Basic FGF Increases Communication between Cells of the Developing Neocortex

Nadarajah, Bagirathy; Makarenkova, Helen P.; Becker, DL; Evans, William Howard; Parnavelas, John G.

doi:10.1523/jneurosci.18-19-07881.1998

Cited by 51 publications

(32 citation statements)

References 50 publications

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“…In vertebrates, growth factors have been shown to selectively diminish (Maldonado et al, 1988;Madhukar et al, 1989;Lau et al, 1992) or enhance (Pepper et al, 1989;Nadarajah et al, 1998;Reuss et al, 1998;Aberg et al, 2000) coupling and connexin expression. In Helisoma, it is believed that trophic factors are among the substances released from isolated ring ganglia when conditioning defined medium (Wong et al, 1981(Wong et al, , 1983(Wong et al, , 1984Barker et al, 1982).…”

Section: Neurotrophic Effects On Synaptic Developmentmentioning

confidence: 99%

Transient Electrical Coupling Delays the Onset of Chemical Neurotransmission at Developing Synapses

Szabo

Faber²,

Zoran³

2004

J. Neurosci.

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Section: Neurotrophic Effects On Synaptic Developmentmentioning

confidence: 99%

Transient Electrical Coupling Delays the Onset of Chemical Neurotransmission at Developing Synapses

Szabo

Faber²,

Zoran³

2004

J. Neurosci.

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“…Transfer of Lucifer Yellow was determined by fluorescence microscopy using filter set 05 (395-440 nm/ 460-470 nm; Zeiss, UK) on an Axiostat microscope (Zeiss, UK). Inhibition of dye transfer was quantified by determining the percentage of injected cells that communicated Lucifer Yellow to < 5, 5-10 and > 10 neighbouring cells (Nadarajah et al 1998). …”

Section: Dye Transfermentioning

confidence: 99%

The endothelial component of cannabinoid‐induced relaxation in rabbit mesenteric artery depends on gap junctional communication

Chaytor

Martin

Evans

et al. 1999

The Journal of Physiology

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150

157

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An endothelium-derived hyperpolarizing factor (EDHF) is now widely recognized to mediate endothelium-dependent vascular relaxations that are independent of nitric oxide (NO) and prostanoid synthesis (Mombouli & Vanhoutte, 1997). Although the chemical identity of EDHF remains controversial, there is accumulating evidence that this mediator normally effects relaxation following diffusion from the endothelium to smooth muscle via myoendothelial gap junctions rather than the extracellular space Taylor et al. 1998;Dora et al. 1999;Hutcheson et al. 1999). Anatomically, this hypothesis is supported by the demonstration of myoendothelial gap junction plaques in rabbit conduit arteries (Spagnoli et al. 1982), and functional dye transfer experiments confirm direct chemical coupling between endothelium and subjacent smooth muscle (Little et al. 1995). Gap junctions are membrane structural proteins which consist of two hemichannels or connexons contributed by apposing cells, with each connexon being formed from six protein subunits or connexins arranged around an aqueous central pore that permits intercellular transfer of electrical current and molecules < 1 kDa in size (Yeager & Nicholson, 1996). Connexin 43 (Cx43) is present in both endothelial and vascular smooth muscle cells, and EDHFmediated relaxations and hyperpolarizations of rabbit

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“…Several studies have shown that connexins accumulate in intracellular stores that correspond to the ERGIC/Golgi in cultured cells (16 -18) and tissues (19), and growth factors appear to regulate connexin transport between these stores and the gap junction (20). Transport of membrane proteins in general from such intracellular stores to the plasma membrane is likely to involve tubulovesicular networks (21,22).…”

mentioning

confidence: 99%

Intracellular Trafficking Pathways in the Assembly of Connexins into Gap Junctions

George

Kendall²,

Evans

1999

Journal of Biological Chemistry

111

103

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Trafficking pathways underlying the assembly of connexins into gap junctions were examined using living COS-7 cells expressing a range of connexin-aequorin (Cx-Aeq) chimeras. By measuring the chemiluminescence of the aequorin fusion partner, the translocation of oligomerized connexins from intracellular stores to the plasma membrane was shown to occur at different rates that depended on the connexin isoform. Treatment of COS-7 cells expressing Cx32-Aeq and Cx43-Aeq with brefeldin A inhibited the movement of these chimera to the plasma membrane by 84 ؎ 4 and 88 ؎ 4%, respectively. Nocodazole treatment of the cells expressing Cx32-Aeq and Cx43-Aeq produced 29 ؎ 16 and 4 ؎ 7% inhibition, respectively. In contrast, the transport of Cx26 to the plasma membrane, studied using a construct (Cx26/43T-Aeq) in which the short cytoplasmic carboxylterminal tail of Cx26 was replaced with the extended carboxyl terminus of Cx43, was inhibited 89 ؎ 5% by nocodazole and was minimally affected by exposure of cells to brefeldin A (17 ؎11%). The transfer of Lucifer yellow across gap junctions between cells expressing wild-type Cx32, Cx43, and the corresponding Cx32-Aeq and Cx43-Aeq chimeras was reduced by nocodazole treatment and abolished by brefeldin A treatment. However, the extent of dye coupling between cells expressing wild-type Cx26 or the Cx26/43T-Aeq chimeras was not significantly affected by brefeldin A treatment, but after nocodazole treatment, transfer of dye to neighboring cells was greatly reduced. These contrasting effects of brefeldin A and nocodazole on the trafficking properties and intercellular dye transfer are interpreted to suggest that two pathways contribute to the routing of connexins to the gap junction.

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Basic FGF Increases Communication between Cells of the Developing Neocortex

Cited by 51 publications

References 50 publications

Transient Electrical Coupling Delays the Onset of Chemical Neurotransmission at Developing Synapses

Transient Electrical Coupling Delays the Onset of Chemical Neurotransmission at Developing Synapses

The endothelial component of cannabinoid‐induced relaxation in rabbit mesenteric artery depends on gap junctional communication

Intracellular Trafficking Pathways in the Assembly of Connexins into Gap Junctions

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