GABA release from cerebellar stellate cells is developmentally regulated by presynaptic GABAB receptors in a target-cell-specific manner

Authors

  • Simone Astori,

    1. Department of Molecular Neurobiology, Max-Planck-Institute for Medical Research, Jahnstrasse 29, D-69120 Heidelberg, Germany
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    • *

      Present address: Department of Cell Biology Morphology, University of Lausanne, Rue du Bugnon 9, CH-1005 Lausanne, Switzerland

  • Rafael Luján,

    1. Departamento de Ciencias Médicas, CRIB-Facultad de Medicina, Universidad Castilla-La Mancha, Campus Biosanitario, Albacete, Spain
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  • Georg Köhr

    1. Department of Molecular Neurobiology, Max-Planck-Institute for Medical Research, Jahnstrasse 29, D-69120 Heidelberg, Germany
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Dr S. Astori, at *Present address below.
E-mail: simone.astori@unil.ch

Abstract

Transmitter release from boutons along a common axon is often regulated depending on the postsynaptic target. Here, GABA release from cerebellar stellate cells onto Purkinje cells and other stellate cells was examined in acute cerebellar slices of 2- and 4-week-old mice. Consistent with previous findings on action potential-dependent GABA release, we found a developmental decrease in inhibitory inputs onto Purkinje cells but not onto stellate cells when recording miniature inhibitory postsynaptic currents (mIPSCs). Although amplitudes of mIPSCs were developmentally reduced in both cell types, mIPSC frequencies were decreased in Purkinje cells but were increased in stellate cells. Similarly, modulation of GABA release by presynaptic GABAB receptors changed during development in Purkinje cells but not in stellate cells, as demonstrated by the baclofen-mediated depression of mIPSC frequency and evoked IPSC (eIPSC) amplitudes. The selectively diminished baclofen effect in 4-week-old Purkinje cells correlated with a selective downregulation of presynaptic GABAB receptors at stellate cell-to-Purkinje cell synapses observed by immunoelectron microscopy analysis. Thus, expression of GABAB receptors in stellate cell axons and presynaptic modulation of GABA release appear to change during development in a target-cell-specific manner.

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