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001-es BibID:	BIBFORM013273
Első szerző:	Teuchner, Barbara
Cím:	VIP, PACAP-38, BDNF and ADNP in NMDA-induced excitotoxicity in the rat retina / Barbara Teuchner, Andreas Dimmer, Christian Humpel, Albert Amberger, Reiner Fischer-Colbrie, Jozsef Nemeth, James A. Waschek, Gerhard Kieselbach, Martina Kralinger, Eduard Schmid, Nikolaos Bechrakis, Josef Troger
Dátum:	2011
Megjegyzések:	To evaluate the effect of intravitreal injection of N-methyl-D-aspartate(NMDA) on brain-derived neurotrophic factor (BDNF), pituitary adenylatecyclase-activating peptide-38 (PACAP-38), vasoactive intestinal peptide (VIP) andthe VIP-associated glial protein activity-dependent neuroprotective protein(ADNP) in the rat retina. These elements have well-documented neuroprotectiveproperties and may thus be integrated in endogenous neuroprotective mechanismsin the retina which break down in NMDA excitotoxicity.Methods: A volume of 2 ll of 100 nmol NMDA was intravitreally injected intoone eye of rats, the untreated eye served as a control. Time-dependent effects ofNMDA on VIP, PACAP-38 and BDNF were detected by radioimmunoassay andELISA, and the effect on the expression of VIP, PACAP-38 and ADNP was evaluatedby quantitative RT-PCR 20 days after NMDA injection. Topical flunarizineserved to find out whether the effect of NMDA is counteracted.Results: Compared to PACAP-38, VIP levels significantly decreased on days 1, 7,14, 28 and 56 after NMDA injection indicating that VIPergic cells are more vulnerablethan PACAP-38-expressing cells. The expression of VIP and ADNP but not ofPACAP-38 was found to be reduced, and application of topical flunarizine counteractedthe decrease of VIP. BDNF levels significantly increased after days 1 and 3.Conclusion: The early upregulation of BDNF seems to act neuroprotectively andleads to a delay of ganglion cell loss. Although there is no direct evidence, thedecrease of VIP and ADNP ? the consequence of the presence of NMDA receptorson these peptide-expressing cells ? might contribute to the breakdown ofendogenous neuroprotective mechanisms given that the decrease of the VIP-relatedADNP runs in parallel with the decrease of VIP. Activating and maintaining thesemechanisms must be the primary aim in the therapy of diseases with retinal neuronaldegeneration.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban ADNP BDNF NMDA PACAP-30 retina VIP
Megjelenés:	Acta Ophthalmologica 89 : 7 (2011), p. 670-675. -
További szerzők:	Dimmer, Andreas Humpel, Christian Amberger, Albert Fischer-Colbrie, Reiner Németh József (1954-) (vegyész, analitikus) Waschek, James A. Kieselbach, Gerhard Kralinger, Martina Schmid, Eduard Bechrakis, Nikolaos Troger, Josef
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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