Regional brain-derived neurotrophic factor mRNA and protein levels following transient forebrain ischemia in the rat

Kokaia, Zaal; Nawa, Hiroyuki; Uchino, Haruto; Elmér, Eskil; Kokaia, Mérab; Carnahan, Josette; Smith, MA; Siesjö, Bo K.; Lindvall, Olle

doi:10.1016/0169-328x(96)00002-2

Cited by 97 publications

(45 citation statements)

References 32 publications

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“…Reactive astrocytes were excluded as the source of GDNF because they do not express GDNF in our model. The BDNF results are consistent with previous studies (Kokaia et al, 1996;Lee et al, 2002), whereas the GDNF results are inconsistent with a study by Miyazaki et al (2001). They reported that GDNF expression in the hippocampal CA1 region increased between 3 and 24 h after ischemia, and then declined to baseline levels.…”

Section: Discussionsupporting

confidence: 73%

Neuroprotective Effect of Exogenous Microglia in Global Brain Ischemia

Imai

Suzuki

Oda

et al. 2006

J Cereb Blood Flow Metab

189

125

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Exogenous microglia pass through the blood-brain barrier and migrate to ischemic hippocampal lesions when injected into the circulation. We investigated the effect of exogenous microglia on ischemic CA1 pyramidal neurons. Microglia were isolated from neonatal mixed brain cultures, labeled with the fluorescent dye PKH26, and injected into the subclavian artery of Mongolian gerbils subjected to ischemia reperfusion neuronal injury. PKH26-labeled microglia migrated to the ischemic hippocampal lesion, resulting in increased numbers of surviving neurons compared with control animals, even when injected 24 h after ischemia. Interferon-c stimulation of isolated microglia enhanced the neuroprotective effect. Administration of exogenous microglia resulted in normal performance in a passive avoidance-learning task. Additionally, administration of exogenous microglia increased the expression of brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor in the ischemic hippocampus, and thus might have induced neurotrophin-dependent protective activity in damaged neurons. Peripherally injected microglia exhibited a specific affinity for ischemic brain lesions, and protected against ischemic neuronal injury in vivo. It is possible that administration of exogenous microglia can be developed as a potential candidate therapy for central nervous system repair after transitory global ischemia.

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Section: Discussionsupporting

confidence: 73%

Neuroprotective Effect of Exogenous Microglia in Global Brain Ischemia

Imai

Suzuki

Oda

et al. 2006

J Cereb Blood Flow Metab

189

125

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“…11 The neuroprotective role of endogenous BDNF is further supported by the observed correlation between BDNF protein levels and resistance to ischemic damage in the various hippocampal subregions. 12 Furthermore, intravenous administration of BDNF 30 min after middle cerebral artery occlusion reduced infarct size in the cerebral cortex and counter-regulated Bcl-2 and Bax expression. 8 Intraventricular injection of BDNF also increased survival of rat hippocampal CA1 pyramidal neurons following transient forebrain ischemia.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotection by BDNF against glutamate-induced apoptotic cell death is mediated by ERK and PI3-kinase pathways

et al. 2005

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Neurotrophins protect neurons against glutamate excitotoxicity, but the signaling mechanisms have not been fully elucidated. We studied the role of the phosphatidylinositol 3-kinase (PI3-K) and Ras/mitogen-activated protein kinase (MAPK) pathways in the protection of cultured hippocampal neurons from glutamate induced apoptotic cell death, characterized by nuclear condensation and activation of caspase-3-like enzymes. Pre-incubation with the neurotrophin brain-derived neurotrophic factor (BDNF), for 24 h, reduced glutamate-evoked apoptotic morphology and caspase-3-like activity, and transiently increased the activity of the PI3-K and of the Ras/MAPK pathways. Inhibition of the PI3-K and of the Ras/MAPK signaling pathways abrogated the protective effect of BDNF against glutamate-induced neuronal death and similar effects were observed upon inhibition of protein synthesis. Moreover, incubation of hippocampal neurons with BDNF, for 24 h, increased Bcl-2 protein levels. The results indicate that the protective effect of BDNF in hippocampal neurons against glutamate toxicity is mediated by the PI3-K and the Ras/MAPK signaling pathways, and involves a longterm change in protein synthesis.

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“…It has been reported that administration of BDNF in ischemic damaged brain reduces neuronal death and even supports new neuron formation 31 . In another study, BDNF mRNA and BDNF protein levels were measured in various regions of brain in time-dependent cerebral ischemia, and it was observed that the amount of post-ischemic BDNF mRNA and protein significantly increased in different regions of the brain after ischemia 32 . Different research showed that BDNF, like other neurotrophic factors, protects developing neurons by inhibiting apoptosis during developmental stage 30 .…”

Section: Discussionmentioning

confidence: 99%

“…Neuroprotective effects of BDNF in hippocampus, especially in ischemic injury, have been reported 31,32 . The irreversible cell death is caused by the activation of Caspases, especially the Caspase-3 33 .…”

Section: Introductionmentioning

confidence: 99%

Apoptotic Effects of Reduced Brain Derived Neurotrophic Factor (BDNF) on Mouse Liver and Kidney

Tezcan¹,

Hacioglu²,

Abidin³

et al. 2017

Dicle Tıp Dergisi

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Objective: Brain-derived neurotrophic factor (BDNF) promotes the development and differentiation of neurons and synapses, as well as neuronal survival, by acting on specific neuronal groups in the central and peripheral nervous systems. However, the direct effect of BDNF on apoptosis in peripheral tissues is not known. The aim of this study was to investigate the relationship between BDNF and apoptosis, and the density and distribution of BDNF receptors in liver and kidney tissues by histological and immunehistochemical methods.Methods: Seven wild-type and 7 BDNF heterozygous (reduced BDNF levels) male mice were used in the study. Caspase-3 and TUNEL immunehistochemical stainings were performed in order to investigate the presence of apoptosis in the liver and kidney tissues of the studied groups. Apoptosis-entering cells were counted and the groups were compared. Concentration and distribution of BDNF receptors, tropomyosin-related kinase B (TrkB) and nerve growth factor receptor p75 (NGFR p75), in liver and kidney tissues were also examined by immunehistochemical analyzes.Results: As a result of Caspase-3 and TUNEL immunehistochemical staining, more cells were counted to enter the apoptotic process in sections of BDNF heterozygous group compared to control group (p<0.0001). In both groups TrkB and NGFR p75 receptors in liver and kidney tissues were determined in trace amounts, but there was no difference in intensity and distribution between the studied groups.Conclusion: According to our histological and immunehistochemical stainings and statistical analysis of cell count between groups, it was found that BDNF is protective against apoptosis in liver and kidney. The lack of difference between the studied groups in terms of intensity and distribution of BDNF receptors, suggests that BDNF receptor distribution in the liver and kidney tissues may be different from the nervous system or that BDNF may differ in affinity for these receptors. Keywords 316 Azaltılmış Beyin Kaynaklı Nörotrofik Faktörün (BDNF), Fare Karaciğer ve Böbrek Dokusuna Apoptotik EtkileriÖzet Amaç: Beyin kökenli nörotrofik faktör (BDNF), merkezi ve periferik sinir sisteminde belirli nöron grupları üzerine etki ederek, nöron ve sinapsların gelişimini ve farklılaşmasını, bunun yanında nöronal sağkalımı desteklemektedir. Periferik dokularda ise BDNF'nin apoptoz ile direkt ilişkisi bilinmemektedir. Bu çalışmada, karaciğer ve böbrek dokularında BDNF'nin apoptoz ile ilişkisi ve bu dokulardaki BDNF reseptörlerinin yoğunluk ve dağılımının histolojik ve immünohistokimyasal yöntemler kullanılarak araştırılması amaçlanmıştır.Yöntemler: Araştırmada 7 adet yabanıl tip ve 7 adet BDNF heterozigot (BDNF düzeyleri yarı yarıya azaltılmış) erkek fare kullanılmıştır. Karaciğer ve böbrek dokusunda apoptozun varlığını araştırmak amacıyla Kaspaz-3 ve TUNEL immünohistokimyasal boyamaları gerçekleştirilmiş ve apoptoza giren hücreler sayılarak gruplar arası karşılaştırma yapılmıştır. BDNF reseptörleri olan tropomiyozin-ilişkili kinaz B (TrkB) ve nerve growth fa...

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Regional brain-derived neurotrophic factor mRNA and protein levels following transient forebrain ischemia in the rat

Cited by 97 publications

References 32 publications

Neuroprotective Effect of Exogenous Microglia in Global Brain Ischemia

Neuroprotective Effect of Exogenous Microglia in Global Brain Ischemia

Neuroprotection by BDNF against glutamate-induced apoptotic cell death is mediated by ERK and PI3-kinase pathways

Apoptotic Effects of Reduced Brain Derived Neurotrophic Factor (BDNF) on Mouse Liver and Kidney

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