Long-term potentiation in Schaffer collateral and commissural systems of the hippocampus: In vitro study in rats pretreated with kainic acid

In the series of experiments reported here we provide evidence that a focal adhesion-like process underlies the induction of long-term potentiation (LTP) in the Schaffer Collateral-CA1 projection in the hippocampus. Here we show that an integrin-binding peptide (RGD) impairs induction of Schaffer Collateral-CA1 LTP in hippocampal slice preparations in vitro. The heparin-binding peptide that binds heparan sulfate proteoglycan (HSPG) and blocks the formation of focal adhesions also impairs induction of LTP. Either the integrin-binding peptide or heparin-binding peptide reduces LTP partially. However, when the two peptides were administered simultaneously, there was no LTP 1 hour after induction. This indicates that these two molecules might function together and that a focal adhesion-like process might be involved in the induction of LTP. Additionally, we report that the RGD effect on LTP is time dependent and occurs only in the first few minutes following LTP induction, that the binding of the RGD peptide in CA1 stratum radiatum increases after LTP induction and that this increased binding depends on Ca2+. Using electron microscopy we show that integrins are present in synapses.

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Chronic in vivo morphine administration facilitates primed-bursts-induced long-term potentiation of Schaffer collateral–CA1 synapses in hippocampal slices in vitro

Brain Research ◽

10.1016/s0006-8993(98)01148-2 ◽

1999 ◽

Vol 815 (2) ◽

pp. 419-423 ◽

Cited By ~ 35

Author(s):

Farshad Alizadeh Mansouri ◽

Fereshteh Motamedi ◽

Yaghoub Fathollahi

Keyword(s):

Hippocampal Slices ◽

Long Term Potentiation ◽

Schaffer Collateral ◽

Morphine Administration ◽

Term Potentiation

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Effect of Arsenic-containing Hydrocarbon on the Long-term Potentiation at Schaffer Collateral-CA1 Synapses from Infantile Male Rat

NeuroToxicology ◽

10.1016/j.neuro.2021.04.002 ◽

2021 ◽

Author(s):

Yu Zheng ◽

Chunxiao Tian ◽

Lei Dong ◽

Lei Tian ◽

Ronald A. Glabonjat ◽

...

Keyword(s):

Long Term Potentiation ◽

Male Rat ◽

Schaffer Collateral ◽

Term Potentiation

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Neuroprotective properties of mitochondria-targeted antioxidants of the SkQ-type

Reviews in the Neurosciences ◽

10.1515/revneuro-2016-0036 ◽

2016 ◽

Vol 27 (8) ◽

pp. 849-855 ◽

Cited By ~ 17

Author(s):

Nickolay K. Isaev ◽

Elena V. Stelmashook ◽

Elisaveta E. Genrikhs ◽

Galina A. Korshunova ◽

Natalya V. Sumbatyan ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Brain Area ◽

Hippocampal Slices ◽

Amyloid Β ◽

Long Term Potentiation ◽

Term Potentiation ◽

Neuroprotective Action

AbstractIn 2008, using a model of compression brain ischemia, we presented the first evidence that mitochondria-targeted antioxidants of the SkQ family, i.e. SkQR1 [10-(6′-plastoquinonyl)decylrhodamine], have a neuroprotective action. It was shown that intraperitoneal injections of SkQR1 (0.5–1 μmol/kg) 1 day before ischemia significantly decreased the damaged brain area. Later, we studied in more detail the anti-ischemic action of this antioxidant in a model of experimental focal ischemia provoked by unilateral intravascular occlusion of the middle cerebral artery. The neuroprotective action of SkQ family compounds (SkQR1, SkQ1, SkQTR1, SkQT1) was manifested through the decrease in trauma-induced neurological deficit in animals and prevention of amyloid-β-induced impairment of long-term potentiation in rat hippocampal slices. At present, most neurophysiologists suppose that long-term potentiation underlies cellular mechanisms of memory and learning. They consider inhibition of this process by amyloid-β1-42as anin vitromodel of memory disturbance in Alzheimer’s disease. Further development of the above studies revealed that mitochondria-targeted antioxidants could retard accumulation of hyperphosphorylated τ-protein, as well as amyloid-β1-42, and its precursor APP in the brain, which are involved in developing neurodegenerative processes in Alzheimer’s disease.

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