The Roles of MAPK Cascades in Synaptic Plasticity and Memory in Aplysia: Facilitatory Effects and Inhibitory Constraints: Figure 1 | Zendy

Shiv K. Sharma | Zendy; Thomas Carew | Zendy

Open Access

The Roles of MAPK Cascades in Synaptic Plasticity and Memory in Aplysia: Facilitatory Effects and Inhibitory Constraints: Figure 1

Author(s) -

Shiv K. Sharma,

Thomas Carew

Publication year - 2004

Publication title -

learning and memory

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.228

H-Index - 136

eISSN - 1549-5485

pISSN - 1072-0502

DOI - 10.1101/lm.81104

Subject(s) - aplysia , neuroscience , neural facilitation , synaptic plasticity , facilitation , metaplasticity , inhibitory postsynaptic potential , nonsynaptic plasticity , neurotransmitter , protein kinase a , synaptic fatigue , sensitization , neuroplasticity , homosynaptic plasticity , chemistry , biology , kinase , microbiology and biotechnology , excitatory postsynaptic potential , central nervous system , biochemistry , receptor

Synaptic plasticity is thought to contribute to memory formation.Serotonin-induced facilitation of sensory-motor (SN-MN) synapses in Aplysia is an extensively studied cellular analog of memory forsensitization. Serotonin, a modulatory neurotransmitter, is released in theCNS during sensitization training, and induces three temporally andmechanistically distinct phases of SN-MN synaptic facilitation. The role ofprotein kinase A and protein kinase C in SN-MN synaptic facilitation is welldocumented. Recently, it has become clear that mitogen-activated proteinkinase (MAPK) cascades also play a critical role in SN-MN plasticity. Here, wesummarize the roles of MAPK cascades in synaptic plasticity and memory forsensitization in Aplysia .

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