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The Journal of Neuroscience, February 1, 2000, 20(3):977-985
ERKI/II Regulation by the Muscarinic Acetylcholine Receptors
in Neurons
Kobi
Rosenblum1,
Marie
Futter2,
Matthew
Jones1,
E. C.
Hulme2, and
T. V. P.
Bliss1
Divisions of 1 Neurophysiology and
2 Physical Biochemistry, National Institute for Medical
Research, Mill Hill, London NW7 1AA, United Kingdom
Muscarinic acetylcholine receptors (mAChRs) are known to be
involved in learning and memory, but the molecular basis of their involvement is not well understood. The availability of new and specific biochemical tools has revealed a crucial role for the mitogen-activated protein kinase (MAPK) family in learning and memory.
Here, we examine the link between mAChRs and MAPK in neurons. Using the
MAPK kinase (MEK)-specific inhibitor PD98059, we first demonstrate a necessary role for active ERKI/II in long-term
potentiation in vivo. Using phospho-specific
antibodies that recognize the activated form of ERKI/II, we find that
the level of ERKI/II activation in brain is regulated by mAChRs.
Carbachol, a muscarinic agonist, induces prolonged activation of
ERKI/II, without effect on the related kinase SAPK/JNK
(stress-activated protein kinase/c-Jun N-terminal protein
kinase) in primary cortical cultures. ERKI/II activation is
Src-dependent and partially phosphoinositide-3 kinase- and Ca2+-dependent but is PKC-independent. M1-M4
mAChR subtypes expressed in COS-7 cells can all induce ERKI/II
activation using a signal transduction pathway similar to that
operating in neurons. The nature of the signal transduction suggests
that ERKI/II can serve as a convergence site for mAChR activation and
other neurotransmitter receptors.
Key words:
mAChR; extracellular regulated kinase; MAPK; neurons; COS-7; LTP; signal transduction
Copyright © 2000 Society for Neuroscience 0270-6474/00/203977-09$05.00/0
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