Electrical stimulation of the amygdala modifies the negative feedback effect of glucocorticoids on the adrenocortical responses to stress.
OBJECTIVE
The amygdala (AMG) plays a facilitatory role in the hypothalamic-pituitary-adrenal (HPA) axis. The effect of the AMG on the negative feedback exerted by glucocorticoids (GC) is not clear. We investigated the effect of repeated electrical stimulation of the AMG on the feedback action of GC upon the adrenocortical (AC) response to stressful stimuli.


METHODS
Rats received electrical stimulation into the central amygdalar nucleus once daily for 4 days. At days 5 and 12 after the onset of stimulation, rats were treated with dexamethasone (Dex) or vehicle and were exposed to either photic or acoustic stress stimuli, and serum corticosterone (CS) was measured. In another group of rats, we measured the binding of Dex to the hippocampal cytosol at 5 and 12 days after the AMG stimulation.


RESULTS
At 5 and 12 days after the onset of stimulation or a sham control, stress increased the serum CS level. In the sham group, Dex completely inhibited the CS response, but at 5 days after stimulation, it was significantly less effective in doing this. At day 12, Dex was as effective as in the control group. AMG stimulation delayed the return of CS response to basal levels and caused a significant decrease in the binding capacity of Dex to hippocampal cytosol.


CONCLUSIONS
Electrical stimulation of the AMG caused a transient impairment of the feedback action of GC upon the stress response. This effect may be due to the decrease in hippocampal corticosteroid receptors. This suggests that the impaired GC feedback caused by AMG stimulation may be involved in the facilitatory effect of the AMG on the function of the AC axis.
Department of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Joseph
J
Weidenfeld
Anna
A
Itzik
Haim
H
Ovadia
D000161:Acoustic Stimulation / Q000009:adverse effects; D000818:Animals; D066274:Central Amygdaloid Nucleus / Q000502:physiology*; D003345:Corticosterone / Q000097:blood; D003907:Dexamethasone / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004558:Electric Stimulation / Q000379:methods*; D005246:Feedback; D005938:Glucocorticoids / Q000097:blood / Q000627:therapeutic use*; D006624:Hippocampus / Q000378:metabolism; D008297:Male; D010775:Photic Stimulation / Q000009:adverse effects; D011863:Radioimmunoassay; D051381:Rats; D013315:Stress, Psychological / Q000097:blood / Q000473:pathology / Q000628:therapy; D013997:Time Factors
D005938:Glucocorticoids; D003907:Dexamethasone; D003345:Corticosterone