Medial prefrontal cortex-basolateral amygdala circuit dysfunction in chronic alcohol-exposed male rats

2021 ◽  
pp. 108912
Author(s):  
Elizabeth J. Crofton ◽  
ManHua Zhu ◽  
Katelin N. Curtis ◽  
Gavin W. Nolan ◽  
Todd K. O'Buckley ◽  
...  
2015 ◽  
Vol 57 (3) ◽  
pp. 305-312 ◽  
Author(s):  
Wendy A. Koss ◽  
Madeline M. Lloyd ◽  
Renee N. Sadowski ◽  
Leslie M. Wise ◽  
Janice M. Juraska

2019 ◽  
Vol 116 (9) ◽  
pp. 3799-3804 ◽  
Author(s):  
Tingting Sun ◽  
Zihua Song ◽  
Yanghua Tian ◽  
Wenbo Tian ◽  
Chunyan Zhu ◽  
...  

Obsessive-compulsive disorder (OCD) affects ∼1 to 3% of the world’s population. However, the neural mechanisms underlying the excessive checking symptoms in OCD are not fully understood. Using viral neuronal tracing in mice, we found that glutamatergic neurons from the basolateral amygdala (BLAGlu) project onto both medial prefrontal cortex glutamate (mPFCGlu) and GABA (mPFCGABA) neurons that locally innervate mPFCGlu neurons. Next, we developed an OCD checking mouse model with quinpirole-induced repetitive checking behaviors. This model demonstrated decreased glutamatergic mPFC microcircuit activity regulated by enhanced BLAGlu inputs. Optical or chemogenetic manipulations of this maladaptive circuitry restored the behavioral response. These findings were verified in a mouse functional magnetic resonance imaging (fMRI) study, in which the BLA–mPFC functional connectivity was increased in OCD mice. Together, these findings define a unique BLAGlu→mPFCGABA→Glu circuit that controls the checking symptoms of OCD.


2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Haley A. Vecchiarelli ◽  
Chaitanya P. Gandhi ◽  
Matthew N. Hill

Tryptophan is an essential dietary amino acid that is necessary for protein synthesis, but also serves as the precursor for serotonin. However, in addition to these biological functions, tryptophan also serves as a precursor for the kynurenine pathway, which has neurotoxic (quinolinic acid) and neuroprotective (kynurenic acid) metabolites. Glucocorticoid hormones and inflammatory mediators, both of which are increased by stress, have been shown to bias tryptophan along the kynurenine pathway and away from serotonin synthesis; however, to date, there is no published data regarding the effects of stress on enzymes regulating the kynurenine pathway in a regional manner throughout the brain. Herein, we examined the effects of an acute psychological stress (120 min restraint) on gene expression patterns of enzymes along the kynurenine pathway over a protracted time-course (1–24 h post-stress termination) within the amygdala, hippocampus, hypothalamus, and medial prefrontal cortex. Time-dependent changes in differential enzymes along the kynurenine metabolism pathway, particularly those involved in the production of quinolinic acid, were found within the amygdala, hypothalamus, and medial prefrontal cortex, with no changes seen in the hippocampus. These regional differences acutely may provide mechanistic insight into processes that become dysregulated chronically in stress-associated disorders.


2014 ◽  
Vol 45 ◽  
pp. 31-42 ◽  
Author(s):  
Sara Sabihi ◽  
Nicole E. Durosko ◽  
Shirley M. Dong ◽  
Benedetta Leuner

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