Neuronal activity up-regulates astroglial gene expression.

Steward, Oswald; Torre, Enrique; Tomasulo, Richard A.; Lothman, Eric W.

doi:10.1073/pnas.88.15.6819

Cited by 168 publications

(104 citation statements)

References 30 publications

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“…Serial sections from all regions of NF1 SynI KO brains were compared to normal counterparts, and no evidence of microgliosis was found (data not shown). Taken together, these results indicate that loss of NF1 in neurons does not elicit the classical morphological features of neuronal degeneration and microgliosis but, rather, may alter normal neuronal physiology, thus exerting an effect on surrounding astrocytes (Kraig et al 1991;Steward et al 1991).…”

Section: Ko Brains Do Not Develop Neuronal Degeneration or Microgliosismentioning

confidence: 82%

“…The simplest model for the observed astrogliosis is that a paracrine effect, mediated by NF1-deficient neurons, induces astroglial hypertrophy and GFAP induction (Rabchevsky et al 1998). Alternatively, loss of NF1 may induce synaptic hyperactivity, which leads to astrocyte reactivity (Kraig et al 1991;Steward et al 1991). One interesting feature in this astrogliosis model is the absence of neuronal degeneration and microgliosis.…”

Section: A Unique Model For Astrogliosis and Learning Disabilitymentioning

confidence: 99%

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Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain

Zhu¹,

Romero²,

Ghosh³

et al. 2001

Genes Dev.

545

557

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Neurofibromatosis type 1 (NF1) is a prevalent genetic disorder that affects growth properties of neural-crest-derived cell populations. In addition, approximately one-half of NF1 patients exhibit learning disabilities. To characterize NF1 function both in vitro and in vivo, we circumvent the embryonic lethality of NF1 null mouse embryos by generating a conditional mutation in the NF1 gene using Cre/loxP technology. Introduction of a Synapsin I promoter driven Cre transgenic mouse strain into the conditional NF1 background has ablated NF1 function in most differentiated neuronal populations. These mice have abnormal development of the cerebral cortex, which suggests that NF1 has an indispensable role in this aspect of CNS development. Furthermore, although they are tumor free, these mice display extensive astrogliosis in the absence of conspicuous neurodegeneration or microgliosis. These results indicate that NF1-deficient neurons are capable of inducing reactive astrogliosis via a non-cell autonomous mechanism.

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Section: Ko Brains Do Not Develop Neuronal Degeneration or Microgliosismentioning

confidence: 82%

Section: A Unique Model For Astrogliosis and Learning Disabilitymentioning

confidence: 99%

Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain

Zhu¹,

Romero²,

Ghosh³

et al. 2001

Genes Dev.

545

557

View full text Add to dashboard Cite

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“…Many mRNAs are affected by acute or chronic drug administration, including neuroleptics (Romano et al, 1987;De la Concha et al, 1991), opiates (Lightman and Young, 1987), and alcohol (Mochly-Rosen et al, 1988). Other influences that may be pertinent for some mRNAs include the time of day at which death occurred (Lausson et al, 1989), dehydration (Rivkees et al, 1989), hypoglycaemia (Suda et al, 1988), stresses of various kinds (Daval et al, 1989;Nichols et al, 1990), and neuronal activity (Nishimori et al, 1989;Steward et al, 1991).…”

Section: The Effect Of As On Brain Rnamentioning

confidence: 99%

Pre‐and Postmortem Influences on Brain RNA

Barton

Pearson

Najlerahim

et al. 1993

Journal of Neurochemistry

243

142

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Many potentially valuable techniques for the understanding of human neurobiological and neuropathological processes require the use of RNA obtained from postmortem tissue. As with earlier neurochemical studies, there are two particular problems posed by such tissue in comparison with tissue from experimental animals. These are the postmortem interval and the condition of the patient prior to death, referred to as the agonal state. We review the nature and extent of the effects of postmortem interval and agonal state on RNA in brain tissue, with particular reference to the study of neuropsychiatric disorders. Perhaps surprisingly, postmortem interval has at most a modest effect on RNA. Abundant intact and biologically active RNA is present in tissue frozen 36 h or more after death. Postmortem interval does not account for the marked variability observed among human brains in all RNA parameters. Despite the overall stability of RNA after death, some evidence suggests that individual RNAs may undergo postmortem decay. Less attention has been paid to the effects of agonal state. The existing data indicate that events in the premortem period such as hypoxia and coma can affect the amount of some messenger RNAs. The nature of agonal state influences depends on the messenger RNA in question, though the basis for this selective vulnerability is unknown. No agonal state effect on overall RNA level or activity has been found. The data show that postmortem brain tissue can be used for RNA research. However, considerable attention must be paid to controlling for the influences of pre-and postmortem factors, especially when quantitative analyses are performed.

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“…In epilepsy, several pathological changes typically occur in the brain, including neuronal loss, gliosis (Penfield, 1929;Steward et al, 1991), dendritic spine degeneration (Isokowa,1998, and abnormal synaptic reorganization (Babb et al, 1991;Mello et al, 1993; www.intechopen.com Leite et al, 1996;Xiang-ming Zha et al, 2005). These changes lead to abnormally increased excitability and synchronization, and eventually to the occurrence of spontaneous seizures (Cavalheiro et al, 1991;Isokawa & Mello,1991;Bothwell et al, 2001).…”

Section: Histopathological Changes Of Neurones In Epilepsymentioning

confidence: 99%