Both electrical and chemical stimulation of the midbrain periaqueductal gray matter (PAG) inhibit baroreflex vagal bradycardia (BVB). The present study was designed to determine the target site of this inhibition about which little is known. Electrical stimulation of the PAG, in particular of its dorsal portion, markedly suppressed BVB provoked by electrical stimulation of the aortic depressor nerve (ADN; percentage of inhibition = 91.0 +/- 9.7%, mean +/- SD; n = 64). To identify the target site of the inhibition, several types of experiments were conducted in rats under chloralose-urethan anesthesia. 2. The inhibition was exclusively of central origin because inhibition of BVB by stimulation of the PAG was unchanged after transection of the spinal cord at the C1 level. According to Wall's method, we examined whether PAG stimulation affects BVB presynaptically by modulating the excitability of ADN terminals in the nucleus tractus solitarius (NTS). However, excitability changes of ADN terminals by the PAG stimulation were not demonstrated. 3. Vagal bradycardia evoked by microinjection of glutamate into the nucleus ambiguus (NA) region was markedly suppressed by the PAG (percentage of inhibition = 85.9 +/- 9.1%; n = 9), an indication that vagal cardiac preganglionic neurons at this site were subject to the inhibitory action of the PAG. Basal vagal tone due to ongoing preganglionic neuronal activity was also subject to inhibitory control by the PAG because basal heart rate was increased by stimulation of the PAG after either C1 transection or NTS lesion. 4. We found that PAG stimulation suppressed ADN-induced field potentials in the NA region (37.7 +/- 13.8% relative to the control; n = 9) but only slightly in the NTS region (95.8 +/- 15.2%; n = 16). In addition, unitary recordings revealed that ADN-evoked unitary responses of neurons in the NA region were suppressed by PAG stimulation, whereas NTS baroreceptor neurons, either ADN responsive or nonresponsive, were scarcely inhibited by PAG stimulation. 5. These findings suggest that the PAG inhibited BVB mainly at the vagal preganglionic cell level and not at the NTS interneuron level. The conclusion is in harmony with our previous reports that the target site of hypothalamic inhibition of BVB in rats is also the preganglionic neurons and that hypothalamic inhibition of BVB is mediated predominantly by the PAG.
