scholarly journals VDCCs and NMDARs Underlie Two Forms of LTP in CA1 Hippocampus In Vivo

1999 ◽  
Vol 82 (2) ◽  
pp. 736-740 ◽  
Author(s):  
S. L. Morgan ◽  
T. J. Teyler
Keyword(s):  
Long Term Potentiation ◽  
Stratum Radiatum ◽  
Mk 801 ◽  
Aspartate Receptor ◽  
Area Ca1 ◽  
Term Potentiation ◽  
Voltage Dependent

N-methyl-d-aspartate receptor/channel (NMDAR) and voltage-dependent calcium channel (VDCC) antagonists applied independently reduce the magnitude of long-term potentiation (LTP) in area CA1 of the hippocampal slice preparation. When used in combination, the antagonists completely block the induction of LTP. In urethan-anesthetized rats we examined the effect of the NMDAR blocker MK-801 (0.1 mg/kg) and the VDCC blocker Verapamil (10 mg/kg) on LTP induction in area CA1. Extracellular recordings were obtained from stratum radiatum following stimulation of Schaffer collaterals. LTP was induced by a 200-Hz/100-ms tetanus repeated 10 times (2 s isi). Tetanus was given in the presence of intraperitoneal saline, MK-801, Verapamil, or both Verapamil and MK-801. When given separately, Verapamil and MK-801 both significantly reduced the magnitude of LTP as compared with control animals. When given together, the drugs blocked the induction of LTP completely. We conclude that like LTP in vitro, VDCCs and NMDAR underlie two forms of LTP in vivo.

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

Aging Differentially Alters Forms of Long-Term Potentiation in Rat Hippocampal Area CA1

1998 ◽  
Vol 79 (1) ◽  
pp. 334-341 ◽  
Author(s):  
Subbakrishna Shankar ◽  
Timothy J. Teyler ◽  
Norman Robbins
Keyword(s):  
Calcium Channel ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Voltage Dependent Calcium Channel ◽  
Area Ca1 ◽  
Age Related ◽  
Term Potentiation ◽  
Voltage Dependent ◽  
Hippocampal Area

Shankar, Subbakrishna, Timothy J. Teyler, and Norman Robbins. Aging differentially alters forms of long-term potentiation in rat hippocampal area CA1. J. Neurophysiol. 79: 334–341, 1998. Long-term potentiation (LTP) of the Schaffer collateral/commissural inputs to CA1 in the hippocampus was shown to consist of N-methyl-d-aspartate receptor (NMDAR) and voltage-dependent calcium channel (VDCC) dependent forms. In this study, the relative contributions of these two forms of LTP in in vitro hippocampal slices from young (2 mo) and old (24 mo) Fischer 344 rats were examined. Excitatory postsynaptic potentials (EPSP) were recorded extracellularly from stratum radiatum before and after a tetanic stimulus consisting of four 200-Hz, 0.5-s trains given 5 s apart. Under control conditions, a compound LTP consisting of both forms was induced and was similar, in both time course and magnitude, in young and old animals. NMDAR-dependent LTP (nmdaLTP), isolated by the application of 10 μM nifedipine (a voltage-dependent calcium channel blocker), was significantly reduced in magnitude in aged animals. The VDCC dependent form (vdccLTP), isolated by the application of 50 μM d,l-2-amino-5-phosphonvalerate (APV), was significantly larger in aged animals. Although both LTP forms reached stable values 40–60 min posttetanus in young animals, in aged animals vdccLTP increased and nmdaLTP decreased during this time. In both young and old animals, the sum of the two isolated LTP forms approximated the magnitude of the compound LTP, and application of APV and nifedipine or genestein (a tyrosine kinase inhibitor) together blocked potentiation. These results suggest that aging causes a shift in synaptic plasticity from NMDAR-dependent mechanisms to VDCC-dependent mechanisms. The data are consistent with previous findings of increased L-type calcium current and decreased NMDAR number in aged CA1 cells and may help explain age-related deficits in learning and memory.

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