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Permanent link (DOI): https://doi.org/10.7939/R3ZC7S517

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Mechanisms involved in the norepinephrine-mediated protection of synapses from depotentiation Open Access

Descriptions

Other title
Subject/Keyword
Norepinephrine
Long term potentiation
Depotentiation
Synaptic plasticity
LTP
DPT
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Rah, Sean S
Supervisor and department
Nguyen, Peter (Physiology)
Examining committee member and department
Gosgnach, Simon (Physiology)
Ali, Declan (Physiology)
Dickson, Clayton (Psychology)
Department
Department of Physiology
Specialization

Date accepted
2016-07-06T11:21:41Z
Graduation date
2016-06:Fall 2016
Degree
Master of Science
Degree level
Master's
Abstract
Norepinephrine (NE) is a key neuromodulator that controls the longevity of synaptic plasticity such as long term potentiation (LTP). Activation of beta-adrenergic receptors (β-ARs) is known to boost persistence of LTP in area CA1 of mouse hippocampal slices. Activity-induced weakening (depotentiation, DPT) via 5Hz stimulation depresses the strength of synaptic transmission at synapses that have recently undergone LTP. I tested the hypothesis that NE primes synapses for subsequent long-lasting LTP, serving to protect potentiated synapses from depotentiation. Using population excitatory postsynaptic potential (EPSP) recordings from CA1 of mouse hippocampal slices, I show that NE (10uM) applied well before weak tetanic stimulation (1 x 100-Hz, 1s) protects synapses from depotentiation. This protection is no longer present when PKA and ERK (downstream protein kinases of the β-AR pathway) have been pharmacologically blocked. I also present evidence suggesting that, in addition to these kinases, NMDA receptors may also play a role in initiating the intracellular mechanisms that protect, or immunize, potentiated synapses from activity-induced weakening.
Language
English
DOI
doi:10.7939/R3ZC7S517
Rights
This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for the purpose of private, scholarly or scientific research. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.
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