50 research outputs found

    ΠœΠ΅Ρ‚ΠΎΠ΄ΠΈ управління Π΅ΠΊΠΎΠ»ΠΎΠ³Ρ–Ρ‡Π½ΠΈΠΌΠΈ Ρ€ΠΈΠ·ΠΈΠΊΠ°ΠΌΠΈ Π² систСмі забСзпСчСння Π΅ΠΊΠΎΠ½ΠΎΠΌΡ–Ρ‡Π½ΠΎΠ³ΠΎ Ρ€ΠΎΠ·Π²ΠΈΡ‚ΠΊΡƒ Ρ€Π΅Π³Ρ–ΠΎΠ½Ρƒ

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    ΠœΠ΅Ρ‚ΠΎΡŽ статті Ρ” дослідТСння ΠΌΠ΅Ρ‚ΠΎΠ΄Ρ–Π² управління Π΅ΠΊΠΎΠ»ΠΎΠ³Ρ–Ρ‡Π½ΠΈΠΌΠΈ Ρ€ΠΈΠ·ΠΈΠΊΠ°ΠΌΠΈ Π² систСмі забСзпСчСння Π΅ΠΊΠΎΠ½ΠΎΠΌΡ–Ρ‡Π½ΠΎΠ³ΠΎ Ρ€ΠΎΠ·Π²ΠΈΡ‚ΠΊΡƒ Ρ€Π΅Π³Ρ–ΠΎΠ½Ρƒ

    Hippocalcin functions as a calcium sensor in hippocampal LTD.

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    It is not fully understood how NMDAR-dependent LTD causes Ca2+-dependent endocytosis of AMPARs. Here we show that the neuronal Ca2+ sensor hippocalcin binds the ?2-adaptin subunit of the AP2 adaptor complex and that along with GluR2 these coimmunoprecipitate in a Ca2+-sensitive manner. Infusion of a truncated mutant of hippocalcin (HIP2-72) that lacks the Ca2+ binding domains prevents synaptically evoked LTD but has no effect on LTP. These data indicate that the AP2-hippocalcin complex acts as a Ca2+ sensor that couples NMDAR-dependent activation to regulated endocytosis of AMPARs during LTD
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