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The Journal of Neuroscience, 1999, 19:RC36:1-8
RAPID COMMUNICATION
Molecular Mechanisms of Long-Term Potentiation in the Insular
Cortex In Vivo
Matthew W.
Jones,
Pim J.
French,
T. V. P.
Bliss, and
Kobi
Rosenblum
Division of Neurophysiology, National Institute for Medical
Research, London NW7 1AA, United Kingdom
We have investigated molecular mechanisms of synaptic plasticity in
the pathway between two forebrain structures important for taste
learning, the basolateral amygdala (BLA) and the insular cortex. We
report here that in vivo long-term potentiation (LTP) induced by BLA stimulation requires functional NMDA receptors and is modulated by muscarinic acetylcholine receptors. In addition, LTP results in the activation of cortical extracellular regulated kinase 1/2 (ERK1/2) and is blocked by inhibitors of ERK1/2 activation. Previous findings demonstrated the involvement of the same molecular mechanisms in the same cortical area during novel taste learning. The
results demonstrate that both synaptic and behavioral plasticity share
common molecular mechanisms in the insular cortex.
Key words:
long-term potentiation; basolateral amygdala; insular
cortex; muscarinic acetylcholine receptors; extracellular-regulated
kinases; ERK1/2; mitogen-activated protein kinase; immediate early
gene
Copyright © 0000 Society for Neuroscience 0270-6474/0/$05.00/0
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