ERIC Number: EJ910256
Record Type: Journal
Publication Date: 2010-Dec
Abstractor: As Provided
Reference Count: 0
"Silent" Priming of Translation-Dependent LTP by [Beta]-Adrenergic Receptors Involves Phosphorylation and Recruitment of AMPA Receptors
Tenorio, Gustavo; Connor, Steven A.; Guevremont, Diane; Abraham, Wickliffe C.; Williams, Joanna; O'Dell, Thomas J.; Nguyen, Peter V.
Learning & Memory, v17 n12 p627-638 Dec 2010
The capacity for long-term changes in synaptic efficacy can be altered by prior synaptic activity, a process known as "metaplasticity." Activation of receptors for modulatory neurotransmitters can trigger downstream signaling cascades that persist beyond initial receptor activation and may thus have metaplastic effects. Because activation of [beta]-adrenergic receptors ([beta]-ARs) strongly enhances the induction of long-term potentiation (LTP) in the hippocampal CA1 region, we examined whether activation of these receptors also had metaplastic effects on LTP induction. Our results show that activation of [beta]-ARs induces a protein synthesis-dependent form of metaplasticity that primes the future induction of late-phase LTP by a subthreshold stimulus. [beta]-AR activation also induced a long-lasting increase in phosphorylation of [alpha]-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) GluA1 subunits at a protein kinase A (PKA) site (S845) and transiently activated extracellular signal-regulated kinase (ERK). Consistent with this, inhibitors of PKA and ERK blocked the metaplastic effects of [beta]-AR activation. [beta]-AR activation also induced a prolonged, translation-dependent increase in cell surface levels of GluA1 subunit-containing AMPA receptors. Our results indicate that [beta]-ARs can modulate hippocampal synaptic plasticity by priming synapses for the future induction of late-phase LTP through up-regulation of translational processes, one consequence of which is the trafficking of AMPARs to the cell surface.
Descriptors: Cognitive Processes, Cues, Brain Hemisphere Functions, Neurological Organization, Biochemistry, Cytology, Drug Use
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Publication Type: Journal Articles; Reports - Research
Education Level: N/A
Authoring Institution: N/A