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Title: Modulation of cholinergic synaptic transmission in the rat hippocampus
Author: Morton, Robin A.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1998
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Intracellular recordings were made from pyramidal neurones in the CA1 region of the rat hippocampus to investigate aspects of cholinergic synaptic transmission in the mammalian brain. In the presence of ionotropic glutamate and GABA receptor antagonists, single shock stimulation of the septohippocampal cholinergic input in stratum oriens evoked a slow excitatory postsynaptic potential (EPSP) which was associated with an increase in input resistance. Stimulation at intensities sub-threshold for evoking a slow EPSP caused a reduction of spike frequency adaptation. Pharmacological analysis of these responses revealed that they were mediated by muscarinic acetylcholine receptors (mAChRs). Having established a protocol for evoking reproducible mAChR-mediated EPSPs (EPSPMs) and mAChR-mediated inhibition of spike frequency adaptation, experiments were conducted to investigate the modulation of these responses by other neurotransmitter receptors. In this respect, activation of adenosine receptors by the broad spectrum adenosine receptor agonist 2-chloroadenosine (CADO) reversibly inhibited mAChR-mediated synaptic responses in a concentration dependent manner. The pharmacological profile of this effect established that it was mediated by adenosine A1 receptors. In conclusion, it is possible to evoke isolated muscarinic acetylcholine receptor mediated synaptic responses with a single stimulus in the CA1 region of the rat hippocampus. Adenosine A1 receptors are present on cholinergic terminals in this region and act to inhibit these responses by an unknown mechanism. GABAB receptor activation also inhibits cholinergic synaptic transmission although the mechanism and site of action of this is unclear. Finally, endogenous adenosine and GABA, acting at adenosine A1 and GABAB receptors respectively, inhibit cholinergic synaptic transmission in vitro. This modulation provides a potentially important mechanism for the control of neuronal excitability in the hippocampus in vivo.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available