Brain-derived neurotrophic factor improves long-term potentiation and cognitive functions after transient forebrain ischemia in the rat

• Verfasst von: Kiprianova, Irina [VerfasserIn]
• Verfasst von: Sandkühler, Jürgen [VerfasserIn]
• Verfasst von: Schwab, Stefan [VerfasserIn]
• Verfasst von: Hoyer, Siegfried [VerfasserIn]
• Verfasst von: Spranger, Matthias [VerfasserIn]
• Titel: Brain-derived neurotrophic factor improves long-term potentiation and cognitive functions after transient forebrain ischemia in the rat
• Verf.angabe: Irina Kiprianova, Jürgen Sandkühler, Stefan Schwab, Siegfried Hoyer, Matthias Spranger
• Jahr: 1999
• Umfang: 9 S.
• Fussnoten: Online 25 May 2002 ; Elektronische Reproduktion der Druck-Ausgabe ; Gesehen am 04.05.2021
• Titel Quelle: Enthalten in: Experimental neurology
• Ort Quelle: Amsterdam [u.a.] : Elsevier, 1959
• Jahr Quelle: 1999
• Band/Heft Quelle: 159(1999), 2, Seite 511-519
• ISSN Quelle: 1090-2430
• DOI: doi:10.1006/exnr.1999.7109
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: BDNF
• Sach-SW: global ischemia
• Sach-SW: long-term potentiation
• Sach-SW: neurotrophic factors
• Sach-SW: reference memory.
• Sach-SW: working memory
• K10plus-PPN: 1757048650

Abstract

We investigated the effect of brain-derived neurotrophic factor (BDNF) on hippocampal long-term potentiation (LTP) and cognitive functions after global cerebral ischemia in the rat. After four-vessel occlusion, BDNF was administered via an osmotic minipump continuously over 14 days intracerebroventricularly. Electrophysiological experiments were performed 14 days after cerebral ischemia. Test stimuli and tetanization were delivered to the Schaffer collaterals of the hippocampus and field excitatory postsynaptic potentials (fEPSP) were recorded in the CA1 region. Cognitive impairment was analyzed repeatedly with a passive avoidance test, a hole-board test, and with an activity center on the same animal. In sham-operated animals, LTP was consistantly induced after delivering a tetanus (increase of initial slope of fEPSP to 173±12% of baseline; n=6). After transient forebrain ischemia LTP could not be induced (117±4% of baseline; n=7). In ischemic animals treated with BDNF, LTP could be induced (168±28% of baseline; n=8). Transient forebrain ischemia resulted in a significant decrease in spatial discrimination performance but not of associative memory. The ratios for working memory (WM) and reference memory (RM) 15 days after ischemia were lower in the ischemic rats (n=10) than in the sham-operated control animals (n=10; WM: 22±6 vs 72±7; RM: 30±7 vs 72±5). Postischemic intracerebroventricular BDNF infusion increased both WM (63±4; n=10) and RM (58±5; n=10). The spontaneous locomotor activity did not differ significantly in the three groups. These data indicate a protective effect of BDNF for synaptic transmission and cognitive functions after transient forebrain ischemia.