Algebraic Groups and Their Generalizations: Quantum and by Haboush W., Parshall B. (eds.)

By Haboush W., Parshall B. (eds.)

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Over subsequent days of training, this timing deficit often gradually resolved. The authors suggested that the lesions damage some, but not all, of the Purkinje cells responsible for the expression of the conditioned responses. If Purkinje cells are learning to suppress the expression of responses early in the CS, removing some Purkinje cells could unmask shorter latency conditioned responses, as was observed. If the lesion spared enough Purkinje cells to support further learning to suppress responding, then the early responses unmasked by the lesions could be suppressed through further learning.

Proceedings of the National Academy of Sciences of the United States of America, 101, 676–681. , & Linden, D. J. (2004). A unique PDZ ligand in PKCα confers induction of cerebellar long-term synaptic depression. Neuron, 44, 585–594. , Mehta, S. , & Tsien, R. Y. (2003). Reversing cerebellar long-term depression. Proceedings of the National Academy of Sciences of the United States of America, 100, 15989–15993. , Wong, S. , Storm, D. , & Tsien, R. Y. (2002). A new form of cerebellar long-term potentiation is postsynaptic and depends on nitric oxide but not cAMP.

C. In mice with a Purkinje cell-specific knockout of calcineurin (L7-PP2B), LTP is blocked, but LTD remains unaffected (Fig. , 2010). Finally, several studies from other laboratories have demonstrated that LTD induction requires, or is supported by, the suppression of PP1/2A (Ajima & Ito, 1995; Eto, Bock, Brautigan, & Linden, 2002; Kawaguchi & Hirano, 2013; Launey, Endo, Sakai, Harano, & Ito, 2004) and that a late phase of LTD requires a downregulation of calcineurin (Fuji & Hirano, 2002). Together, these studies support the notion that phosphatases PP1, PP2A, and PP2B negatively regulate LTD rather than promote it (also note that calcineurin and PP1 have been suggested to act in tandem; Lisman, 1989).

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