Post-tetanic Potentiation and Depression in Hippocampal Neurons in a Rat Model of Alzheimer’s Disease: Effects of Teucrium Polium Extract

The plant Teucrium polium ( T.p. ) possesses a wide range of pharmacological activities due to the presence, in particular, of different phytochemicals, phenols and flavonoids. We examined the effects of the T.p. extract on impulse activity of hippocampal neurons in rats with a model of Alzheimer’s...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Neurophysiology (New York) 2019-09, Vol.51 (5), p.332-343
Hauptverfasser: Simonyan, K. V., Galstyan, H. M., Chavushyan, V. A.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The plant Teucrium polium ( T.p. ) possesses a wide range of pharmacological activities due to the presence, in particular, of different phytochemicals, phenols and flavonoids. We examined the effects of the T.p. extract on impulse activity of hippocampal neurons in rats with a model of Alzheimer’s disease. Adult albino rats were divided into three groups (5 animals in each). The control group C obtained intracerebroventricular (i.c.v.) infusions of saline, animals of group Aβ were i.c.v. infused with amyloid β peptide 25–35, Aβ(25–35), and group Aβ+ T.p. was treated by both Aβ(25–35) infusions and introductions of the T.p. extract. In group Aβ, a greater proportion of hippocampal neurons with post-tetanic depression after high-frequency stimulation of the entorhinal cortex, lower values of the frequency of background activity generated by the above neurons, and relatively weaker modifications of spike activity (post-tetanic potentiation and depression) were observed. Daily administrations of the T.p. extract partially but considerably reversed the above-mentioned negative shifts in spike activity of hippocampal neurons caused by Aβ(25–35). We suggest that T.p. extract containing important phytochemicals is capable of ameliorating the memory dysfunction caused by Aβ(25–35) via blocking amyloid deposition and a positive influence on the functions of hippocampal neurons.
ISSN:0090-2977
1573-9007
DOI:10.1007/s11062-020-09827-8