At present, little is known about the brain origin of stress-induced cardiac sympathetic drive responsible for stress-induced tachycardia. Our aim was to determine the effect of bilateral microinjections of the GABA(A) receptor agonist, muscimol, into the amygdaloid complex on both the heart rate and cardiac autonomic activity during restraint stress. Experiments were performed in male Sprague-Dawley rats (n=9), with pre-implanted electrocardiographic electrodes. Heart rate increased sharply after the onset of the restraint and reached a peak 1-2 min later (from 344+/-6-440+/-20 BPM). Subsequently, heart rate began to fall, and during the next 10-15 min approached the steady-state level of 384+/-11. After vehicle, mean heart rate during each of three 10-min restraint epochs was significantly higher compared with the pre-restraint level. After muscimol, mean heart rate was significantly elevated only during the first 10 min of restraint. There was no difference in the early peak tachycardia between both conditions. Muscimol substantially accelerated the fall of the HR from the peak to the steady-state level, and thus the area under the curve value for muscimol (503+/-162 BPM x min) was significantly smaller than that for vehicle (1221+/-231 BPM x min); P<0.05. After vehicle, the high-frequency spectral power of the heart rate decreased and the low-frequency power increased during the restraint, resulting in a significant rise of the low frequency/high frequency ratio from 1.2+/-0.2-2.8+/-0.6 (n=9, P<0.05). Muscimol suppressed these stress-induced effects. We conclude that inhibition of the amygdala neurons abolishes the sustained component of tachycardia during the restraint, has no effect on the early tachycardic component, and prevents stress-induced alterations in the heart rate variability indices.