Richard S Surwit
Sep 1, 1988; 37:1163-1167
Original Article

Stress alters brain function by modifying the structure and function of neurons and astrocytes. The fine processes of astrocytes are critical for the clearance of neurotransmitters during synaptic transmission. Thus, experience-dependent remodeling of glial processes is anticipated to alter the output of neural circuits. However, the molecular mechanisms that underlie glial structural plasticity are not known. Here we show that a single exposure of male and female mice to an acute stress produced a long-lasting retraction of the lateral processes of cerebellar Bergmann glial cells. These cells express the GluA1 subunit of AMPA-type glutamate receptors, and GluA1 knockdown is known to shorten the length of glial processes. We found that stress reduced the level of GluA1 protein and AMPA receptor-mediated currents in Bergmann glial cells, and these effects were absent in mice devoid of CPEB3, a protein that binds to GluA1 mRNA and regulates GluA1 protein synthesis. Administration of a β-adrenergic receptor blocker attenuated the reduction in GluA1, and deletion of adenylate cyclase 5 prevented GluA1 suppression. Therefore, stress suppresses GluA1 protein synthesis via an adrenergic/adenylyl cyclase/CPEB3 pathway, and reduces the length of astrocyte lateral processes. Our results identify a novel mechanism for GluA1 subunit plasticity in non-neuronal cells and suggest a previously unappreciated role for AMPA receptors in stress-induced astrocytic remodeling.

SIGNIFICANCE STATEMENT Astrocytes play important roles in synaptic transmission by extending fine processes around synapses. In this study, we showed that a single exposure to an acute stress triggered a retraction of lateral/fine processes in mouse cerebellar astrocytes. These astrocytes express GluA1, a glutamate receptor subunit known to lengthen astrocyte processes. We showed that astrocytic structural changes are associated with a reduction of GluA1 protein levels. This requires activation of β-adrenergic receptors and is triggered by noradrenaline released during stress. We identified adenylyl cyclase 5, an enzyme that elevates cAMP levels, as a downstream effector and found that lowering GluA1 levels depends on CPEB3 proteins that bind to GluA1 mRNA. Therefore, stress regulates GluA1 protein synthesis via an adrenergic/adenylyl cyclase/CPEB3 pathway in astrocytes and remodels their fine processes.

Hello

The document I referenced is https://filebox.ece.vt.edu/~symort/rfworkshop/Mixer_workshop_instruction.pdf. (This is cadence workshop document)

While following the pxf simulation in the above article, the results are different and I have a question.

My result picture is shown below.

<my result error>

<document result>

<my direct plot>

<document direct plot>

The difference with the documentation is that in the direct plot screen after the pxf simulation,

1.output harmonics-> input sideband

2.Frequency axis: out-> frequency axis: absin

3.The results for port0 (RF port) are also different (see photo below).

4.The frequency values in the box are different.

My screen shows 5G, 10G, 1K ~ 10M, but the document is the same as 1K ~ 10M.

Ask for a solution. Thank you.

aircrack-ng is a set of tools for auditing wireless networks. It's an enhanced/reborn version of aircrack. It consists of airodump (an 802.11 packet capture program), aireplay (an 802.11 packet injection program), aircrack (static WEP and WPA-PSK cracking), airdecap (decrypts WEP/WPA capture files), and some tools to handle capture files (merge, convert, etc.).

TC52

TC56

TC56*

TC534

TC530

TC520A

TC514

TC510

TC500

TC500A

IEEE / Institute of Electrical and Electronics Engineers Incorporated

IEEE / Institute of Electrical and Electronics Engineers Incorporated