Molecular mechanisms of long-term potentiation in the insular cortex in vivo.

Content Provider	Semantic Scholar
Author	Rosenblum, Kobi
Copyright Year	1999
Abstract	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.
Starting Page	RC36
Ending Page	RC36
Page Count	1
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://www.jneurosci.org/content/jneuro/19/21/RC36.full.pdf
PubMed reference number	10531470v1
Volume Number	19
Issue Number	21
Journal	The Journal of neuroscience : the official journal of the Society for Neuroscience
Language	English
Access Restriction	Open
Subject Keyword	Amygdaloid structure Biologics License Application Cerebral cortex Cholinergic Receptors Insula of Reil Learning Disorders Long-Term Potentiation Muscarinic Acetylcholine Receptor N-Methyl-D-Aspartate Receptors N-Methylaspartate Neuronal Plasticity Prosencephalon Set of basolateral nuclei of amygdala central amygdalar nucleus chemosensitization/potentiation
Content Type	Text
Resource Type	Article