Protein kinase A inhibitors prevent the maintenance of hippocampal long-term potentiation.
The possible involvement of cAMP-dependent protein kinase A (PKA) in mechanisms of long-term potentiation of the Schaffer collateral-commissural input of rat CA1 neurones was investigated using several inhibitors in vitro. If 10 microM H-8, 100 nM KT5720 or 50 microM Rp-cAMPs was applied to the bath before a triple 100 Hz/0.5 s tetanization, post-tetanic and short-term potentiation developed almost normally. However, from about 3 h after tetanization the long-term potentiation (LTP) of the field-EPSP declined with respect to the control in an irreversible manner. These data suggest that besides protein kinase C the synergistic activation of PKA is necessary for the maintenance of LTP.
Matthies
H
H
Institute for Neurobiology, Department of Neurophysiology, Magdeburg, Germany.
Reymann
K G
KG
D000818:Animals; D002227:Carbazoles; D004558:Electric Stimulation; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D007211:Indoles / Q000494:pharmacology; D007546:Isoquinolines / Q000494:pharmacology; D008297:Male; D009473:Neuronal Plasticity / Q000187:drug effects*; D010766:Phosphorylation; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D047428:Protein Kinase Inhibitors; D011758:Pyrroles / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013569:Synapses / Q000502:physiology
D002227:Carbazoles; D007211:Indoles; D007546:Isoquinolines; D047428:Protein Kinase Inhibitors; D011758:Pyrroles; C057416:KT 5720; C053177:N-(2-(methylamino)ethyl)-5-isoquinolinesulfonamide; D011493:Protein Kinase C