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Abstract and Poster Instructions

We encourage all participants to consider presenting a paper at the meeting. The abstracts of the conference will be subject to review and published on our website, www.otago.ac.nz/awcbr in the Proceedings of the International Australasian Winter Conference on Brain Research. Please make your abstracts as complete as possible, including a full description of the experimental results, while adhering to the 300 total word limit. Unacceptable abstracts will be returned to the authors, who will be asked to submit a revised abstract. No changes to the abstract can be accepted after 7 July 2017.

Note: Only one abstract is permitted per presenter.

Abstract instructions

Head the abstract with the title in upper and lower case; authors (presenter first); affiliation and address. Each of these should be on a separate line.

  • No abstract should exceed 300 words including title, affiliation, etc.
  • No references should be cited at the end of abstracts and abstracts over the 300 word limit will be sent back to authors to amend.

The abstract style should conform to the APA guidelines (see back issues of the Proceedings on our website). All abstracts should be submitted online via the AWCBR website (www.otago.ac.nz/awcbr). Abstracts should contain a statement of the problem, brief methods, clear results, and a statement of the conclusions or significance of the findings. Abstracts will be reviewed and may be returned to the authors for modification.

Note: The abstract file should be titled with the FIRST author’s name as: “lastname-firstname-AWCBR”. The first author must be the presenting author.

Sample abstract

Apoptotic Purkinje Cell Death in the Neonatal Rat Cerebellum Following a Single Exposure to Ethanol on Postnatal Days 0 to 4

N. M. IDRUS and R. M. A. NAPPER

Department of Anatomy and Structural Biology
University of Otago, Dunedin, New Zealand

The cerebellar Purkinje cells (Pcells) have been studied extensively in the rodent, and a temporal window of vulnerability to ethanol-induced death exists from postnatal day (PD) 4 to 6. The endpoint of this temporal window has been thoroughly investigated, but the time of onset has not. This study aimed to determine the earliest timepoint postnatally following exposure to ethanol, at which Pcells express active caspase-3, a key enzyme involved in the initiation and regulation of apoptotic cell death. On G22 (PD 0), the pups of timed pregnant Sprague-Dawley dams were randomly assigned to groups – alcohol-exposed (AE), intubation controls, and suckle controls (SC) – and to days PD 0-4. On each day, pups were perfusion-fixed at 8, 10, and 12 hours after the initial ethanol exposure. Cerebella were removed, wax-embedded, and serial 5um-thick sections cut. Sections were immunolabeled for active caspase-3 and the number of caspase-3 positive Pcells counted using the physical disector method. The number of labeled Pcells in the cerebellar vermis was significantly greater (p<0.05) in ethanol-treated animals compared to controls for all days studied (e.g. mean number of caspase-3 positive Pcells: AE = 74.33 compared to SC = 18.00 for PD1). This study shows that the window of vulnerability for Pcells to ethanol exposure during development is longer than previously thought.

Poster instructions

Posters should have a maximum width of 1.0 m. They should be self-contained, and be self-explanatory.