Inhibition of apamin-sensitive calcium dependent potassium channels facilitate the induction of long-term potentiation in the CA1 region of rat hippocampus in vitro

1998 ◽  
Vol 253 (2) ◽  
pp. 91-94 ◽  
Author(s):  
Thomas Behnisch ◽  
Klaus G Reymann
Keyword(s):  
Potassium Channels ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Calcium Dependent ◽  
Ca1 Region ◽  
Term Potentiation

Oxaloacetate restores the long-term potentiation impaired in rat hippocampus CA1 region by 2-vessel occlusion

2009 ◽  
Vol 604 (1-3) ◽  
pp. 51-57 ◽  
Author(s):  
Máté Marosi ◽  
János Fuzik ◽  
Dávid Nagy ◽  
Gabriella Rákos ◽  
Zsolt Kis ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Vessel Occlusion ◽  
Ca1 Region ◽  
Term Potentiation

The modulation of long-term potentiation by delta-9-tetrahydrocannabinol in the rat hippocampus, in vitro

1987 ◽  
Vol 19 (6) ◽  
pp. 663-672 ◽  
Author(s):  
Alexander V. Nowicky ◽  
Timothy J. Teyler ◽  
Richard M. Vardaris
Keyword(s):  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Term Potentiation

Bidirectional Associative Plasticity of Unitary CA3-CA1 EPSPs in the Rat Hippocampus In Vitro

1997 ◽  
Vol 77 (5) ◽  
pp. 2851-2855 ◽  
Author(s):  
Dominique Debanne ◽  
Beat H. Gähwiler ◽  
Scott M. Thompson
Keyword(s):  
Hippocampal Slice ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Absolute Level ◽  
Postsynaptic Activity ◽  
Term Potentiation ◽  
Transmission Failures ◽  
Expression Mechanism

Debanne, Dominique, Beat H. Gähwiler, and Scott M. Thompson. Bidirectional associative plasticity of unitary CA3-CA1 EPSPs in the rat hippocampus in vitro. J. Neurophysiol. 77: 2851–2855, 1997. Associative long-term potentiation (LTP) and depression of compound and unitary CA3-CA1 excitatory postsynaptic potentials (EPSPs) were investigated in rat hippocampal slice cultures. The induction of LTP with synchronous pairing of synaptic activation and postsynaptic depolarization resulted in an increase in the amplitude of EPSPs to the same absolute level, regardless of whether the input was naive or had been previously depressed by asynchronous pairing of pre- and postsynaptic activity. Saturated LTP of compound and unitary EPSPs was reversed by asynchronous pairing and could be reinduced by synchronous pairing. The likelihood that an action potential in a presynaptic CA3 cell failed to trigger an unitary EPSP in a postsynaptic CA1 cell decreased after induction of associative potentiation and increased after induction of associative depotentiation. These changes in the rate of transmission failures were accompanied by large changes in the amplitude of nonfailure EPSPs. We conclude that the same CA3-CA1 synapses can alternatively undergo associative potentiation and depression, perhaps through opposite changes in a single expression mechanism.

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