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Estradiol and Metabotropic Glutamate Receptors interaction within the anxiety neural circuitry at behavioral and protein levels
Author(s) -
De Jesus-Burgos Maria Ines,
Gonzalez-Garcia Stephanie,
Cruz Yanira,
Gonzalez Gabriela,
Gonzalez Beatriz,
Portela Lucila,
Pérez-Acevedo Nivia L
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.918.7
Subject(s) - metabotropic glutamate receptor , metabotropic glutamate receptor 2 , medicine , endocrinology , amygdala , basolateral amygdala , metabotropic glutamate receptor 5 , glutamate receptor , elevated plus maze , ovariectomized rat , agonist , receptor , chemistry , neuroscience , anxiety , psychology , estrogen , psychiatry
Anxiety is the most common psychiatric disorders affecting females twice more than males. In hippocampal cells, estradiol regulates group I/II metabotropic glutamate receptors (mGluR1a/5 and mGluR2/3, respectively) activation. Thus, estradiol might modulate female anxiety within the basolateral amygdala (BLA) through mGluRs. We hypothesized that: 1) BLA activation of mGluRs might produce anxiolytic‐like effects; and 2) mGluR protein expression will be up‐regulated, in an estradiol dependent manner. Ovariectomized female rats, with (OVX+EB) and without (OVX) estradiol treatment were compared to male rats. We infused (S)‐3,5‐dihydroxyphenylglycin (DHPG), a group I mGluR agonist into the BLA. Anxiety was analyzed with the elevated plus maze and risk assessment behaviors (RABs); and protein expression by western blots analysis. DHPG (1.0 μM) increased the time and entries in open arms; and reduced RABs in OVX+EB (p<0.05), but not OVX and/or male rats. In the amygdala, protein expression of mGluR1a and mGluR2/3 were up‐regulated in OVX+EB (p<0.05) than OVX and/or male rats. No differences were found for mGluR5. Thus, activation of group I mGluRs, within the BLA, depends upon estradiol to modulate female anxiety. This effect might be underlined by region‐specific estradiol genomic and nongenomic effects. Grant Funding Source : NIH‐EARDA 1G11H046326, MBRS‐RISE GM61838 and NSF DBI‐0932955