Comments and Questions:


1) This paper reveals that how OT elicits GFAP plasticity. The major finding is that activation of OTR can activate ERK 1/2 and PKA in an antagonistic but coordinated manner with microdomain-specific features, which determines the spatiotemporal features of GFAP metabolisms. Firstly, the finding confirms that OT can efficiently facilitate neuronal activity via eliciting retraction of astrocyte processes. Secondly, the change in GFAP plasticity is accompanied with alterations of the activity of pERK1/2 and PKA. The former promote GFAP monomers to decompose or polymerize; the latter increases GFAP monomers via a process opposite to the effect of pERK1/2. This study provides a novel approach to alter astrocyte functions by targeting GFAP metabolism through pharmacological modulation of the activity of different protein kinases. Since GFAP-associated astrocytic plasticity is extensively involved in physiological processes, such as OT secretion in lactation, reproduction, and immunological activity, as well as VP secretion in hyponatremia and ischemic stroke in addition to psychiatric disorders, neurodegenerative diseases and many other diseases. Further exploration of the approaches to selectively changing the activity of pERK 1/2 and PKA in different compartments of astrocytes has broad therapeutic potentials in clinical field.



1) What is the significance of applying patch-clamp technique on non-excitable cells?

2) What is the role of GFAP fragments in the formation of GFAP filaments?

3) What is the effect of oxytocin on GFAP metabolism?

4) What is the signaling pathway from OTR activation to the activation of different protein kinases?

5) Are there any specific phosphorylation/dephosphorylation sites of GFAP to pERK 1/2 or PKA?

6) How to explain the apparent contradictory effect of pERK 1/2 in facilitation of GFAP monomer decomposition and filament formation? So does the activated PKA.

7) What is the difference in the time course between increases in pERK 1/2 and PKA in downstream to Gbetagamma signaling?

8) In lactation rats, how to explain the co-existence of cPKA and pERK 1/2 in astrocytic processes immediately following the milk-ejection reflex.

9) Is there any specific agent that can modulate GFAP plasticity?

10) How can we change GFAP metabolism in a microdomain-specific manner?


2017-11- 03 Literature Analysis

Oxytocin Rapidly Changes Astrocytic GFAP Plasticity by Differentially Modulating the Expressions of pERK 1/2 and Protein Kinase A. Ping Wang, Frontiers in Molecular Neuroscience(2017) doi: 10.3389/fnmol.2017.00262 Presented by Dan Cui; Edited by Xiaoran Wang

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