N-methyl-D-aspartate and TrkB receptor activation in cerebellar granule cells: an in vitro model of preconditioning to stimulate intrinsic survival pathways in neurons
Delineating the mechanisms of survival pathways that exist in neurons will provide important insight into how neurons utilize intracellular proteins as neuroprotectants against the causes of acute neurodegeneration. We have employed cultured rat cerebellar granule cells as a model for determining th...
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Published in | Annals of the New York Academy of Sciences Vol. 993; no. 1; pp. 134 - 145 |
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01.05.2003
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Abstract | Delineating the mechanisms of survival pathways that exist in neurons will provide important insight into how neurons utilize intracellular proteins as neuroprotectants against the causes of acute neurodegeneration. We have employed cultured rat cerebellar granule cells as a model for determining the mechanisms of these intraneuronal survival pathways. Glutamate has long been known to kill neurons by an N-methyl-d-aspartate (NMDA) receptor-mediated mechanism. Paradoxically, subtoxic concentrations of NMDA protect neurons against glutamate-mediated excitotoxicity. Because NMDA protects neurons in physiologic concentrations of glucose and oxygen, we refer to this phenomenon as physiologic preconditioning. One of the major mechanisms of NMDA neuroprotection involves the activation of NMDA receptors leading to the rapid release of brain-derived neurotrophic factor (BDNF). BDNF then binds to and activates its cognate receptor, receptor tyrosine kinase B (TrkB). The efficient utilization of these two receptors confers remarkable resistance against millimolar concentrations of glutamate that kill more than eighty percent of the neurons in the absence of preconditioning the neurons with a subtoxic concentration of NMDA. Exactly how the neurons mediate neuroprotection by activation of both receptors is just beginning to be understood. Both NMDA and TrkB receptors activate nuclear factor kappaB (NF-kappaB), a transcription factor known to be involved in protecting neurons against many different kinds of toxic insults. By converging on survival transcription factors, such as NF-kappaB, NMDA and TrkB receptors protect neurons. Thus, crosstalk between these very different receptors provides a rapid means of neuronal communication to upregulate survival proteins through release and transcriptional activation of messenger RNA. |
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Delineating the mechanisms of survival pathways that exist in neurons will provide important insight into how neurons utilize intracellular proteins as neuroprotectants against the causes of acute neurodegeneration. We have employed cultured rat cerebellar granule cells as a model for determining the mechanisms of these intraneuronal survival pathways. Glutamate has long been known to kill neurons by an
N
‐methyl‐d‐aspartate (NMDA) receptor‐mediated mechanism. Paradoxically, subtoxic concentrations of NMDA protect neurons against glutamate‐mediated excitotoxicity. Because NMDA protects neurons in physiologic concentrations of glucose and oxygen, we refer to this phenomenon as physiologic preconditioning. One of the major mechanisms of NMDA neuroprotection involves the activation of NMDA receptors leading to the rapid release of brain‐derived neurotrophic factor (BDNF). BDNF then binds to and activates its cognate receptor, receptor tyrosine kinase B (TrkB). The efficient utilization of these two receptors confers remarkable resistance against millimolar concentrations of glutamate that kill more than eighty percent of the neurons in the absence of preconditioning the neurons with a subtoxic concentration of NMDA. Exactly how the neurons mediate neuroprotection by activation of both receptors is just beginning to be understood. Both NMDA and TrkB receptors activate nuclear factor kappaB (NF‐κB), a transcription factor known to be involved in protecting neurons against many different kinds of toxic insults. By converging on survival transcription factors, such as NF‐κB, NMDA and TrkB receptors protect neurons. Thus, crosstalk between these very different receptors provides a rapid means of neuronal communication to upregulate survival proteins through release and transcriptional activation of messenger RNA. Delineating the mechanisms of survival pathways that exist in neurons will provide important insight into how neurons utilize intracellular proteins as neuroprotectants against the causes of acute neurodegeneration. We have employed cultured rat cerebellar granule cells as a model for determining the mechanisms of these intraneuronal survival pathways. Glutamate has long been known to kill neurons by an N-methyl-d-aspartate (NMDA) receptor-mediated mechanism. Paradoxically, subtoxic concentrations of NMDA protect neurons against glutamate-mediated excitotoxicity. Because NMDA protects neurons in physiologic concentrations of glucose and oxygen, we refer to this phenomenon as physiologic preconditioning. One of the major mechanisms of NMDA neuroprotection involves the activation of NMDA receptors leading to the rapid release of brain-derived neurotrophic factor (BDNF). BDNF then binds to and activates its cognate receptor, receptor tyrosine kinase B (TrkB). The efficient utilization of these two receptors confers remarkable resistance against millimolar concentrations of glutamate that kill more than eighty percent of the neurons in the absence of preconditioning the neurons with a subtoxic concentration of NMDA. Exactly how the neurons mediate neuroprotection by activation of both receptors is just beginning to be understood. Both NMDA and TrkB receptors activate nuclear factor kappaB (NF-kappaB), a transcription factor known to be involved in protecting neurons against many different kinds of toxic insults. By converging on survival transcription factors, such as NF-kappaB, NMDA and TrkB receptors protect neurons. Thus, crosstalk between these very different receptors provides a rapid means of neuronal communication to upregulate survival proteins through release and transcriptional activation of messenger RNA. |
Author | Lipsky, Robert Marini, Ann M Jiang, Xueying Strauss, Kenneth I Banaudha, Krishna Okagaki, Peter Wu, Xuan Zhu, Daming Mearow, Karen |
Author_xml | – sequence: 1 givenname: Xueying surname: Jiang fullname: Jiang, Xueying organization: Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA – sequence: 2 givenname: Daming surname: Zhu fullname: Zhu, Daming – sequence: 3 givenname: Peter surname: Okagaki fullname: Okagaki, Peter – sequence: 4 givenname: Robert surname: Lipsky fullname: Lipsky, Robert – sequence: 5 givenname: Xuan surname: Wu fullname: Wu, Xuan – sequence: 6 givenname: Krishna surname: Banaudha fullname: Banaudha, Krishna – sequence: 7 givenname: Karen surname: Mearow fullname: Mearow, Karen – sequence: 8 givenname: Kenneth I surname: Strauss fullname: Strauss, Kenneth I – sequence: 9 givenname: Ann M surname: Marini fullname: Marini, Ann M |
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Snippet | Delineating the mechanisms of survival pathways that exist in neurons will provide important insight into how neurons utilize intracellular proteins as... A bstract : Delineating the mechanisms of survival pathways that exist in neurons will provide important insight into how neurons utilize intracellular... |
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SubjectTerms | Animals Autocrine Communication Brain-Derived Neurotrophic Factor - genetics Brain-Derived Neurotrophic Factor - metabolism Brain-Derived Neurotrophic Factor - pharmacology Cells, Cultured Cerebellum - cytology Cerebellum - drug effects Cerebellum - metabolism Genes, bcl-2 Glutamic Acid - toxicity Ischemic Preconditioning - methods N-Methylaspartate - metabolism N-Methylaspartate - pharmacology Neurons - cytology Neurons - drug effects Neurons - metabolism Neuroprotective Agents - metabolism NF-kappa B - metabolism Oligonucleotides, Antisense - metabolism Receptor, trkB - metabolism Receptors, N-Methyl-D-Aspartate - metabolism |
Title | N-methyl-D-aspartate and TrkB receptor activation in cerebellar granule cells: an in vitro model of preconditioning to stimulate intrinsic survival pathways in neurons |
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