Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252451
Title: Involvement of voltage-sensitive calcium channels in activity-dependent depression of neuronal signalling in the adult rat hippocampus
Author: Marsden, David Peter
ISNI:       0000 0001 3619 380X
Awarding Body: University of Southampton
Current Institution: University of Southampton
Date of Award: 2002
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Abstract:
Synaptic activity and network excitability in area CA1 of adult rat hippocampal slices were investigated using field potential recordings. Changes in network excitability associated with long-term depression (LTD) were measured using EPSP-to-spike (E-S) curves. Network inhibition was evaluated using a paired-pulse stimulation protocol with a 20 ms inter-pulse interval. The participation of voltage-sensitive calcium channels (VSCCs) in the induction of LTD and in E-S coupling (and dissociation of this E-S relationship) was investigated pharmacologically. A critical assessment was made of published methods of analysing E-S data. Application of low-frequency stimulation (LFS, 1Hz, 900 pulses) to the Schaffer collateral-commissural fibres of slices at both room temperature and 32°C (at which further work was carried out), induced NMDA receptor-dependent LTD of field EPSP slope (EPSP-S) and population spike amplitude (PS-A), which lasted for at least 30 minutes. Interestingly, after LFS, there was only a small E-S depression but, importantly, paired-pulse inhibition of the PS-A persisted. This novel observation was not due to inability of these slices to express E-S potentiation. Induction of long-term potentiation, as well as application of GABA_A antagonists, caused significant E-S potentiation, but with large decreases in inhibition. The full range of changes to the E-S relationship has not been fully described previously, however here; slices were shown to be able to also undergo significant E-S depression when responses to paired-pulse stimuli were compared, i.e. paired-pulse inhibition of the spike lead to E-S depression. The R/T-type VSCC blocker NiCl₂ (50mM) caused highly significant reductions of both EPSP-S and PS-A and a decrease in inhibition. However, paired-pulsed inhibition remained functional (>80%) and only a non-significant E-S depression was observed. NiCl₂ significantly reduced the amount of LTD of the PS-A but did not block LTD of the EPSP-S and did not alter the E-S relationship found after LFS under control conditions.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.252451  DOI: Not available
Keywords: Electrophysiology
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