The role of postsynaptic spiking and muscarinic acetylcholine receptors in the induction of synaptic plasticity at the Schaffer collateral synapse in the rat hippocampus
The induction of NMDA receptor-dependent long-term. potentiation (LTP) requires the coincidence of presynaptic glutamate release and postsynaptic depolarisation. The postsynaptic depolarisation requirement for LTP induction can be supplied by a variety of mechanisms including; the temporal summation...
| Main Author: | |
|---|---|
| Published: |
University of Bristol
2007
|
| Subjects: | |
| Online Access: | http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486127 |
| Summary: | The induction of NMDA receptor-dependent long-term. potentiation (LTP) requires the coincidence of presynaptic glutamate release and postsynaptic depolarisation. The postsynaptic depolarisation requirement for LTP induction can be supplied by a variety of mechanisms including; the temporal summation of presynaptic inputs, the back-propagation of somatic action potentials and the initiation of locally restricted dendritic spikes. The work described in this thesis demonstrates that the mechanism providing the postsynaptic depolarisation required for the induction of LTP at the Schaffer collateral to CA1 pyramidal cell synapse changes during development in the rat hippocampus. In acute slices from adult animals there is a reliance on the coincidence of presynaptic inputs and bursts of somatic action potentials for the induction of LTP. In slices from juvenile rats, LTP can occur independently of somatic action potentials and instead requires strong presynaptic stimulation or prolonged somatic depolarisation during trains of postsynaptic spikes. Numerous studies have I indicated the importance of the precise timing of presynaptic and postsynaptic spikes in dictating the direction and magnitUde of synaptic plasticity. In experiments carried out here the induction of LTP is spike timing independent in slices from juvenile rats and instead displays a dependency on spike frequency. I also show that the postsynaptic depolarisation requirement for LTP induction in juvenile hippocampal slices can be modulated through the activation of muscarinic acetylcholine receptors. The specific activation of M1 muscarinic acetylcholine receptors lowers the threshold for LTP induction independently of somatic activity through depolarisation of CA1 pyramidal cell dendrites. |
|---|