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

1999 ◽  
Vol 815 (2) ◽  
pp. 419-423 ◽  
Author(s):  
Farshad Alizadeh Mansouri ◽  
Fereshteh Motamedi ◽  
Yaghoub Fathollahi
Keyword(s):  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Schaffer Collateral ◽  
Morphine Administration ◽  
Term Potentiation

scholarly journals Preconditioning In Vivo Ischemia Inhibits Anoxic Long-Term Potentiation and Functionally Protects CA1 Neurons in the Gerbil

1998 ◽  
Vol 18 (3) ◽  
pp. 288-296 ◽  
Author(s):  
Kensuke Kawai ◽  
Tadayoshi Nakagomi ◽  
Takaaki Kirino ◽  
Akira Tamura ◽  
Nobufumi Kawai
Keyword(s):  
Nmda Receptor ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Forebrain Ischemia ◽  
Term Potentiation ◽  
Induced Tolerance

Preconditioning with sublethal ischemia induces tolerance to subsequent lethal ischemia in neurons. We investigated electrophysiologic aspects of the ischemic tolerance phenomenon in the gerbil hippocampus. Gerbils were subjected to 2 minutes of forebrain ischemia (preconditioning ischemia). Some of them were subjected to a subsequent 5 minutes of forebrain ischemia 2 to 3 days after the preconditioning ischemia (double ischemia). Hippocampal slices were prepared from these gerbils subjected to the preconditioning or double ischemia, and field excitatory postsynaptic potentials were recorded from CA1 pyramidal neurons. Capacity for long-term potentiation triggered by tetanic stimulation (tetanic LTP) was transiently inhibited 1 to 2 days after the double ischemia but then recovered. Latency of anoxic depolarization was not significantly different between slices from preconditioned gerbils and those from sham-operated gerbils when these slices were subjected to in vitro anoxia. Postanoxic potentiation of N-methyl-D-aspartate (NMDA) receptor-mediated transmission (anoxic LTP) was inhibited in slices from gerbils 2 to 3 days after the preconditioning ischemia, whereas it was observed in slices from sham-operated gerbils and gerbils 9 days after the preconditioning ischemia. These results suggest that protection by induced tolerance is (1) not only morphologic but also functional, and (2) expressed in inhibiting postischemic overactivation of NMDA receptor-mediated synaptic responses.

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.

P4-378: REVERSAL OF AB-INDUCED DEFICITS IN LONG-TERM POTENTIATION (LTP) IN VITRO AND IN VIVO BY MRZ-99030

2014 ◽  
Vol 10 ◽  
pp. P926-P926
Author(s):  
Christopher G. Parsons ◽  
Ross David Jeggo ◽  
Lydia Staniaszek ◽  
David Spanswick ◽  
Gerhard Rammes
Keyword(s):  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals In vivo and in vitro exposure to PCB 153 reduces long-term potentiation.

2000 ◽  
Vol 108 (9) ◽  
pp. 827-831 ◽  
Author(s):  
R J Hussain ◽  
J Gyori ◽  
A P DeCaprio ◽  
D O Carpenter
Keyword(s):  
Long Term Potentiation ◽  
Term Potentiation ◽  
In Vitro Exposure

Blockade of long-term potentiation by phencyclidine and σ opiates in the hippocampus in vivo and in vitro

1983 ◽  
Vol 280 (1) ◽  
pp. 127-138 ◽  
Author(s):  
Janet L. Stringer ◽  
L. John Greenfield ◽  
John T. Hackett ◽  
Patrice G. Guyenet
Keyword(s):  
Long Term Potentiation ◽  
Term Potentiation

In vivo injected mitochondria-targeted plastoquinone antioxidant SkQR1 prevents β-amyloid-induced decay of long-term potentiation in rat hippocampal slices

2011 ◽  
Vol 76 (12) ◽  
pp. 1367-1370 ◽  
Author(s):  
N. A. Kapay ◽  
N. K. Isaev ◽  
E. V. Stelmashook ◽  
O. V. Popova ◽  
D. B. Zorov ◽  
...  
Keyword(s):  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Β Amyloid

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.

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