BELGIAN BRAIN CONGRESS 2008
Kursaal-Oostende
Friday Oct 24 and Saturday Oct 25

1.	Abstract presentation

Marges :
	up	2.5 cm	down	2.5 cm
	left	3 cm	right	2.5 cm

Title : Arial, 14 pt, Bold, Capital letters, maximum 120 characters 

Author(s) : Arial, 11 pt, single space. The name of the presenting author should be underlined.

Example :

Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HT1 receptor signaling 

D. Hoyaux1, C. C.W. Heizmann2, T. Vogel3, B.W. 

1 Laboratory of Histology, Faculty of Medicine Université Libre de Bruxelles, Brussels (Belgium)
2 Division of Clinical Chemistry and Biochemistry, Dpt Pediatrics, University of Zürich, Zürich (Switzerland)
3 Institute of Experimental Dermatology, Westfälische Wilhelms-Universität Münster, Münster (Germany)

Institution : Arial, 10 pt, single space. 
Text : Arial, 11 pt, 1.5 space, justified. MAX 300 WORDS  with OBJECTIVES, BACKGROUND, RESULTS, CONCLUSION

Example:
OBJECTIVES: Roles of CGRP and 5-HT in glutamate release from cultured trigeminal cells. BACKGROUND: The aberrant release of the neurotransmitters, glutamate and calcitonin-gene related peptide (CGRP), from trigeminal neurons has been implicated in migraine. The voltage-gated P/Q-type calcium channel has a critical role in controlling neurotransmitter release and has been linked to Familial Hemiplegic Migraine. Therefore, we examined the importance of voltage-dependent calcium channels in controlling release of glutamate and CGRP from trigeminal ganglion neurons isolated from either male or female rats and grown in culture. Serotonergic pathways are likely involved in migraine, as triptans, a class of 5-HT1 receptor agonists, are effective in the treatment of migraine and their effectiveness may be due to inhibiting neurotransmitter release from trigeminal neurons. We also studied the effect of serotonin receptor activation on release of glutamate and CGRP from trigeminal neurons grown in culture. RESULTS: P/Q-, N- and L-type channels each mediate a significant fraction of potassium-stimulated release of glutamate and CGRP. We determined that 5-HT significantly inhibits potassium-stimulated release of both glutamate and CGRP. Serotonergic inhibition of both CGRP and glutamate release can be blocked by pertussis toxin and NAS-181, a 5-HT1B/1D antagonist. Stimulated release of CGRP is unaffected by Y-25130, a 5-HT3 antagonist and SB 200646, a 5-HT2B/2C antagonist. CONCLUSIONS: These data suggest that release of both glutamate and CGRP from trigeminal neurons is controlled by calcium channels and modulated by 5-HT signaling in a pertussis-toxin dependent manner and probably via 5-HT1 receptor signaling. This is the first characterization of glutamate release from trigeminal neurons grown in culture.

Keywords : maximum 6 keywords. 

2.	Abstract submission form

Contact name : Chaballe Linda	

E-mail address : L.Chaballe@student.ulg.ac.be	

Address : Avenue de l’Hôpital 1, tour de pathologie, batiment B36 +1   CNCM	

City : Liège		Postal Code : 4000	

Country : Belgium	

3.	
Abstract

Expression and Role of Placental Growth Factor (PLGF) in the inflammatory context resulting from nerve injury, the Wallerian Degeneration

Linda  Chaballe1, Murielle Wouters1, Maxime Sempels1, Lieve Moons2, Peter Carmeliet3, Jean Schoenen1, Rachelle Franzen1.

1Research Centre for Cellular and Molecular Neurobiology, research unit on cephalic pain and axonal regeneration, University of Liège, Liège, Belgium.
2Laboratory of Neural Circuit Development and Regeneration, Zoological Institute K.U.Leuven, Belgium.
3The Centre for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology, KU Leuven, Leuven, Belgium.

OBJECTIVES: Expression and roles of PLGF during Wallerian degeneration. BACKGROUND: Wallerian degeneration (WD) is an inflammatory process of axonal degeneration. It includes axonal fragmentation, myelin breakdown and debris clearance by Schwann cells and macrophages, providing a favourable environment to successful axonal regeneration after nerve injury. Placental growth factor (PLGF) is a glycoprotein of the VEGF (Vascular Endothelial Growth Factor) family. Originally identified in the placenta, it has also been detected in other organs, like brain, especially when cells are activated or stressed. In addition to its pro-angiogenic action, PLGF has various properties like monocyte activation and attraction, ability to increase expression of pro-inflammatory cytokines and chemokines, as well as axonal guidance that could make it a candidate involved in the WD process, and in the success of axonal regeneration. RESULTS: In normal adult mice, PLGF is expressed in axons as well as in the cell body of dorsal root ganglion neurons. In the axon, PLGF is periaxonal, and its expression is interrupted at the nodes of Ranvier. Early after injury, PLGF is only detected in Schwann cells which also express the marker p75NGFr. At further post-injury delays, PLGF is again detected in regenerating axons, while its expression in Schwann cells decreases. We also demonstrate that in absence of PLGF, Wallerian degeneration events, like macrophage invasion and Schwann cell dedifferentiation are delayed in Pgf-/- mice compared to wild-type mice. CONCLUSIONS: These results strongly support our hypothesis that PLGF plays a role in the inflammatory process of WD. Further work will focus on various cytokines whose expression is influenced by PLGF and known to play a role in WD.