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GABAergic mIPSCs in rat cerebellar Purkinje cells are modulated by TrkB and mGluR1-mediated stimulation of Src

Andrew R. Boxall

1. Whilst protein tyrosine kinase (PTK) activity can modulate expressed GABA_A receptors in cell culture, the physiological consequences on synaptic GABA_A receptors are unknown. This was examined using whole-cell recording of bicuculline-sensitive mIPSCs in Purkinje cells (PCs) in cerebellar slices.

2. Postsynaptic application of a peptide activator of the non-receptor PTK Src (Src-peptide) enhanced mIPSC amplitudes by 39 % in the presence of brain-derived neurotrophic factor (BDNF) only; neurotrophin-3 (NT-3) was ineffective in this regard. Thus Src and TrkB (the receptor for BDNF) can physiologically interact to modulate synaptic GABA_A receptors.

3. In the presence of BDNF, pharmacological activation of metabotrophic glutamate receptor subtype 1 (mGluR1) by (S)-3,5-dihydrophenylglycine (3,5-DHPG) also lead to a 32 % enhancement of mIPSCs. This enhancement was blocked by intracellular dialysis of PCs with PP1, a selective inhibitor of Src.

4. It is concluded that, whilst GABA_A receptors are not constitutively regulated by endogenous PTK activity in PCs, co-activation of TrkB by BDNF and Src by mGluR1 is required to modulate GABAergic synapses in PCs.

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