The effect of dopaminergic D1 receptor blockade during tetanization on the expression of long-term potentiation in the rat CA1 region in vitro

1991 ◽  
Vol 129 (1) ◽  
pp. 111-114 ◽  
Author(s):  
Uwe Frey ◽  
Henry Matthies ◽  
Klaus G. Reymann ◽  
Hansjürgen Matthies
Keyword(s):  
Long Term Potentiation ◽  
D1 Receptor ◽  
Receptor Blockade ◽  
Ca1 Region ◽  
Term Potentiation

The effects of angiotensin IV analogs on long-term potentiation within the CA1 region of the hippocampus in vitro

2001 ◽  
Vol 897 (1-2) ◽  
pp. 114-121 ◽  
Author(s):  
Enikö A Kramár ◽  
Deborah L Armstrong ◽  
Saiko Ikeda ◽  
Matthew J Wayner ◽  
Joseph W Harding ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Angiotensin Iv ◽  
Ca1 Region ◽  
Term Potentiation

Aβ25–35-Induced Depression of Long-Term Potentiation in Area CA1 In Vivo and In Vitro Is Attenuated by Verapamil

2003 ◽  
Vol 89 (6) ◽  
pp. 3061-3069 ◽  
Author(s):  
D. B. Freir ◽  
D. A. Costello ◽  
C. E. Herron
Keyword(s):  
Long Term Potentiation ◽  
Slice Preparation ◽  
Ca1 Region ◽  
Combined Application ◽  
Significant Reversal ◽  
Term Potentiation ◽  
Prior Application

The effect of intracerebroventricular (icv) injection of Aβ25–35 and/or intraperitoneal (ip) application of the L-type calcium channel (VDCC) blockers verapamil or diltiazem were examined in vivo. To by-pass possible systemic actions of these agents, their effects on long-term potentiation (LTP) in the CA1 region of the in vitro hippocampal slice preparation were also examined. Application of Aβ25–35 (10 nmol in 5 μl, icv) significantly impaired LTP in vivo, as did IP injection of verapamil (1 or 10 mg/kg) or diltiazem (1 or 10 mg/kg). In the in vitro slice preparation, LTP was also depressed by prior application of Aβ25–35 (500 nmol), verapamil (20 μM), or diltiazem (50 μM). Combined application of Aβ25–35 and verapamil in either the in vivo or in vitro preparation resulted in a significant reversal of the LTP depression observed in the presence of either agent alone. However, co-application of diltiazem and Aβ25–35 failed to attenuate the depression of LTP observed in the presence of either agent alone in vivo or in vitro. Since LTP is a cellular correlate of memory and Aβ is known to be involved in Alzheimer's disease (AD), these results indicate that verapamil, a phenylalkylamine, may be useful in the treatment of cognitive deficits associated with AD.

Hippocampal long-term potentiation and spatial learning in the rat: effects of GABAB receptor blockade

Neuroscience ◽  
1996 ◽  
Vol 74 (2) ◽  
pp. 331-339 ◽  
Author(s):  
F.H Brucato ◽  
E.D Levin ◽  
D.D Mott ◽  
D.V Lewis ◽  
W.A Wilson ◽  
...  
Keyword(s):  
Spatial Learning ◽  
Gabab Receptor ◽  
Long Term Potentiation ◽  
Receptor Blockade ◽  
Term Potentiation

Spatial performance correlates with long-term potentiation of the dentate gyrus but not of the CA1 region in rats with fimbria–fornix lesions

2001 ◽  
Vol 307 (3) ◽  
pp. 159-162 ◽  
Author(s):  
Kazuhito Nakao ◽  
Yuji Ikegaya ◽  
Maki K Yamada ◽  
Nobuyoshi Nishiyama ◽  
Norio Matsuki
Keyword(s):  
Dentate Gyrus ◽  
Long Term Potentiation ◽  
Ca1 Region ◽  
Term Potentiation ◽  
Spatial Performance

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

2016 ◽  
Vol 27 (8) ◽  
pp. 849-855 ◽  
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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