Abstract Format for FEPS 2015 Kaunas (according to Acta Physiologica journal style)
Up to 300 Words (including the title, authors and affiliations)
Title
Authors
Affiliations
Aim:
Methods
Results:
Conclusions:
Abstract example for Plenary Lecture and Lecture of Invited speaker
DEVELOPMENT OF THE BUILDING PLAN OF THE HEART
Antoon F M Moorman
Department of Anatomy, Embryology & Physiology, Academic Medical Centre, Amsterdam
One of the most fascinating aspects in the formation of the heart is the very early development of the
electrical patterning as can be registered by the ECG, which is the registration of the rhythmic waves
of depolarizing activity over the cardiac muscle. In the mature heart, the conduction system is held
responsible for the rhythmic excitations and contractions. However, in chicken embryos a sinusoidal
type of ECG can already be derived from the linear heart tube stages at about two days of
development onward, and less than one day later when chamber formation has just been initiated, an
adult type of ECG can be monitored. The presence of an adult type of ECG in these early embryonic
hearts betrays the development of fast-conducting chambers rather than the presence of a conduction
system. We now know that the primary heart tube as seen in the early embryo contains the precursors
for the left ventricle only, or even less, whereas the precursor cells for the remainder of the cardiac
components are continuously added to both the venous and arterial pole of the heart tube during
further development from a single center of growth outside the heart. Therefore, it is impossible that
the straight heart tube contains the precursors for the conduction system as rings separating the
purported cardiac segments. While the primary heart tube is growing by addition of cells it does not
show significant cell proliferation, until chamber differentiation and expansion starts locally in the tube.
The transcriptional repressors Tbx2 and Tbx3 locally repress the chamber-specific program of gene
expression, by which these regions are allowed to differentiate into the distinct components of the
conduction system. The cardiac building plan and the underlying mechanisms of its formation are
conserved from fish to man. Detailed reconstructions of the developmental patterns of expression of
Tbx3 during development in mouse and human have revealed, that Tbx3 is expressed in those areas
of the heart tube that do not become chamber, i.e. in the sinu-nodal region, internodal region,
atrioventricular junction, atrioventricular bundle and bundle branches. These areas comprise not only
the conventional conduction system, but also the highly controversial areas of the internodal region
and the entire atrioventricular junction. Also the (right) ventricular outflow tract initially expresses these
transcriptional repressors, preventing it from chamber differentiation. These observations provide an
embryonic basis why some areas in the heart are more arrhythmogenic than other regions.
References:
Moorman AFM & Christoffels VM (2003). Physiol Rev 83:1223–1267.
van den Berg G et al. (2009). Circ Res 104:179-188.
Christoffels VM & Moorman AFM (2009). Circulation 2: 195-207.
Sizarov A et al (2011). Morphogenesis, Growth and Differentiation. Circulation 2011; 123:1125-1135.
Abstract example for Oral and Poster Presentations
Neuroprotective efficacy of the peroxisome proliferator activated receptor gamma ligand in
chronic cerebral hypoperfusion
Hale Sayan Ozaçmak1, Veysel Haktan Özaçmak1, Figen Barut2, Ewa Jakubowska Dogru3
1Department of Physiology,
2Pathology, Zonguldak Karaelmas University, Zonguldak, Turkey
3Department of Biology, Middle East Technical University, Ankara, Turkey
Aim: Chronic cerebral hypoperfusion can cause learning and memory impairment and neuronal
damage resembling the effects observed in vascular dementia. The present study was designed to
evaluate possible neuroprotective effects of rosiglitazone, a PPAR-gamma agonist, in rat model of
chronic cerebral hypoperfusion.
Methods: Cerebral hypoperfusion was induced by permanent bilateral occlusion of the common
carotid arteries. Oral administration of rosiglitazone (1.5, 3, and 6 mg/kg/day) or vehicle was carried
out for 5 weeks, starting one week before the surgery. Cognitive performance was assessed using the
Morris water maze. The density of the OX-42-labeled microglial activation and hippocampal neuronal
death were estimated. Synaptogenesis was also evaluated by the measurement of synaptophysin, the
pre-synaptic vesicular protein, and level via western blotting technique.
Results: Cerebral hypoperfusion for 30 days induced a significant cognitive impairment along with
hyperactivation of microglial and astroglial cells, hippocampal neuronal loss, and reduction of
synaptophysin level. The escape latencies for both 3 and 6 mg/kg of rosiglitazone-treated groups were
significantly shorter than in the ischemia control group (P<0.05). For the group treated with 3 mg/kg of
rosiglitazone, the number of OX-42 positive cells significantly decreased, as compared with two other
treatment groups (P<0.05). Compared to the sham-operated group, the amounts of synaptophysin
protein in the ischemia, 1.5 mg/kg, and 3 mg/kg rosiglitazone-treated groups, were statistically lower
(P<0.05), whereas in the group treated with 6 mg/kg of rosiglitazone, no significant difference was
noted.
Conclusions: Our results suggest that the chronic administration of rosiglitazone significantly
prevents chronic cerebral hypoperfusion-induced brain damage, at least, partly through suppressing
glial activation and preserving synaptic plasticity.