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Synchronizing neurons in acute hippocampal slices for generation of epileptiform activity

Sakka, Vasiliki (2017) MOBN01 20162
Degree Projects in Molecular Biology
Popular Abstract
The etiology of epileptic seizures is not completely understood. Literature results estimate that the main reason for epileptiform activity is a shift in the fine-tuned balance between excitation and inhibition in neural circuits, leading to hyperexcitability. Normal brain function is dependent on local inhibitory GABAergic input of interneurons on pyramidal cells. GABAergic interneurons and loss and formation of new abnormal GABAergic terminals leads to dysfunctional regulation of activity and a network more prone to seizures. However, other studies support that activation of inhibitory interneurons can initiate epileptic discharges by synchronizing principle cells through GABAA-receptor signalling.
With all the above as background, the... (More)
The etiology of epileptic seizures is not completely understood. Literature results estimate that the main reason for epileptiform activity is a shift in the fine-tuned balance between excitation and inhibition in neural circuits, leading to hyperexcitability. Normal brain function is dependent on local inhibitory GABAergic input of interneurons on pyramidal cells. GABAergic interneurons and loss and formation of new abnormal GABAergic terminals leads to dysfunctional regulation of activity and a network more prone to seizures. However, other studies support that activation of inhibitory interneurons can initiate epileptic discharges by synchronizing principle cells through GABAA-receptor signalling.
With all the above as background, the aim of this master thesis project was to test if it is possible to produce seizure-like discharges by optogenetic activation of principal cells only, or interneurons only.
To this end, I used two transgenic mouse strains, specifically expressing channelrhodopsin ChR2 under the Cre-dependent promoter for CamKII neurons or PV interneurons. Extracellular synaptic field potentials were performed in stratum lucidum of CA3 and stratum radiatum of CA1.
Selective light activation of PV inhibitory interneurons was not sufficient to initiate discharges detected with field recordings. Whole-cell patch-clamp recordings performed in subiculum supports these results, were the number of cells that had epileptic bursts was no significant. However, activating the excitatory neuronal circuit in kainite-injected animals (KA) resulted in a facilitation of depolarization events in stratum radiatum of CA1.

Master’s Degree Project in Molecular Biology 45 credits 2017
Department of Biology, Lund University

Advisor: My Andersson
Advisors Unit/Department Epilepsy Center (Less)
Please use this url to cite or link to this publication:
author
Sakka, Vasiliki
supervisor
organization
course
MOBN01 20162
year
type
H2 - Master's Degree (Two Years)
subject
language
English
id
8907470
date added to LUP
2017-05-18 15:49:38
date last changed
2017-05-18 15:49:38
@misc{8907470,
  author       = {Sakka, Vasiliki},
  language     = {eng},
  note         = {Student Paper},
  title        = {Synchronizing neurons in acute hippocampal slices for generation of epileptiform activity},
  year         = {2017},
}