Increase of hypoxic tolerance in rat hippocampal slices following 3-nitropropionic acid is not mediated by endogenous nerve growth factor

Riepe, Matthias W.; Kasischke, Karl A.; Gericke, Christian A.; Löwe, Andrea; Hellweg, Rainer

doi:10.1016/0304-3940(96)12699-9

Cited by 29 publications

(8 citation statements)

References 24 publications

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“…In nontolerant rats subjected to a long-term cerebral ischemia, neuronal necrosis is definitely higher than in preconditioned brains. Endogenous NGF has been shown previously not to mediate 3-nitropropionic-acid-induced tolerance in rat hippocampal slices [19]. …”

Section: Discussionmentioning

confidence: 99%

Neurotrophic Factor Expression after Focal Brain Ischemia Preceded by Different Preconditioning Strategies

Pera

Zawadzka²,

Kamińska³

et al. 2005

Cerebrovasc Dis

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Background: Both prolonged brain ischemia and preconditioning (PC) induce expression of neurotrophic factors. However, the influence of PC on their expression after a long-term ischemia remains vague. Previously, we have found various effects of PC on mRNA levels of different cytokines after focal brain ischemia. Thus, we investigated mRNA expression of nerve growth factor, brain-derived neurotrophic factor (BDNF) and ciliary neurotrophic factor after 90-min middle cerebral artery occlusion (MCAo) preceded by ischemic or chemical PC. Methods: MCAo was induced in rats using the suture method. PC had been carried out 3 days earlier. There were 4 experimental groups: MCAo alone; ischemic PC and MCAo; chemical PC and MCAo, and sham-operated rats. Expression of mRNAs in the ipsi- and contralateral cortex was studied by semiquantitative RT-PCR at 12 and 24 h after MCAo. Results: Despite clearly neuroprotective effects of both PC strategies, mRNA levels of neurotrophic factors were similar in tolerant and nontolerant rats. Only BDNF mRNA expression, 12 h after reperfusion, was lower when ischemic PC was applied prior to long-term ischemia. Conclusions: These results suggest that PC generally does not change the expression of neurotrophic factor expression after a long-term focal brain ischemia compared to the nontolerant state.

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Section: Discussionmentioning

confidence: 99%

Neurotrophic Factor Expression after Focal Brain Ischemia Preceded by Different Preconditioning Strategies

Pera

Zawadzka²,

Kamińska³

et al. 2005

Cerebrovasc Dis

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“…There are a large number of different paradigms used to induce ischemic tolerance. For example, sublethal global64 or focal cerebral ischemia,65 cortical spreading depression,66,67 chronic hypoxia,68 hypothermia,69 and different pharmacological agents70-72 have been used to induce ischemic tolerance.…”

Section: Tolerance/preconditioning and Metabolic Depressionmentioning

confidence: 99%

Metabolic Downregulation

Yenari

Kitagawa

Lyden

et al. 2008

Stroke

142

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Background and Purpose-The search for effective neuroprotectants remains frustrating, particularly with regard to specific pharmaceuticals. However, laboratory studies have consistently shown remarkable neuroprotection with 2 nonpharmacological strategies-therapeutic hypothermia and ischemic preconditioning. Recent studies have shown that the mechanism of protection underlying both of these treatments is correlated to downregulation of cellular and tissue metabolism. Thus, understanding the mechanisms underlying such robust protective effects could lead to appropriate translation at the clinical level. In fact, hypothermia is already being used at many centers to improve neurological outcome from cardiac arrest. Methods-A systematic review of both topics is presented in terms of underlying pathophysiological mechanisms and application at the clinical level. Results-Although the mechanisms of protection for both therapeutic strategies are multifold, both share features of downregulating metabolism. Both therapeutic strategies are robust neuroprotectants, but translating them to the clinical arena is challenging, though not impossible, and clinical studies have shown or suggest benefits of both treatments. Conclusions-The strategy of metabolic downregulation should be further explored to identify effective neuroprotectants that can be easily applied clinically.

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“…To determine if astrocytes also express ␤-and ␥-crystallins in response to hypoxia, we used 3-nitropropionic acid, an irreversible inhibitor of mitochondrial succinate dehydrogenase activity (Cavaliere et al, 2001). It can be considered a model substance to study hypoxic neuronal damage (Riepe et al, 1996). As shown in Figure 9, when fetal human astrocytes in culture were exposed to 3-NP, there was induction not only of VEGF within 6 hr, as expected, but also ␤-and ␥-crystallins.…”

Section: Induction Of Vegf and ␤-And ␥-Crystallins In Cultured Human mentioning

confidence: 99%

A potential role for β‐ and γ‐crystallins in the vascular remodeling of the eye

Zhang¹,

Gehlbach²,

Gongora³

et al. 2005

Developmental Dynamics

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We demonstrate that expression of ␤-and ␥-crystallins is associated with intraocular vessels during normal vascular development of the eye and also in the Nuc1 rat, a mutant in which the hyaloid vascular system fails to regress normally. Real-Time RT PCR, Western blot and metabolic labeling studies indicate an increased expression of ␤-and ␥-crystallins in Nuc1 retina. The increased expression of crystallins was localized to the astrocytes surrounding the intraocular vessels. A similar pattern of crystallin expression was also observed in the retinal vessels during normal development. Cultured human astrocytes exposed to 3-nitropropionic acid, an established model of neuronal hypoxia, increased VEGF expression, as expected, but also increased expression of crystallins. Our data suggest that crystallins may function together with VEGF during vascular remodeling. Interestingly, in human PFV (persistent fetal vasculature) disease, where the hyaloid vasculature abnormally persists after birth, we show that astrocytes express both VEGF and crystallins. Developmental Dynamics 234:36 -47, 2005.

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Increase of hypoxic tolerance in rat hippocampal slices following 3-nitropropionic acid is not mediated by endogenous nerve growth factor

Cited by 29 publications

References 24 publications

Neurotrophic Factor Expression after Focal Brain Ischemia Preceded by Different Preconditioning Strategies

Neurotrophic Factor Expression after Focal Brain Ischemia Preceded by Different Preconditioning Strategies

Metabolic Downregulation

A potential role for β‐ and γ‐crystallins in the vascular remodeling of the eye

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