Cerebral ischemia in gerbils: polyribosomal function during progression and recovery.

Morimoto, Kazuyoshi; Yanagihara, Takehiko

doi:10.1161/01.str.12.1.105

Cited by 47 publications

(16 citation statements)

References 22 publications

(21 reference statements)

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“…The stability of polyribosome integrity during the ischemic period (as evidenced by unchanged in vitro activity in these studies) is in keeping with that observed in other models of complete ischemia (Kleihues and Hossmann, 1971 ;Cooper et al, 1977), and we have demonstrated stable incorporation through at least 1 h following decapitation (Nowak et al, 1984). This is in contrast to unilateral ischemia in the gerbil, which may result in less than complete cessation of blood flow and that generally leads to a progressive loss of polysome aggregation with time (Yanagihara, 1978;Morimoto and Yanagihara, 1981).…”

Section: Discussionmentioning

confidence: 99%

“…The effects of experimental ischemia on various aspects of brain biochemistry have been investigated using a number of animal models. In contrast to the relatively rapid recovery of most measures of brain energy status following transient ischemia (Ljunggren et al, 1 9 7 4~;Kobayashi et al, 1977), brain protein synthesis has been shown to return relatively slowly to control levels, using experimental protocols involving cats, rats, and gerbils (Kleihues and Hossmann, 1971;Cooper et al, 1977;Dienel et al, 1980;Morimoto and Yanagihara, 1981). The evidence is consistent with a deficit in protein synthesis initiation arising from the ischemic episode, although the mechanism responsible for this effect remains unknown.…”

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confidence: 99%

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Changes in Brain Energy Metabolism and Protein Synthesis Following Transient Bilateral Ischemia in the Gerbil

Nowak

Fried

Lust

et al. 1985

Journal of Neurochemistry

178

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The time course of the reduction in brain protein synthesis following transient bilateral ischemia in the gerbil was characterized and compared with changes in a number of metabolites related to brain energy metabolism. The recovery of brain protein synthesis was similar following ischemic periods of 5, 10, or 20 min; in vitro incorporation activity of brain supernatants was reduced to approximately 10% of control at 10 or 30 min recirculation, showed slight recovery at 60 min, and returned to 60% of control activity by 4 h. Protein synthesis activity was indistinguishable from control at 24 h. One minute of ischemia produced no detectable effect on protein synthesis measured after 30 min reperfusion; longer periods of ischemia resulted in progressive inhibition, with 5 min producing the maximal effect. Pentobarbital (50 mg/kg) increased by 1-2 min the threshold ischemic duration required to produce a given effect. Whereas most metabolites recovered quickly following 5 min ischemia, glycogen showed a delayed recovery comparable to that seen for protein synthesis. These results are discussed in relation to possible mechanisms for the coordinate regulation of brain energy metabolism and protein synthesis. An improved method for the fluorimetric measurement of guanine nucleotides is described.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Changes in Brain Energy Metabolism and Protein Synthesis Following Transient Bilateral Ischemia in the Gerbil

Nowak

Fried

Lust

et al. 1985

Journal of Neurochemistry

178

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“…Glutamate toxicity in vitro, in turn, differs from both focal and global ischemia. Both ischemic conditions are associated with an immediate disag gregation of ribosomes (Morimoto and Yanagihara, 1981;Bonnekoh et aI., 1992) and near-complete in hibition of protein synthesis (Mies et aI., 1991;Wid mann et aI., 1991), but glutamate toxicity results in gradually progressing disaggregation, which, more over, is present only if the culture medium is de prived of trophic factors (Dux et aI., 1992). These differences suggest that neuronal death results from different p athophysiologies in which glutamate is involved in various ways.…”

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confidence: 99%

Cortical Negative DC Deflections following Middle Cerebral Artery Occlusion and KCl-Induced Spreading Depression: Effect on Blood Flow, Tissue Oxygenation, and Electroencephalogram

Back

Kohno

Hossmann

1994

J Cereb Blood Flow Metab

286

130

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Summary: In the periphery of ischemic brain lesions, transient spreading depression-like direct current (DC) deflections occur that may be of pathophysiological im portance for determining the volume of the ischemic in farct. The effect of these deflections on cerebral blood flow, tissue oxygen tension, and electrophysiology was studied in rats submitted to intraluminal thread occlusion of the middle cerebral artery (MCA) and compared with the changes following potassium chloride (KCl)-induced spreading depression of intact animals, Immediately after MCA occlusion, cortical laser-Doppler flow (LDF) in the periphery of the MCA territory sharply decreased to 35 ± 14% of control (mean ± SD; p < 0,05), tissue P02 de clined from 28 ± 4 to 21 ± 3 mm Hg (p < 0.05), and EEG power fell to -80% of control. During 7-h occlusion, 3-11 DC deflections with a mean duration of 5.2 ± 4.8 min occurred at irregular intervals, and EEG power gradually During the last years, several laboratories have been able to show that glutamate antagonists reduce the volume of ischemic infarcts (Ozyurt et aI. , 1988; Park et aI., 1988; Dirnagl et aI., 1990). The thera peutical effect could not be attributed to increased cerebral blood flow (Park et aI., 1989; Iijima et aI., 1992), indicating that molecular mechanisms are in volved. This observation is widely held to support an excitotoxic mechanism of brain infarcts in anal ogy to glutamate toxicity in vitro (Choi, 1985) and the phenomenon of delayed neuronal death in se lectively vulnerable brain regions following a period of global ischemia (Suzuki et aI., 1983). The com-

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“…Temporary occlusion of the left carotid artery affected clinical IS], histochemical [9,10], histological [lo, 111, biochemical [12,13] and electrophysiological [14] signs. Moreover, in this study temporary occlusion of the left carotid artery modified the BAEPs of gerbil.…”

Section: Discussionmentioning

confidence: 99%

The auditory evoked potentials of gerbils after temporary occlusion of the left carotid artery

Delbarre¹,

Delbarre²,

Ferger³

et al. 1991

Brain Injury

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This study examined brain-stem auditory evoked potentials response (BAEP) changes in the gerbil after temporary occlusion of the left carotid artery. Fourteen adult gerbils were subjected to unilateral left carotid ligation for 30 min. BAEPs were registered before and 5 min after occlusion, then 5 min, 60 min, 120 min, 24 h, 7 days and 28 days after release of the clip. Waves I (cochlear nerve), III (superior olivary complex) and V (inferior colliculus) were examined. Results were analysed using paired Student's t-test. Transient ischaemia increased latencies of waves I, III and V and the changes were more severe 5 min after release of the clip. In the gerbil, BAEPs might be a suitable method to study cerebral ischaemia.

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Cerebral ischemia in gerbils: polyribosomal function during progression and recovery.

Cited by 47 publications

References 22 publications

Changes in Brain Energy Metabolism and Protein Synthesis Following Transient Bilateral Ischemia in the Gerbil

Changes in Brain Energy Metabolism and Protein Synthesis Following Transient Bilateral Ischemia in the Gerbil

Cortical Negative DC Deflections following Middle Cerebral Artery Occlusion and KCl-Induced Spreading Depression: Effect on Blood Flow, Tissue Oxygenation, and Electroencephalogram

The auditory evoked potentials of gerbils after temporary occlusion of the left carotid artery

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