Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27457815
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27457815
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Mol+Psychiatry
2017 ; 22
(10
): 1440-1447
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Cellular and molecular basis for stress-induced depression
#MMPMID27457815
Seo JS
; Wei J
; Qin L
; Kim Y
; Yan Z
; Greengard P
Mol Psychiatry
2017[Oct]; 22
(10
): 1440-1447
PMID27457815
show ga
Chronic stress has a crucial role in the development of psychiatric diseases,
such as anxiety and depression. Dysfunction of the medial prefrontal cortex
(mPFC) has been linked to the cognitive and emotional deficits induced by stress.
However, little is known about the molecular and cellular determinants in mPFC
for stress-associated mental disorders. Here we show that chronic restraint
stress induces the selective loss of p11 (also known as annexin II light chain,
S100A10), a multifunctional protein binding to 5-HT receptors, in layer II/III
neurons of the prelimbic cortex (PrL), as well as depression-like behaviors, both
of which are reversed by selective serotonin reuptake inhibitors (SSRIs) and the
tricyclic class of antidepressant (TCA) agents. In layer II/III of the PrL, p11
is highly concentrated in dopamine D2 receptor-expressing (D2(+)) glutamatergic
neurons. Viral expression of p11 in D2(+) PrL neurons alleviates the
depression-like behaviors exhibited by genetically manipulated mice with D2(+)
neuron-specific or global deletion of p11. In stressed animals, overexpression of
p11 in D2(+) PrL neurons rescues depression-like behaviors by restoring
glutamatergic transmission. Our results have identified p11 as a key molecule in
a specific cell type that regulates stress-induced depression, which provides a
framework for the development of new strategies to treat stress-associated mental
illnesses.