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Journal Article

γ-Aminobutyric acidB autoreceptors in substantia nigra and neostriatum of the weaver mutant mouse

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Radnikow,  Gabriele
Cortical Circuits, Max Planck Institute for Medical Research, Max Planck Society;
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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https://www.sciencedirect.com/science/article/pii/S0304394001014963/pdfft?md5=5caf508fe1fa6846e6787e9b46c0e686&pid=1-s2.0-S0304394001014963-main.pdf
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https://doi.org/10.1016/S0304-3940(01)01496-3
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Citation

Radnikow, G., Titz, S., Mades, S., Bäurle, J., & Misgeld, U. (2001). γ-Aminobutyric acidB autoreceptors in substantia nigra and neostriatum of the weaver mutant mouse. Neuroscience Letters, 299(1-2), 81-84. doi:10.1016/S0304-3940(01)01496-3.


Cite as: https://hdl.handle.net/21.11116/0000-0000-3F8F-A
Abstract
The weaver mutation causes cell loss in the center of the substantia nigra, pars compacta. We compared the depression of γ-aminobutyric acid (GABA)A synaptic currents by the GABAB agonist R-baclofen in pars compacta neurons of weaver mice which were largely spared from cell degeneration and of wild-type mice. In weaver neurons the suppression of GABAA synaptic currents by R-baclofen was reduced compared to wild-type neurons. The EC50 of R-baclofen was 6.3 times higher in weaver than in wild-type mice. In the neostriatum, which is not a target of the mutation, such a difference did not exist. We conclude that in the pars compacta the weaver mutation leads to a reduced presynaptic autoinhibition through GABAB receptors which may promote survival of a subset of weaver neurons in the pars compacta.