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Suppressed kindling epileptogenesis in mice with ectopic overexpression of galanin

In English

Författare

  • Merab Kokaia
  • Kristina Holmberg
  • Avtandil Nanobashvili
  • Zhi-Qing D. Xu
  • Zaal Kokaia
  • Urban Lendahl
  • Susanne Hilke
  • Elvar Theodorsson
  • Ulrika Kahl
  • Tamas Bartfai
  • Olle Lindvall
  • Tomas Hökfelt
Visa allt

Summary, in English

The neuropeptide galanin has been shown to suppress epileptic seizures. In cortical and hippocampal areas, galanin is normally mainly expressed in noradrenergic afferents. We have generated a mouse overexpressing galanin in neurons under the platelet-derived growth factor B promoter. RIA and HPLC analysis revealed up to 8-fold higher levels of galanin in transgenic as compared with wild-type mice. Ectopic galanin overexpression was detected especially in dentate granule cells and hippocampal and cortical pyramidal neurons. Galanin-overexpressing mice showed retardation of seizure generalization during hippocampal kindling, a model for human complex partial epilepsy. The high levels of galanin in mossy fibers found in the transgenic mice were further increased after seizures. Frequency facilitation of field excitatory postsynaptic potentials, a form of short-term synaptic plasticity assessed in hippocampal slices, was reduced in mossy fiber-CA3 cell synapses of galanin-overexpressing mice, indicating suppressed glutamate release. This effect was reversed by application of the putative galanin receptor antagonist M35. These data provide evidence that ectopically overexpressed galanin can be released and dampen the development of epilepsy by means of receptor-mediated action, at least partly by reducing glutamate release from mossy fibers.

Avdelning/ar

Publiceringsår

2001

Språk

Engelska

Sidor

14006-14011

Publikation/Tidskrift/Serie

Proceedings of the National Academy of Sciences

Volym

98

Issue

24

Dokumenttyp

Artikel i tidskrift

Förlag

National Academy of Sciences

Ämne

  • Neurosciences
  • Neurology

Aktiv

Published

ISBN/ISSN/Övrigt

  • ISSN: 1091-6490