Formation of AP-1 transcription factors during learning in Helix.
Gel shift assays were used to study the formation of transcription factors of the AP-1 family in the CNS of Helix during the acquisition of a conditioned defensive reflex based on food aversion. Increases in the DNA-binding activity of AP-1 factors were seen 1-3 h after training. Modeling of "learning" in an in situ system (incubation of the CNS in the presence of serotonin and the Ca2+ ionophore A23187 or the protein kinase C activator phorbol ester (TPA)) also increased the DNA-binding activity of this transcription complex. The DNA-binding activity induced by serotonin acting alone was significantly less than that in controls, while that in the presence of A23187 and TPA was the same as or less than that in controls. The calcium/calmodulin-dependent protein kinase inhibitor KN62 produced significant suppression of the effects of simultaneous exposure to serotonin and calcium on the activation of transcription factors of the AP-1, while greater suppression was obtained with the mitogen-activated protein kinase (ERK) inhibitor PD98059. Cooperative induction of the activation of AP-1 transcription factors in the CNS of the common snail by the serotonin-induced and calcium-dependent regulatory systems may be a mechanism underlying the formation of conditioned defensive reflexes in these animals. Lesions of the formation of transcription factors of the AP-1 family in animals unable to learn defensive forms of behavioral plasticity may be explained in terms of the presence of inhibitory forms of transcription factors interacting with the SRE element.
Grinkevich
L N
LN
I. P. Pavlov Institute of Physiology, Russian Academy of Sciences, 6 Makarov Bank, 199034 St. Petersburg, Russia.
Lisachev
P D
PD
Merkulova
T I
TI
D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D022762:CCAAT-Enhancer-Binding Proteins / Q000187:drug effects; D000001:Calcimycin / Q000494:pharmacology; D047390:Casein Kinase II; D002490:Central Nervous System / Q000187:drug effects / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000187:drug effects / Q000378:metabolism*; D004347:Drug Interactions; D024202:Electrophoretic Mobility Shift Assay / Q000379:methods; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005095:Exoribonucleases; D005419:Flavonoids / Q000494:pharmacology; D019833:Genistein / Q000494:pharmacology; D006372:Helix, Snails; D007476:Ionophores / Q000494:pharmacology; D007858:Learning / Q000187:drug effects / Q000502:physiology*; D010703:Phorbol Esters / Q000494:pharmacology; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology / Q000502:physiology; D018808:Transcription Factor AP-1 / Q000096:biosynthesis* / Q000145:classification
D022762:CCAAT-Enhancer-Binding Proteins; D004268:DNA-Binding Proteins; D004791:Enzyme Inhibitors; D005419:Flavonoids; D007476:Ionophores; D010703:Phorbol Esters; D018808:Transcription Factor AP-1; D012701:Serotonin; D000001:Calcimycin; C063302:KN 62; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D019833:Genistein; D047390:Casein Kinase II; D017346:Protein Serine-Threonine Kinases; D005095:Exoribonucleases; C065486:oligonucleotidase; C093973:2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one