MR mediated effects in the brain
The MR became a central focus as a moderator of early stress responses
since the receptor was found to mediate non-genomic rapid and transient
effects of corticosteroids on neurotransmission and synaptic plasticity
in the hippocampus and amygdala after stress (Karst and Joëls, 2005;
Karst et al. , 2010; Nahar et al. , 2015; Treviño and
Gorelick, 2021). This was specifically shown with the rapid and
transient increase of miniature excitatory postsynaptic currents (mEPSC)
following treatment with corticosterone, whereby signaling was
transduced by MRs located pre-synaptically at the plasma membrane
regulating the eventual release of glutamate, in contrast to genomic
receptors (Karst et al. , 2010; Groeneweg et al. , 2012). A
distinct mechanism of non-genomic MR signaling could involve receptor
dissociation from chaperone complexes within the cytoplasm
(Gutierrez-Mecinas et al. , 2011) in concert with mediators like
noradrenalin and CRH. Of note, non-genomic MR effects can determine
subsequent genomic mechanisms, which has been termed metaplasticity
(Karst et al. , 2010; Chatterjee and Sikdar, 2014; Sarabdjitsinghet al. , 2014).