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Regulation of muscarinic acetylcholine receptor-mediated synaptic responses by GABA_B receptors in the rat hippocampus

Robin A. Morton *†, Nick A. Manuel †, Diederick O. Bulters †, Stuart R. Cobb†‡ and Ceri H. Davies †§

1. Both GABA_B and muscarinic acetylcholine receptors (mAChRs) influence hippocampal-dependent mnemonic processing. Here the possibility of a direct interaction between GABA_B receptors and mAChR-mediated synaptic responses has been studied using intracellular recording in rat hippocampal slices.
2. The GABA_B receptor agonist (-)-baclofen (5-10 µM) depressed an atropine-sensitive slow EPSP (EPSP_M) and occluded the GABA_B-receptor-mediated IPSP (IPSP_B) which preceded it. These inhibitory effects were accompanied by postsynaptic hyperpolarization (9 ± 2 mV) and a reduction in cell input resistance (12 ± 3 %).
3. The selective GABA_B receptor antagonist CGP 55845A (1 µM) fully reversed the depressant effects of (-)-baclofen (5-10 µM) such that in the combined presence of (-)-baclofen and CGP 55845A the EPSP_M was 134 ± 21 % of control.
4. (-)-Baclofen (5-10 µM) caused a small (28 ± 11 %) inhibition of carbachol-induced (3.0 µM) postsynaptic depolarizations and increases in input resistance.
5. CGP 55845A (1 µM) alone caused an increase in the amplitude of the EPSP_M (253 ± 74 % of control) and blocked the IPSP_B that preceded it.
6. In contrast, the selective GABA uptake inhibitor NNC 05-0711 (10 µM) increased the amplitude of the IPSP_B by 141 ± 38 % and depressed the amplitude of the EPSP_M by 58 ± 10 %. This inhibition was abolished by CGP 55845A (1 µM).
7. Taken together these data provide good evidence that synaptically released GABA activates GABA_B receptors that inhibit mAChR-mediated EPSPs in hippocampal CA1 pyramidal neurones. The mechanism of inhibition may involve both pre- and postsynaptic elements.

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