Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.702111
Title: Plasticity of NMDA receptor-mediated transmission and metaplasticity in the CA1 region of the hippocampus
Author: Bhouri, Mehdi
Awarding Body: University of Bristol
Current Institution: University of Bristol
Date of Award: 2013
Availability of Full Text:
Access from EThOS:
Abstract:
The hippocampus is a key structure of the brain for learning and memory processes. Two inputs to the CA1 region, the Schaffer collateral (SC) and the temporoammonic (TA) pathways, have different roles in these processes. N-methyl-D-aspartate receptors (NMDAR) are crucial for induction of synaptic plasticity and learning and memory processes, and are themselves subject to plasticity. Plasticity of NMDAR-mediated transmission can therefore change the threshold for induction of future synaptic plasticity and affect learning and memory. However, little is known about the effect of NMDAR-mediated plasticity on subsequent longterm potentiation (L TP) and long-term depression (L TO). In this study a combination of whole-cell recordings from CA1 pyramidal neurons and field recordings in the CA 1 area of the hippocampus was used to show that the SC-CA 1 input is subject to metaplasticity whereas the TA-CA1 input is not. Indeed L TO of NMDAR-mediated transmission is selectively induced in the SC pathway but not in the TA pathway. This LTD of NMDA EPSCs can prevent subsequent induction of L TP of AMPA receptor-mediated transmission via an increase of the threshold. The L TO of NMDAR-mediated transmission was shown to be mGlu1 receptor-dependent. However, LTD of AMPAR-mediated transmission in both inputs was not affected by the prior induction of L TO of NMDAR-mediated transmission. Therefore, these results show that the SC-CA 1 input can undergo meta plasticity whereas the TA-CA 1 input does not. These differences could explain the distinct roles of the two inputs in memory. In some neurodegenerative diseases such as Alzheimer's disease ,(AD) memory is impaired. AD is a tauopathy characterized by the aggregation of AB, a derivative of amyloid precursor protein (APP), and Tau, a microtubule-associated protein, which lead to synaptic loss and neuronal degeneration.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.702111  DOI: Not available
Share: