Neurotrophin-4 selectively promotes survival of striatal neurons in organotypic slice culture

Ardelt, Agnieszka; Flaris, Nikolaos; Roth, Kevin A.

doi:10.1016/0006-8993(94)91333-1

Cited by 50 publications

(23 citation statements)

References 28 publications

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“…In this regard, we did not find a significant change in proposed that NT-4/5 can replace BDNF deficiency to promote the survival [43] of specific striatal neuronal populations [44] . We have demonstrated that NT-4/5 becomes detectable in striatal cells after BDNF during postnatal development [45] , and since there is no evidence that it comes from the cortex, it is possible that NT-4/5 is produced by cells that are not as sensitive to 3-NP as those that respond to BDNF.…”

Section: Neurotrophincontrasting

confidence: 56%

3-Nitropropionic acid modifies neurotrophin mRNA expression in the mouse striatum: 18S-rRNA is a reliable control gene for studies of the striatum

2012

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Objective The aim of the present study was to determine the changes in the mRNA levels of neurotrophins and their receptors in the striatal tissue of mice treated with 3-nitropropionic acid (3-NP). Methods At 1 and 48 h after the last drug administration, the mRNA expression of nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4/5 as well as their receptors p75, TrkA, TrkB and TrkC, was evaluated using semi-quantitative (semi-Q) and real-time RT-PCR. β-actin mRNA and ribosomal 18S (18S rRNA) were tested as internal controls. Results 3-NP treatment did not affect mRNA expression of all neurotrophins and their respective receptors equally. Also, differences in neurotrophin and receptor mRNA expression were observed between semi-Q and real-time RT-PCR. Real-time RT-PCR was more accurate in evaluating the mRNA expression of the neurotrophins than semi-Q, and 18S rRNA was more reliable than β-actin as an internal control. Conclusion Neurotrophins and their receptors expression is differentially affected by neuronal damage produced by inhibition of mitochondrial respiration with 3-NP treatment in low, sub-chronic doses in vivo.

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Section: Neurotrophincontrasting

confidence: 56%

3-Nitropropionic acid modifies neurotrophin mRNA expression in the mouse striatum: 18S-rRNA is a reliable control gene for studies of the striatum

2012

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“…They provide a versatile bridge between isolated cell culture and in vivo experiments wherein the cytoarchitecture and structural relationships of cells are maintained, allowing for parameters 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 of neural regeneration, e.g. neuronal survival [19], nerve fiber regeneration [20,21] and collateral axon sprouting to be evaluated [22]. These models offer several advantages including the ease of manipulation/observation of in vitro preparations [18]; several ages, neuroanatomical areas and species, including human foetuses [23] and transgenic models [24,25] can be used as tissue donor sources, offering high flexibility to study neural pathologies and disease mechanisms.…”

Section: Introductionmentioning

confidence: 99%

An in vitro spinal cord injury model to screen neuroregenerative materials

Weightman¹,

Pickard²,

Yang³

et al. 2014

Biomaterials

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Implantable 'structural bridges' based on nanofabricated polymer scaffolds have great promise to aid spinal cord regeneration. Their development (optimal formulations, surface functionalizations, biocompatibility, topographical influences and degradation profiles) is heavily reliant on live animal injury models. These have several disadvantages including invasive surgical procedures, ethical issues, high animal usage, technical complexity and expense. In vitro 3-D organotypic slice arrays could offer a novel solution to overcome these challenges, but their utility for nanomaterials testing is undetermined. We have developed an in vitro model of spinal cord injury that replicates stereotypical cellular responses to neurological injury in vivo, viz. reactive gliosis, microglial infiltration and limited nerve fibre outgrowth. We describe a facile method to safely incorporate aligned, poly-lactic acid nanofiber meshes (± poly-lysine + laminin coating) within injury sites using a lightweight

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“…Specific effects on embryonic telencephalic cell populations have been reported. For example, BDNF promotes survival of primary cortical neurons in vitro (Ghosh et al, 1994), and NT-4/5 causes increased survival of developing striatal neurons (Garcia et al, 1992;Ardelt et al, 1994). The inability of these factors to promote survival in the present study may reflect the fact that few studies have used telencephalic cells isolated as early as E12.…”

Section: Discussionmentioning

confidence: 74%

Trophic support promotes survival of bcl-x-deficient telencephalic cells in vitro

et al. 1998

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Survival of immature neurons is regulated by Bcl-x L , as targeted disruption of bcl-x significantly increases cell death in vivo and in vitro. Death of cultured bcl-x-deficient and wildtype telencephalic cells can be prevented by fetal calf serum or chemically-defined medium (ITS), suggesting trophic factors in these media potentiate survival through a pathway independent of Bcl-x L . Addition of trophic factors to basal medium revealed that insulin and insulin-like growth factors (IGFs), but not other trophic factors, reduced apoptosis of wild-type and bcl-x-deficient telencephalic cells. Antibodies raised against IGF-I receptors and wortmannin both attenuated the effects of IGF-I, indicating survival was mediated by IGF-I receptors and phosphatidylinositol 3'-kinase signaling, whereas effects of ITS were only partially reduced by these agents. The survival promoting effects of ITS were reduced in cells lacking both bcl-x and bcl-2, indicating Bcl-2 plays a supportive role to Bcl-x L in maintaining telencephalic cell survival. Furthermore, the ratio of expression of the pro-apoptotic bax gene to the anti-apoptotic bcl-2 gene was reduced in bcl-x-deficient cultures grown in ITS, suggesting that the interaction between these bcl-2 family members may, in part, regulate a Bcl-x L independent survival pathway. Finally, the pro-apoptotic bad gene does not appear to play a role in these interactions as targeted disruption of bad did not alter apoptosis in telencephalic cultures.

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Neurotrophin-4 selectively promotes survival of striatal neurons in organotypic slice culture

Cited by 50 publications

References 28 publications

3-Nitropropionic acid modifies neurotrophin mRNA expression in the mouse striatum: 18S-rRNA is a reliable control gene for studies of the striatum

3-Nitropropionic acid modifies neurotrophin mRNA expression in the mouse striatum: 18S-rRNA is a reliable control gene for studies of the striatum

An in vitro spinal cord injury model to screen neuroregenerative materials

Trophic support promotes survival of bcl-x-deficient telencephalic cells in vitro

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