Call for Abstracts
The scientific program highlighting North Dakota INBRE investigators will consist of both invited oral presentations and a poster session. All authors may submit their abstracts by following the directions below. The deadline for submission of abstracts is on September 28 at noon. Please limit abstracts to 250 words or less.
Abstract Submission Deadline: September 28, 2022 at noon.
NOTE: If you would like your abstract in the Symposium booklet, your abstract needs to be
submitted by September 28, 2022.
READ THE GUIDELINES FIRST BEFORE SUBMITTING YOUR ABSTRACT.
ABSTRACTS NOT FORMATTED CORRECTLY WILL BE RETURNED AS UNACCEPTABLE.
Guidelines and Rules for Submission
It is the author's responsibility to see that the following guidelines and instructions are followed to ensure optimal results.
1. Size. The entire abstract, including title, author(s), university, department and text must fit on half a sheet of (8.5" x 11") paper. The body of the abstract may have no more than 250 words, including any footnotes or acknowledgements.
2. Format. Use an Arial 11 pt. font; set 1" margins on all sides; single space only; do not use text boxes, tables, figures or diagrams.
3. Title. The title should be brief, clearly indicating the nature of the presentation. The title should be in bold type.
4. Authors. Include all authors' full first and last names. The presenting author's name should be listed first and underlined. Include all authors' department and university affiliations. If there are multiple authors with multiple affiliations (i.e. universities/departments) indicate affiliations according to the sample below.
Knockout mouse models reveal that activation of the α1A-adrenergic receptor reduces epileptiform event frequency in the mouse CA3 hippocampus
Jason A. Powers1,2, Joseph P. Biggane2, Theda P. Knauth1,2, Dianne M. Perez3, Van A. Doze2 1Department of Pathology, University of North Dakota, Grand Forks, ND; 2Department of Biomedical Sciences, University of North Dakota, Grand Forks, ND; 3Department of Molecular Cardiology, Cleveland Clinic Foundation, Cleveland, OH
Norepinephrine (NE) is a powerful modulatory neurotransmitter with well-described antiepileptic effects (Giorgi et al., 2004). The effects of NE are mediated by adrenergic receptor (AR) signaling, but it remains unclear which receptor subtypes mediate its antiepileptic actions. Previous studies suggest that activation of the α1A-AR increases inhibitory tone, via modulation of interneuron activity, and potentially reduces epileptiform activity (Bergles et al., 1996; Hillman et al., 2009). Of particular interest, long-term α1A-AR stimulation leads to improved memory, mood, and synaptic plasticity, making this receptor subtype an attractive therapeutic target (Doze et al., 2011). This study used brain slices prepared from α1A-AR knockout (KO), α1B-AR-KO, or wild-type (WT) control mice to further elucidate the role of each receptor subtype in reducing epileptiform activity. Using field potential recordings to measure epileptiform burst activity in the CA3 region of the hippocampus induced with low-magnesium artificial cerebrospinal fluid, dose-response curves were generated via application of increasing concentrations of the selective α1-AR agonist phenylephrine. In hippocampal slices from either WT control or α1B-AR-KO mice, phenylephrine application caused a concentration-dependent reduction in epileptiform event frequency. In contrast, application of phenylephrine resulted a small increase in epileptiform activity in α1A-AR-KO mice slices. Taken together, these data suggest that the α1A-AR is the sole AR subtype mediating the decrease in epileptiform burst frequency by phenylephrine. This data also suggest that the α1A-AR may be a promising target for attenuating hippocampal CA3 epileptiform activity.
5. No fax copies will be accepted in lieu of electronic submission.
6. Deadline: Submit your abstract by noon on September 28, 2022. Abstracts received after
the deadline will not be accepted.
NOTE: If you would like your abstract in the online Symposium booklet, your abstract needs to be
submitted by September 28, 2022.