Related Experiment Video
Updated: Jul 13, 2026

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
Published on: March 20, 2014
A pharmacological activator of AMP-activated protein kinase (AMPK) induces astrocyte stellation
Carlita B Favero1, James W Mandell
1Neuroscience Graduate Program, University of Virginia, Charlottesville, VA 22908, USA.
Abstract:
AMP-activated protein kinase (AMPK) represents a key energy-sensing molecule in many cell types. Because astrocytes are key mediators of metabolic signaling in the brain, we have initiated studies on the expression and activation of AMPK in these cells. Treatment of cultured rat cortical astrocytes with a pharmacological AMPK activator, AICA-riboside (AICAR) resulted in a time- and concentration-dependent increase in phosphorylation of AMPK and acetyl-CoA carboxylase (ACC), a direct substrate. AICAR treatment also induced a transition from epithelioid to stellate morphology in a time- and concentration-dependent manner. As stellation is indicative of actin cytoskeletal reorganization, the formation of stress fibers and focal adhesions in response to AICAR was assessed. AICAR-induced stellation correlated with F-actin disassembly and focal adhesion dispersal. Furthermore, transient transfection of an activated RhoA construct prevented AICAR-induced stellation, indicating a mechanism upstream of RhoA. Use of pharmacological inhibitor compound C prevented AICAR-induced stellation demonstrating necessity of AMPK activity for the response. Our findings suggest that AMPK mediates morphological alterations of astrocytes in response to energy depletion.
More Related Videos
Related Concept Videos
cAMP-dependent Protein Kinase Pathways
PI3K/mTOR/AKT Signaling Pathway
GPCRs Regulate Adenylyl Cylase Activity
Two...
Amplifying Signals via Enzymatic Cascade
MAPK Signaling Cascades
Amplifying Signals via Second Messengers

