffre; J L Graham; C Moncada; A G Chapman; B S Meldrum
Journal:  J Neurochem       Date:  1994-04       Impact factor: 5.372

10.  Complete cerebral ischemia with short-term survival in rats induced by cardiac arrest. I. Extracellular accumulation of Alzheimer's beta-amyloid protein precursor in the brain.

Authors:  R Pluta; E Kida; A S Lossinsky; A A Golabek; M J Mossakowski; H M Wisniewski
Journal:  Brain Res       Date:  1994-06-27       Impact factor: 3.252

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