Abstract
Although the function of the p42/p44 mitogen-activated protein (MAP) kinase pathway in long-term potentiation at hippocampal CA3-CA1 synapses has been well described, relatively little is known about the importance of the p38 MAP kinase pathway in synaptic plasticity. Here we show that the p38 MAP kinase pathway, a parallel signaling cascade activated by distinct upstream kinases, mediates the induction of metabotropic glutamate receptor-dependent long-term depression at CA3-CA1 synapses. Thus, two parallel MAP kinase pathways contribute to opposing forms of long-term plasticity at a central synapse.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Electric Stimulation
-
Enzyme Inhibitors / pharmacology
-
Excitatory Postsynaptic Potentials / drug effects
-
Excitatory Postsynaptic Potentials / physiology*
-
Hippocampus / cytology
-
Hippocampus / drug effects
-
Hippocampus / physiology*
-
MAP Kinase Signaling System / drug effects
-
MAP Kinase Signaling System / physiology*
-
Mitogen-Activated Protein Kinase 1 / physiology
-
Mitogen-Activated Protein Kinases / physiology*
-
Neuronal Plasticity / drug effects
-
Neuronal Plasticity / physiology*
-
Rats
-
Rats, Sprague-Dawley
-
Signal Transduction
-
Synapses / drug effects
-
Synapses / physiology*
-
p38 Mitogen-Activated Protein Kinases
Substances
-
Enzyme Inhibitors
-
Mitogen-Activated Protein Kinase 1
-
Mitogen-Activated Protein Kinases
-
p38 Mitogen-Activated Protein Kinases