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Compensation for PKMζ in long-term potentiation and spatial long-term memory in mutant mice.
Tsokas, Panayiotis; Hsieh, Changchi; Yao, Yudong; Lesburguères, Edith; Wallace, Emma Jane Claire; Tcherepanov, Andrew; Jothianandan, Desingarao; Hartley, Benjamin Rush; Pan, Ling; Rivard, Bruno; Farese, Robert V; Sajan, Mini P; Bergold, Peter John; Hernández, Alejandro Iván; Cottrell, James E; Shouval, Harel Z; Fenton, André Antonio; Sacktor, Todd Charlton.
Afiliación
  • Tsokas P; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Hsieh C; Department of Anesthesiology, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Yao Y; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Lesburguères E; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Wallace EJC; Center for Neural Science, New York University, New York, United States.
  • Tcherepanov A; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Jothianandan D; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Hartley BR; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Pan L; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Rivard B; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Farese RV; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Sajan MP; Department of Internal Medicine, James A Haley Veterans Hospital, University of South Florida, Tampa, United States.
  • Bergold PJ; Department of Internal Medicine, James A Haley Veterans Hospital, University of South Florida, Tampa, United States.
  • Hernández AI; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Cottrell JE; Department of Pathology, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Shouval HZ; Department of Anesthesiology, State University of New York Downstate Medical Center, Brooklyn, United States.
  • Fenton AA; Department of Neurobiology and Anatomy, University of Texas Medical School at Houston, Houston, United States.
  • Sacktor TC; Department of Physiology and Pharmacology, The Robert F Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, United States.
Elife ; 52016 05 17.
Article en En | MEDLINE | ID: mdl-27187150
PKMζ is a persistently active PKC isoform proposed to maintain late-LTP and long-term memory. But late-LTP and memory are maintained without PKMζ in PKMζ-null mice. Two hypotheses can account for these findings. First, PKMζ is unimportant for LTP or memory. Second, PKMζ is essential for late-LTP and long-term memory in wild-type mice, and PKMζ-null mice recruit compensatory mechanisms. We find that whereas PKMζ persistently increases in LTP maintenance in wild-type mice, PKCι/λ, a gene-product closely related to PKMζ, persistently increases in LTP maintenance in PKMζ-null mice. Using a pharmacogenetic approach, we find PKMζ-antisense in hippocampus blocks late-LTP and spatial long-term memory in wild-type mice, but not in PKMζ-null mice without the target mRNA. Conversely, a PKCι/λ-antagonist disrupts late-LTP and spatial memory in PKMζ-null mice but not in wild-type mice. Thus, whereas PKMζ is essential for wild-type LTP and long-term memory, persistent PKCι/λ activation compensates for PKMζ loss in PKMζ-null mice.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteína Quinasa C / Potenciación a Largo Plazo / Memoria a Largo Plazo / Hipocampo Límite: Animals Idioma: En Revista: Elife Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteína Quinasa C / Potenciación a Largo Plazo / Memoria a Largo Plazo / Hipocampo Límite: Animals Idioma: En Revista: Elife Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido