Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus

Abstract

The goal of the present study was to determine the effect of activating vagal afferent fibers on the discharge of median preoptic (MnPO) neurons responsive to peripheral angiotensin II (ANG II) and osmotic inputs. Vagal afferents were activated by electrical stimulation of the proximal end of the transected cervical vagus nerve (3 pulses, 100 Hz, 1 ms, 100–500 μA). Of 21 MnPO neurons, 19 were antidromically activated from the hypothalamic paraventricular nucleus (PVH) (latency: 10.3 ± 1.3 ms, threshold: 278 ± 25 μA). MnPO-PVH cells had an average spontaneous discharge of 2.1 ± 0.4 Hz. Injection of ANG II (150 ng) and/or hypertonic NaCl (1.5 Osm/L, 100 μl) through the internal carotid artery significantly ( P < 0.01) increased the firing rate of most MnPO-PVH neurons (16/19, 84%). Vagus nerve stimulation significantly ( P < 0.01) decreased discharge (− 73 ± 9%) in 10 of 16 (63%) neurons with an average onset latency of 108 ± 19 ms. Among the remaining 6 MnPO-PVH neurons vagal activation either increased discharge (177 ± 100%) with a latency of 115 ± 15 ms ( n = 2) or had no effect ( n = 4). Pharmacological activation of chemosensitive vagal afferents with phenyl biguanide produced an increase ( n = 3), decrease ( n = 2), or no change ( n = 6) in discharge. These observations indicate that a significant proportion of ANG II- and/or osmo-sensitive MnPO neurons receive convergent vagal input. Although the sensory modalities transmitted by the vagal afferents to MnPO-PVH neurons are not presently known, the presence of inhibitory and excitatory vagal-evoked responses indicates that synaptic processing by these cells integrates humoral and visceral information to subserve potentially important cardiovascular and body fluid homeostatic functions.