Ablation of glucocorticoid receptor in the hindbrain of the mouse provides a novel model to investigate stress disorders.
Anne-Louise GannonLaura O'HaraJ Ian MasonDiane RebourcetSarah SmithAdriana TraveresCarlos Jose Alcaide-CorralHanne FrederiksenAnne JørgensenLaura MilneRod Thomas MitchellLee B SmithPublished in: Scientific reports (2019)
The hypothalamic-pituitary-adrenal (HPA) axis regulates responses to internal and external stressors. Many patients diagnosed with conditions such as depression or anxiety also have hyperactivity of the HPA axis. Hyper-stimulation of the HPA axis results in sustained elevated levels of glucocorticoids which impair neuronal function and can ultimately result in a psychiatric disorder. Studies investigating Glucocorticoid Receptor (GR/NR3C1) in the brain have primarily focused on the forebrain, however in recent years, the hindbrain has become a region of interest for research into the development of anxiety and depression, though the role of GR signalling in the hindbrain remains poorly characterised. To determine the role of glucocorticoid signalling in the hindbrain we have developed a novel mouse model that specifically ablates hindbrain GR to ascertain its role in behaviour, HPA-axis regulation and adrenal structure. Our study highlights that ablation of GR in the hindbrain results in excessive barbering, obsessive compulsive digging and lack of cage exploration. These mice also develop kyphosis, elevated circulating corticosterone and severe adrenal cortex disruption. Together, this data demonstrates a role for hindbrain GR signalling in regulating stress-related behaviour and identifies a novel mouse model to allow further investigation into the pathways impacting stress and anxiety.
Keyphrases
- mouse model
- end stage renal disease
- obsessive compulsive disorder
- sleep quality
- chronic kidney disease
- ejection fraction
- mental health
- stress induced
- prognostic factors
- electronic health record
- depressive symptoms
- genome wide
- patient reported outcomes
- multiple sclerosis
- high fat diet induced
- dna methylation
- cerebral ischemia
- physical activity
- deep brain stimulation
- insulin resistance
- weight gain