gms | German Medical Science

55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

25. bis 28.04.2004, Köln

Gabapentin-lactam as a neuroprotective agent on E14 rat ventral mesencephalon dissociated embryonic cell cultures

Gabapentin-lactam ist ein neuroprotektiver Wirkstoff fr dopaminerge Neurone in Zellkulturen des embryonalen Mescencephalins

Meeting Abstract

  • corresponding author Anna Papazoglou - Labor fr Molekulare Neurochirurgie, Abt. fr Funktionelle und Stereotaktische Neurochirurgie, Universit酹sklinikum Freiburg, Freiburg
  • A. Klein - Sektion Neuropharmakologie der Neurologischen Klinik, Universit酹sklinikum Freiburg, Freiburg
  • T. Feuerstein - Sektion Neuropharmakologie der Neurologischen Klinik, Universit酹sklinikum Freiburg, Freiburg
  • J. Wessolleck - Labor fr Molekulare Neurochirurgie, Abt. fr Funktionelle und Stereotaktische Neurochirurgie, Universit酹sklinikum Freiburg, Freiburg
  • B. Baumer - Labor fr Molekulare Neurochirurgie, Abt. fr Funktionelle und Stereotaktische Neurochirurgie, Universit酹sklinikum Freiburg, Freiburg
  • G. Nikkhah - Labor fr Molekulare Neurochirurgie, Abt. fr Funktionelle und Stereotaktische Neurochirurgie, Universit酹sklinikum Freiburg, Freiburg

Deutsche Gesellschaft fr Neurochirurgie. Ungarische Gesellschaft fr Neurochirurgie. 55. Jahrestagung der Deutschen Gesellschaft fr Neurochirurgie e.V. (DGNC), 1. Joint Meeting mit der Ungarischen Gesellschaft fr Neurochirurgie. K闤n, 25.-28.04.2004. Dsseldorf, K闤n: German Medical Science; 2004. DocP 03.24

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2004/04dgnc0307.shtml

Published: April 23, 2004

© 2004 Papazoglou et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Objective

Parkinson's disease (PD) is one of the most common neurodegenerative diseases. During the early onset in the disease, dopamine (DA)-containing neurons in the substantia nigra pars compacta (SNc) degenerate, leading to slower movements, rigidity, resting tremor and postural imbalance. In contrast to other neurodegenerative disorders, a relatively good symptomatic therapy for PD does exist consisting mainly of dopamine replacement and adjuvant surgical therapy that relieves most motor symptoms. However, there is still a need for a novel therapy preventing cell death ('neuroprotective') or restoring degenerating neurons in PD ('neurorestorative'). In this study, a potential neuroprotective agent gabapentin-lactam (GBP-L) is evaluated in vitro.

Methods

In order to test the effect of GBP-L on primary cultures of dopaminergic (DAergic) neurons, the ventral mesencephalon of E14 Spargue Dawley rat embryos was removed and dissociated. Cells were plated at a concentration of 100,000 cells/cm2 in 48-well plates precoated with 0.01% poly-L-ornithine. At 4 days in vitro, cultures were treated for 24h with 10然, 15然 or 30然 concentrations of hydroxydopamine (6-OHDA) in the absence or presence of 500然, 250然, 100然 or 50然 GBP-L. Quantitative and morphometric analysis were focussed on cell cultures stained for tyrosine hydroxylase (TH), DAPI and β-tubulin (Tub-1).

Results

6-OHDA treatment resulted in a dose-depended decrease of TH+ neurons from 1.7% at 10然, 0.9% at 15然 and 0.2% at 30然 (p<0.05% for the two latter). 500m然 GBL-P treatment resulted in a significant and complete protection at 30然 6-OHDA induced toxicity (p<0.05). Similar results are obtained with GBP-L pre-treatment at 500然 (p<0.05%) and 250然 (p<0.05%) GBP-L concentrations but not at 100然 GBP-L.

Conclusions

To conclude, our results showed that GBP-L can protect dopamine neurons in vitro after neurotoxin treatment with 6-OHDA. These data indicate that GBP-L has neuroprotective potentials with possible clinical implications. Further studies will be interesting to evaluate the neuroprotective mechanism of GBP-L and its in vivo potentials.