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Sample Abstract
(List of items to include in your abstract)
1. Abstract Title: Mechanisms of cerebral hyperexcitability induction by antiviral acute
phase response
2. All Authors: Miranda Reed, PhD, Auburn University; Holly Hunsberger, PhD, Auburn University, Gregory
Konat, PhD, West Virginia University
Presenters: Miranda Reed, PhD, Auburn University
3.
4. Short Description of what will be discussed during the presentation
A body of clinical evidence has demonstrated that viral infections in the periphery exacerbate neurodegenerative
conditions, e.g., multiple sclerosis, Parkinson disease, Alzheimer Disease (AD), and seizures. For example, peripheral
infections increase the propensity and severity of seizures in susceptible populations, and AD patients suffering from
systemic infections develop symptoms earlier and exhibit greater cognitive impairments than patient with less
infectious insults. Although experimental studies strongly indicate the initial response of the innate immune system
to infection, i.e., the acute phase response (APR), as the primarily trigger, the underlying mechanisms have not been
defined. In a quest to elucidate these mechanisms, we have shown that APR instigated by a viral mimic, polyinosinicpolycytidylic acid (PIC), elicits protracted hyperexcitability of cerebral networks by robustly increasing the levels of
resting extracellular glutamate. These levels gradually return to baseline values within four days. While pre-synaptic
potassium-evoked glutamate release is not affected, glutamate uptake is profoundly impaired and non-vesicular
glutamate release is augmented, indicating functional alterations of astrocytes. Electrophysiological examination of
hippocampal slices from PIC-challenged mice reveals a several fold increase in the basal synaptic transmission as
compared to control slices. PIC challenge also increased the probability of pre-synaptic glutamate release as seen
from a reduction of paired-pulse facilitation. Furthermore, twenty-four hours after PIC challenge, the mice feature
an approximately 3-fold increase in cumulative seizure scores and 2-fold increase in the duration of status
epilepticus induced by subcutaneous (s.c.) injection of 12 mg/kg of kainic acid. Seizure scores positively correlated
with pre-seizure tonic glutamate. Moreover, seizures resulted in a profound (76%) elevation of extracellular
glutamate in the CA1 of PIC-challenged but not saline-injected mice. Our results implicate the increase of
extracellular glutamate as a mediator of seizure hypersusceptibility induced by peripheral viral challenge. Finally,
our findings that similar alterations in glutamatergic functioning (i.e., increased extracellular levels and decreased
glutamate uptake) are observed in mouse models of AD early suggests one possible mechanism by which peripheral
infections accelerate the onset and progression of AD.
5. What will the audience take away from your presentation? (Try to list 3-5 specific items)

Explain how the audience will be able to use what they learn?
The elucidation of underlying mechanisms by which peripheral infections increase hyperexcitability will vertically
advance and expand understanding of the mechanistic link between viral infections in the periphery and the
exacerbation of neurodegeneration, an important consideration given the number of neurodegenerative diseases in
which increased glutamatergic signaling is observed. The proposed study is significant because it will provide a
foundation for the development of innovative therapeutic strategies to attenuate or even prevent the progression
of neurological deficits in patients afflicted with neurodegenerative disorders.

How will this help the audience in their job? Is this research that other faculty could use to expand their
research or teaching? Does this provide a practical solution to a problem that could simplify or make a
designer’s job more efficient? Will it improve the accuracy of a design, or provide new information to assist
in a design problem? List all other benefits.
In addition to the general knowledge, we will discuss a novel method to examine glutamatergic levels in awake,
behaving animals. This methodology allows for correlation with behavioral tasks, allowing for more nuanced
experimental questions.
6. Is this abstract connected to an organized session? If yes, please provide full session
title. No
7. Biography of presenting author (about 100 words)
Dr. Miranda N. Reed is an Associate Professor of Drug Discovery and Development at Auburn University. Trained in
psychology, neuroscience, and neurology, her postdoctoral studies focused on the consequences of tau
mislocalization into dendritic spines in the context of Alzheimer’s disease at University of Minnesota under the
direction of Karen Hsiao Ashe. Her current work focuses on alterations in glutamatergic functioning and the
resultant consequences of these alterations in various neurodegenerative conditions, including Alzheimer’s disease
and seizures.
Author Details:
Full Name: Miranda Nicole Reed
Contact Number: 334-844-7401
Country: USA
Category: Oral
Session Name: Neurodegenerative conditions
Email: [email protected]