SUMMARY1. Electrical stimulation of the central nucleus of the amygdala in the urethane or a-chloralose anaesthetized rabbit evokes a bradyeardia with a rapid onset and a concomitant fall in arterial blood pressure.2. Extracellular neuronal activity was recorded in the ipsilateral nucleus tractus solitarius and dorsal vagal nucleus whilst stimulating the ipsilateral central nucleus of the amygdala, the aortic and vagus nerves.3. A total of 213 neurones were activated by stimulation of at least one of these inputs. 93 of these neurones received a marked excitatory input from the central nucleus with a wide range of latencies (2-100 ms). 50 of these cells also received inputs from either the aortic or vagus nerves, or both.4. The activity of42 vagal preganglionic neurones was recorded in the dorsal vagal nucleus of which 22 had properties typical of cardioinhibitory neurones. 9 of these vagal motoneurones received inputs from the central nucleus with latencies between 2 and 100 ms. Of these, 5 had physiological properties indicating they were cardioinhibitory neurones.5. We conclude that neurones in the nucleus tractus solitarius and dorsal vagal nucleus can be influenced by descending inputs arising from the central nucleus of the amygdala. Some of these neurones are also likely to be influenced by afferents innervating the thoracic viscera and arterial baroreceptors. The implications of these observations on the role of forebrain-brain-stem interactions in cardiovascular control are discussed.

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SUMMARY1. The cardiovascular responses to electrical stimulation of the central nucleus of the amygdala (c.n.) have been studied in chloralose-anaesthetized rabbits. A pattern of response involving bradyeardia, hypotension and hind-limb vasodilatation, accompanied by an increase in the rate of phrenic nerve discharge, was evoked only in response to stimulation within the medial portion of the c.n.2. The cardiovascular responses were not secondary to the changes in respiratory activity since they were unaffected by altering central respiratory drive by either hypo-or hyperventilation of the animal.3. The bradycardia was attenuated by the administration of atropine sulphate and abolished by the subsequent administration of propranolol, which when given alone attenuated the bradyeardia. Atropine or propranolol given alone also attenuated the hypotension evoked by medial c.n. stimulation but the concurrent hind-limb vasodilatation was unaffected.4. Atenolol, which unlike propranolol does not cross the blood-brain barrier, had little effect on the bradyeardia in response to medial c.n. stimulation, but the subsequent administration of atropine abolished it. The hypotension in response to medial c.n. stimulation was also unaffected by atenolol.5. The vasodilatation in response to medial c.n. stimulation was abolished by administration of guanethidine even after restoration of hind-limb perfusion pressure to control values by the infusion of angiotensin II into the hind-limb perfusion circuit.6. Electrical stimulation of areas within 0-5 mm of the medial c.n. also resulted in bradycardia but then it was accompanied by hypertension and hind-limb vasoconstriction. Stimulation of areas 1-0 mm distant to the medial c.n. resulted in small and inconsistent cardiovascular responses. 7. These results show that hind-limb vasodilatation, mediated by withdrawal of sympathetic tone, occurs in response to stimulation within the medial c.n. of the rabbit and is in part responsible for the observed hypotension. It has also been confirmed that the bradycardia in response to medial c.n. stimulation is mediated by the vagus nerves.

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