Data from: Glucocorticoid induces incoordination between glutamatergic and GABAergic neurons in the amygdala

Background: Stressful life leads to mood disorders. Chronic mild stress is
presumably major etiology for depression, and acute severe stress leads to
anxiety. These stressful situations may impair
hypothalamus-pituitary-adrenal axis and in turn induce synapse
dysfunction. However, it remains elusive how the stress hormones mess up
subcellular compartments and interactions between excitatory and
inhibitory neurons, which we have investigated in mouse amygdala, a
structure related to emotional states. Methods and Results: Dexamethasone
was chronically given by intraperitoneal injection once a day for one week
or was acutely washed into the brain slices. The neuronal spikes and
synaptic transmission were recorded by whole-cell patching in amygdala
neurons of brain slices. The chronic or acute administration of
dexamethasone downregulates glutamate release as well as upregulates GABA
release and GABAergic neuron spiking. The chronic administration of
dexamethasone also enhances the responsiveness of GABA receptors.
Conclusion: The upregulation of GABAergic neurons and the downregulation
of glutamatergic neurons by glucocorticoid impair their balance in the
amygdala, which leads to emotional disorders during stress.