2011
Tchumatchenko, Tatjana; Malyshev, A; Wolf, F; Volgushev, M
Ultrafast population encoding by cortical neurons Journal Article
In: Journal of Neuroscience, vol. 31, no. 34, pp. 12171–12179, 2011.
@article{Tchumatchenko2011_ultrafast,
title = {Ultrafast population encoding by cortical neurons},
author = {Tatjana Tchumatchenko and A Malyshev and F Wolf and M Volgushev},
year = {2011},
date = {2011-01-01},
journal = {Journal of Neuroscience},
volume = {31},
number = {34},
pages = {12171–12179},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
2010
Dudanova, Irina; Gatto, Graziana; Klein, Rüdiger
GDNF acts as a chemoattractant to support ephrinA-induced repulsion of limb motor axons. Journal Article
In: Current biology : CB, vol. 20, no. 23, pp. 2150–6, 2010, ISSN: 1879-0445.
@article{Dudanova2010,
title = {GDNF acts as a chemoattractant to support ephrinA-induced repulsion of limb motor axons.},
author = {Irina Dudanova and Graziana Gatto and Rüdiger Klein},
url = {http://www.ncbi.nlm.nih.gov/pubmed/21109439},
doi = {10.1016/j.cub.2010.11.021},
issn = {1879-0445},
year = {2010},
date = {2010-12-01},
journal = {Current biology : CB},
volume = {20},
number = {23},
pages = {2150–6},
abstract = {Despite the abundance of guidance cues in vertebrate nervous systems, little is known about cooperation between them. Motor axons of the lateral motor column (LMC(L)) require two ligand/receptor systems, ephrinA/EphA4 and glial cell line-derived neurotrophic factor (GDNF)/Ret, to project to the dorsal limb. Deletion of either EphA4 or Ret in mice leads to rerouting of a portion of LMC(L) axons to the ventral limb, a phenotype enhanced in EphA4;Ret double mutants. The guidance errors in EphA4 knockouts were attributed to the lack of repulsion from ephrinAs in the ventral mesenchyme. However, it has remained unclear how GDNF, expressed dorsally next to the choice point, acts on motor axons and cooperates with ephrinAs. Here we show that GDNF induces attractive turning of LMC(L) axons. When presented in countergradients, GDNF and ephrinAs cooperate in axon turning, indicating that the receptors Ret and EphA4 invoke opposite effects within the same growth cone. GDNF also acts in a permissive manner by reducing ephrinA-induced collapse and keeping the axons in a growth-competent state. This is the first example of two opposing cues promoting the same trajectory choice at an intermediate target.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Despite the abundance of guidance cues in vertebrate nervous systems, little is known about cooperation between them. Motor axons of the lateral motor column (LMC(L)) require two ligand/receptor systems, ephrinA/EphA4 and glial cell line-derived neurotrophic factor (GDNF)/Ret, to project to the dorsal limb. Deletion of either EphA4 or Ret in mice leads to rerouting of a portion of LMC(L) axons to the ventral limb, a phenotype enhanced in EphA4;Ret double mutants. The guidance errors in EphA4 knockouts were attributed to the lack of repulsion from ephrinAs in the ventral mesenchyme. However, it has remained unclear how GDNF, expressed dorsally next to the choice point, acts on motor axons and cooperates with ephrinAs. Here we show that GDNF induces attractive turning of LMC(L) axons. When presented in countergradients, GDNF and ephrinAs cooperate in axon turning, indicating that the receptors Ret and EphA4 invoke opposite effects within the same growth cone. GDNF also acts in a permissive manner by reducing ephrinA-induced collapse and keeping the axons in a growth-competent state. This is the first example of two opposing cues promoting the same trajectory choice at an intermediate target.
Tchumatchenko, Tatjana; Geisel, T; Volgushev, M; Wolf, F
Correlations and synchrony in threshold neuron models Journal Article
In: Physical Review Letters, vol. 104, no. 5, pp. 058102, 2010.
@article{Tchumatchenko2010_correlations,
title = {Correlations and synchrony in threshold neuron models},
author = {Tatjana Tchumatchenko and T Geisel and M Volgushev and F Wolf},
year = {2010},
date = {2010-01-01},
journal = {Physical Review Letters},
volume = {104},
number = {5},
pages = {058102},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
