Hayward LF (2012) Neurotoxic lesion of CRF-R1 neurons in the amygdala selectively attenuates the heart rate response to acute stress in the spontaneously hypertensive rat. Neuroscience 2012 Abstracts 281.28. Society for Neuroscience, New Orleans, LA.
Summary: The magnitude of a person’s autonomic response to mental stress is predictive of one’s risk for the development of cardiovascular disease and has been linked to indicators of exaggerated neuronal activity in the amygdala. Recent evidence from our lab identified a link between changes in the expression of the neuropeptide corticotrophin-releasing factor (CRF) within the central nucleus of the amygdala (CEA) to exaggerated cardiovascular responses to acute stress in the spontaneously hypertensive rat (SHR). The present study was undertaken to evaluate the impact of selective lesion of CRF-R1 neurons in the amygdala on the cardiovascular response to acute air jet stress (AJS) in the SHR. Male SHR rats underwent local bilateral microinjections of 10 nanograms/200 nl per side of blank-saporin (n=4) or CRF-receptor (R1) targeting saporin (n=4) into the region of the CEA. Following 7-10 days of recovery and two days following arterial catheter instrumentation, animals underwent AJS testing. CRH-R1 lesion in the amygdala produced a small reduction in resting systolic blood pressure (160±6 vs 173±4 mmHg, p<0.1) but not change in heart rate (354±16 vs 352±+4 bpm). CRH-R1 lesion also significantly attenuated the mean rise heart rate in response to AJS (72±21 vs 130±13 bpm) and facilitated a more rapid heart rate recovery independent of any effect on the blood pressure response to AJS. The findings demonstrate for the first time that CRF-R1 activation in the amygdala selectively contributes to the elevated heart rate response to stress in individuals with hypertension, thus providing a link between the exaggerated activity in the amygdala and a specific cardiovascular response to stress.
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