TY - JOUR
T1 - Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus
AU - Stocker, Sean D.
AU - Toney, Glenn M.
N1 - Funding Information:
This work was supported by NIH Grants HL-056834 (GMT) and HL-071645 (GMT), a NIH National Research Service Award HL-073661 (SDS), a Scientist Development Award Grant 0630202N from the American Heart Association (SDS), and the University of Kentucky College of Medicine.
PY - 2007/2/2
Y1 - 2007/2/2
N2 - 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.
AB - 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.
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U2 - 10.1016/j.brainres.2006.11.001
DO - 10.1016/j.brainres.2006.11.001
M3 - Article
C2 - 17161831
AN - SCOPUS:33846012925
SN - 0006-8993
VL - 1131
SP - 118
EP - 128
JO - Brain research
JF - Brain research
IS - 1
ER -