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γ−Aminobutyric acid_B 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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Zitation

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

Zusammenfassung

The weaver mutation causes cell loss in the center of the substantia nigra, pars compacta. We compared the depression of small gamma, Greek−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