Increased expression of trkB and trkC messenger RNAS in the rat forebrain after focal mechanical injury

Mudó, G.; Persson, Håkan; Timmusk, Tõnis; Funakoshi, Hiroshi; Bindoni, M; Belluardo, Natale

doi:10.1016/0306-4522(93)90036-f

Cited by 66 publications

(22 citation statements)

References 42 publications

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“…The increased levels of mRNA after the injury returned to control levels a few hours after the injury. Pretreatment of the animals with the ketamine completely prevented the changes of trkB and trkC messenger RNAs, suggesting that the brain injury caused a release of glutamate with subsequent activation of NMDA receptor [54]. In the present study, rats were allowed 5 days before the test to recover from surgery so the changes of mRNA levels after the injury may be returned to control levels after the recovery days.…”

Section: Discussionmentioning

confidence: 69%

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

Razavi¹,

Haeri-Rohani²,

Eidi³

et al. 2014

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Section: Discussionmentioning

confidence: 69%

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

Razavi¹,

Haeri-Rohani²,

Eidi³

et al. 2014

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“…Viral labeling strategies, to our knowledge, would provide the best alternate means for comparing newborn cells labeled at different time points, although a recent report demonstrating fusion of viral-labeled microglia to mature neurons raises concerns (Ackman et al, 2006). Moreover, infusion of virus invariably leads to brain injury, which can alter the expression of numerous genes, including the neurotrophins (Ballarin et al, 1991;Mudo et al, 1993). Neurotrophins are implicated in epileptogenesis (Danzer et al, 2002;He et al, 2004).…”

Section: Advantages and Limitations Of The Present Approachmentioning

confidence: 99%

Pilocarpine-Induced Seizures Cause Selective Time-Dependent Changes to Adult-Generated Hippocampal Dentate Granule Cells

Walter¹,

Murphy²,

Pun³

et al. 2007

J. Neurosci.

163

176

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Aberrantly interconnected granule cells are characteristic of temporal lobe epilepsy. By reducing network stability, these abnormal neurons may contribute directly to disease development. Only subsets of granule cells, however, exhibit abnormalities. Why this is the case is not known. Ongoing neurogenesis in the adult hippocampus may provide an explanation. Newly generated granule cells may be uniquely vulnerable to environmental disruptions relative to their mature neighbors. Here, we determine whether there is a critical period after neuronal birth during which neuronal integration can be disrupted by an epileptogenic insult. By bromodeoxyuridine birthdating cells in green fluorescent protein-expressing transgenic mice, we were able to noninvasively label granule cells born 8 weeks before (mature), 1 week before (immature), or 3 weeks after (newborn) pilocarpineepileptogenesis. Neuronal morphology was examined 4 and 8 weeks after pilocarpine treatment. Strikingly, almost 50% of immature granule cells exposed to pilocarpine-epileptogenesis exhibited aberrant hilar basal dendrites. In contrast, only 9% of mature granule cells exposed to the identical insult possessed basal dendrites. Moreover, newborn cells were even more severely impacted than immature cells, with 40% exhibiting basal dendrites and an additional 20% exhibiting migration defects. In comparison, Ͻ5% of neurons from normal animals exhibited either abnormality, regardless of age. Together, these data demonstrate the existence of a critical period after the birth of adult-generated neurons during which they are vulnerable to being recruited into epileptogenic neuronal circuits. Pathological brain states therefore may pose a significant hurdle for the appropriate integration of newly born endogenous, and exogenous, neurons.

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“…Every molecule has its own specific temporospatial pattern in injured nerves after trauma and during healing [49,50]. Similar effects have also been detected in glial cells of the central nervous system [51]. Increased expression of neurotrophins and their recptors in glia could result in auto/paracrine induction of glial cell proliferation and may be one of the events leading to scar tissue formation that prevents regeneration in the brain after trauma.…”

Section: Perspectivesmentioning

confidence: 67%

Genes for neurotrophic factors and their receptors: structure and regulation

Metsis

2001

CMLS, Cell. Mol. Life Sci.

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Neurotrophins and their receptors have attracted much interest during the last two decades. Although the mode of action of molecules of the neurotrophin system has been studied extensively, information on molecular mechanisms governing their expression is mosaic and incomplete. This review attempts to summarize the data available on gene structure and transcriptional regulation of neurotrophins and their receptors, and outlines perspectives for the future in this field.

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Increased expression of trkB and trkC messenger RNAS in the rat forebrain after focal mechanical injury

Cited by 66 publications

References 42 publications

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

Pilocarpine-Induced Seizures Cause Selective Time-Dependent Changes to Adult-Generated Hippocampal Dentate Granule Cells

Genes for neurotrophic factors and their receptors: structure and regulation

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