Learning-induced modulation of SK channels-mediated effect on synaptic transmission.
Although small conductance (SK)-mediated calcium-dependent potassium currents are usually mostly thought to modulate neuronal adaptation by suppressing repetitive spike firing, recent evidence suggests that these channels also modulate synaptic transmission. SK2 channels were shown to be activated in dendritic spines following calcium entry via N-methyl-d-aspartate (NMDA) receptor. Such activation of potassium currents terminates the NMDA-dependent postsynaptic potential (PSP). Synaptic potentials in pyramidal neurons in the piriform cortex from olfactory-discrimination-trained rats have enhanced rise time 3 days after learning, and their dendritic spines are significantly smaller at this time. In the present study we examined whether the SK channel-mediated effect on PSPs is modified after learning. The SK channels inhibitor, apamin, that selectively blocks the SK channels-mediated potassium currents enhanced the width of the PSP in neurons from trained rats only. This effect is abolished in the presence of the NMDA-channel blocker, APV. The learning-induced reduction in paired-pulse facilitation was not affected by apamin. Although the effect of the SK channels is increased after learning, the protein expression level of the SK2 channels, the type located in dendritic spines, was decreased after learning. The protein expression level of the SK3 channel, suggested to be located mainly in axon terminals, was not modified by learning. We suggest that the enhanced effect of the SK channels on NMDA-mediated synaptic transmission is the result of the reduction in the spine volume after learning. Moreover, these data indicate that spines are more excitable after learning, and are thus more predisposed to activity-dependent modifications.
Brosh
Inbar
I
Department of Neurobiology and Ethology, Faculty of Sciences and Center for Brain and Behavior, Haifa University, Israel.
Rosenblum
Kobi
K
Barkai
Edi
E
D000704:Analysis of Variance; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001522:Behavior, Animal / Q000502:physiology; D001921:Brain / Q000166:cytology* / Q000502:physiology; D004307:Dose-Response Relationship, Radiation; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D007858:Learning / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D018408:Patch-Clamp Techniques / Q000379:methods; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D051640:Small-Conductance Calcium-Activated Potassium Channels / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology; D014868:Water Deprivation / Q000502:physiology
D018691:Excitatory Amino Acid Antagonists; D051640:Small-Conductance Calcium-Activated Potassium Channels; D001030:Apamin; C056639:2-amino-5-phosphopentanoic acid; D014633:Valine