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

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Astori,  Simone
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Köhr,  Georg
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Astori, S., Luján, R., & Köhr, G. (2009). GABA release from cerebellar stellate cells is developmentally regulated by presynaptic GABAB receptors in a target-cell-specific manner. European Journal of Neuroscience: European Neuroscience Association, 30(4), 551-559. doi:10.1111/j.1460-9568.2009.06856.x.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002C-0BFC-2
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.