p38 MAP Kinase Mediates Both Short-Term and Long-Term Synaptic Depression in Aplysia

• Published in: The Journal of neuroscience Vol. 23; no. 19; pp. 7317 - 7325
• Main Authors: Guan, Zhonghui, Kim, Joung-Hun, Lomvardas, Stavros, Holick, Kerri, Xu, Shiqin, Kandel, Eric R, Schwartz, James H
• Format: Journal Article
• Language: English
• Published: United States Soc Neuroscience 13.08.2003; Society for Neuroscience
• Subjects: Activating Transcription Factor 2; Animals; Aplysia; Arachidonic Acid - metabolism; Cells, Cultured; Cellular/Molecular; Cyclic AMP Response Element-Binding Protein - antagonists & inhibitors; Cyclic AMP-Dependent Protein Kinases - physiology; Enzyme Inhibitors - pharmacology; FMRFamide - pharmacology; Histone Deacetylases - metabolism; Long-Term Synaptic Depression - drug effects; MAP Kinase Signaling System; Marine; Mitogen-Activated Protein Kinases - antagonists & inhibitors; Mitogen-Activated Protein Kinases - physiology; Models, Biological; Nerve Tissue Proteins - metabolism; Neuronal Plasticity - drug effects; Neurons - drug effects; Neurons - enzymology; p38 Mitogen-Activated Protein Kinases; Phospholipases A - metabolism; Phospholipases A2; Phosphorylation; Repressor Proteins - metabolism; Serotonin - pharmacology; Transcription Factors - antagonists & inhibitors

At Aplysia sensory-to-motor neuron synapses, the inhibitory neuropeptide Phe-Met-Arg-Phe-NH2 (FMRFa) produces depression, and serotonin (5-HT) produces facilitation. Short-term depression has been found to result from the activation of a phospholipase A2. The released arachidonate is metabolized by...