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Role of protein kinase C family in the cerebellum‐dependent adaptive learning of horizontal optokinetic response eye movements in mice
Author(s) -
Shutoh Fumihiro,
Katoh Akira,
Ohki Masafumi,
Itohara Shigeyoshi,
Tonegawa Susumu,
Nagao Soichi
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02717.x
Subject(s) - optokinetic reflex , mutant , flocculus , microbiology and biotechnology , protein kinase c , biology , neuroscience , climbing fiber , retinal , cerebellum , wild type , knockout mouse , kinase , purkinje cell , eye movement , genetics , receptor , biochemistry , gene
Among the subtypes of the Ca 2+ ‐dependent protein kinase C (PKC), which play a crucial role in long‐term depression (LTD), both α and γ are expressed in the cerebellar floccular Purkinje cells. To reveal the functional differences of PKC subtypes, we examined the adaptability of ocular reflexes of PKCγ mutant mice, which show mild ataxia and normal LTD. In mutant mice, gains of the horizontal optokinetic eye response (HOKR) were reduced. Adaptation of the HOKR was not affected but its retinal slip dependency was altered in mutant mice. Sustained 1‐h sinusoidal screen oscillation, which induced a relatively large amount of retinal slips in both mutant and wild‐type mice, increased the HOKR gain in wild‐type mice but not in mutant mice. In contrast, exposure to 1 h of sustained slower screen oscillations, which induced relatively small retinal slips in mutant and wild‐type mice, increased the HOKR gain in both mutant and wild‐type mice. Adaptation of the HOKR of the mutant mice to slow screen oscillation and those of wild‐type mice to fast and slow screen oscillations were all abolished by local applications of a PKC inhibitor (chelerythrine) within the flocculi. Electrophysiological and anatomical studies showed no appreciable changes in the sources and magnitudes of climbing fibre inputs, which mediate retinal slip signals to the flocculus in the mutant mice. These results suggest that PKCγ has a modulatory role in determining retinal slip dependency, and other PKC subtypes, e.g. PKCα, may play a crucial role in the adaptation of the HOKR.