scholarly journals Quantal analysis of long-term potentiation of combined neuronal postsynaptic potentials on hippocampal slices in vitro

1991 ◽  
Vol 22 (4) ◽  
pp. 341-347 ◽  
Author(s):  
L. L. Voronin ◽  
U. Kuhnt ◽  
G. Hess
Keyword(s):  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Postsynaptic Potentials ◽  
Term Potentiation ◽  
Quantal Analysis

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.

Dynamic aspects of neuronal interphase nuclei: Visualization of subnuclear domains by phase contrast microscopy, confocal microscopy & ultrastructural cytochemistry

1992 ◽  
Vol 50 (1) ◽  
pp. 562-563
Author(s):  
Umberto De Boni ◽  
Kosta Milankov ◽  
Kwame S. Amankwah ◽  
Paul C. Park
Keyword(s):  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Interphase Nuclei ◽  
3 Dimensional ◽  
Term Potentiation ◽  
Nuclear Rotation ◽  
Chromosome Pattern ◽  
Altered Gene

Neuronal chromatin moves, in a saltatory and periodic manner, within the 3-dimensional (3-D) space of interphase nuclei in vitro. This is generally known as nuclear rotation (NR) which has been proposed to function, during differentiation, in the transposition of specific chromatin domains into a cytotypic chromosome pattern, a pattern which, in part, may also be related to the functional state of the cell. Exposure of neurons in vitro to nerve growth factor or to neurotransmitters results in altered gene expression, in altered rates of NR, as well as in a reorganization of chromosome patterns. Moreover, long term potentiation, induced in neurons in hippocampal slices, reduces the number of detectable satellite DNA signals, possibly by increased clustering.

Long-term potentiation in hippocampal slices induced by temporary suppression of glycolysis

1995 ◽  
Vol 74 (6) ◽  
pp. 2763-2766 ◽  
Author(s):  
S. Tekkok ◽  
K. Krnjevic
Keyword(s):  
Nmda Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Excitatory Postsynaptic Potentials ◽  
Postsynaptic Potentials ◽  
After Effects ◽  
Population Spikes ◽  
Term Potentiation

1. Temporary suppression of glycolysis by 2-deoxy-D-glucose (2-DG)-long enough to abolish CA1 population spikes (PSs) and reduce field excitatory postsynaptic potentials (EPSPs) by two-thirds-is followed by a sustained rebound of EPSPs and PSs (both up by 70-150%). 2. Post 2-DG long-term potentiation (2-DG-LTP) is prevented by block of N-methyl-D-aspartate (NMDA) receptors (NMDARs). Though 2-DG-LTP is normally expressed by other receptors, in presence of picrotoxin 2-DG causes similar LTP of NMDAR-mediated EPSPs. 3. Stimulation at 1 s-1 fully depotentiates 2-DG-LTP. 4. Unlike tetanic LTP, 2-DG-LTP is not pathway-specific, is not occluded by a preceding tetanic LTP (or vice versa) and is insensitive to block of NO synthesis. 5. Hypoglycemic states may have long-lasting after-effects on cerebral synaptic function.

Distinct synaptic loci of Ca2+/calmodulin-dependent protein kinase II necessary for long-term potentiation and depression

1996 ◽  
Vol 76 (3) ◽  
pp. 2097-2101 ◽  
Author(s):  
P. K. Stanton ◽  
A. T. Gage
Keyword(s):  
Pyramidal Neurons ◽  
De Novo ◽  
Hippocampal Slices ◽  
Low Frequency ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Bath Application ◽  
Dependent Protein

1. Extracellular bath application of the selective Ca2+/calmodulin-dependent kinase II (CaMKII) inhibitor KN-62 to hippocampal slices in vitro blocked the induction of long-term depression (LTD) by low-frequency Schaffer collateral stimulation (1 Hz/15 min) of the same concentration as has been shown previously to prevent induction of long-term potentiation (LTP) at these synapses. 2. In contrast, postsynaptic intracellular infusion of KN-62 into single CA1 pyramidal neurons did not prevent induction of LTD, although it was quite effective in blocking LTP. 3. We conclude that there is a presynaptic CaMKII that must be activated to induce LTD, whereas postsynaptic CaMKII stimulation is needed to evoke LTP. 4. Bath application of KN-62 also blocked depotentiation by low-frequency stimuli of previously induced LTP, suggesting that induction of depotentiation and de novo LTD may require the same CaMKII-dependent mechanisms.

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