Responses of median preoptic neurons projecting to the hypothalamic paraventricular nucleus to osmotic stimulation in Wistar-Kyoto and spontaneously hypertensive rats

Tanaka, Junichi; Ushigome, Akihiko; Matsuda, Michihiko; Saitō, Hideo

doi:10.1016/0304-3940(95)11555-4

Cited by 17 publications

(13 citation statements)

References 19 publications

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“…These observations are consistent with the ability of these stimuli to increase neuronal discharge of MnPO neurons in vivo (McAllen et al, 1990;Tanaka et al, 1995;Aradachi et al, 1996;Stocker and Toney, 2005). In addition, changes in circulating blood volume have been reported to increase Fos immunoreactivity in MnPO neurons (Potts et al, 2000).…”

Section: Discussionsupporting

confidence: 83%

“…In some cases, Fos immunoreactivity was reported in MnPO neurons that project to the hypothalamic paraventricular nucleus (PVH) and/or supraoptic nucleus (Oldfield et al, 1994;Larsen and Mikkelsen, 1995). Consistent with the notion that osmolality and ANG II increase the excitability of MnPO neurons, electrophysiological studies in vivo have demonstrated that hyperosmolality and circulating ANG II significantly increased the neuronal firing rates of MnPO neurons (McAllen et al, 1990;Tanaka et al, 1993;Tanaka et al, 1995;Aradachi et al, 1996;Stocker and Toney, 2005).…”

Section: Introductionmentioning

confidence: 70%

“…In this regard, our laboratory (Stocker and Toney, 2005) and others (Knuepfer et al, 1985;McAllen et al, 1990;Tanaka et al, 1993;Tanaka et al, 1995;Aradachi et al, 1996) have shown that MnPO neurons are responsive to changes in plasma osmolality, circulating ANG II, and/or changes in ABP. Since the central nervous system integrates these stimuli along with the prevailing level of blood volume to result in appropriate behavioral, neuroendocrine, and autonomic responses to body fluid homeostatic challenges, we examined whether the ongoing activity of MnPO neurons is altered by activation of vagal afferent fibers and whether vagal afferent input specifically targeted MnPO-PVH neurons that were responsive to forebrain ANG II and osmotic stimulation.…”

Section: Discussionmentioning

confidence: 91%

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

Stocker

Toney

2007

Brain Research

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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 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 vagalevoked 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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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 91%

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

Stocker

Toney

2007

Brain Research

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“…The parastrial nucleus also sends projections to the brainstem that appear to end in the lateral parabrachial nucleus (Moga et al, 1990), which may represent an additional pathway for the involvement of AVPV neurons in fluid homeostasis. The AVPV may also play a role in the neural control of fluid homeostasis through its projections to the subfornical organ, or to the MPN, which participate in neural pathways regulating cardiovascular function (McKinley et al, 1994;da Silva et al, 1995;Tanaka et al, 1995; also see Bourque et al, 1994;Saper, 1995, for reviews).…”

Section: Descending Projectionsmentioning

confidence: 98%

Projections of the sexually dimorphic anteroventral periventricular nucleus in the female rat

1997

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The anteroventral periventricular nucleus of the hypothalamus (AVPV) is a sexually dimorphic nucleus in the preoptic region that appears to be a nodal point in forebrain circuits, mediating hormonal feedback on gonadotropin secretion. The results of anterograde transport experiments indicate that the AVPV sends ascending projections to the ventral part of the lateral septal nucleus, the parastrial nucleus, and the region adjacent to the vascular organ of the lamina terminalis (OVLT) that contains a subpopulation of gonadotropin releasing hormone (GnRH)-containing neurons. The majority of projections from the AVPV pass caudally through the periventricular zone of the hypothalamus and form dense terminal fields in the periventricular nuclei, parvicellular parts of the paraventricular nucleus, and in the arcuate nucleus. Inputs to medial zone nuclei are more limited, with substantial projections to only the medial preoptic and dorsomedial nuclei. The AVPV sends few projections to the caudal brainstem, but terminals were observed reliably in the periaqueductal gray and medial part of the nucleus of the solitary tract. Anterograde double-labeling experiments demonstrate terminals derived from neurons in the AVPV in close apposition to GnRH-containing neurons in the preoptic region, and to dopaminergic neurons in the arcuate nucleus. Thus, the organization of projections from the AVPV in female rats suggests that neurons in this nucleus may influence the secretion of luteinizing hormone and prolactin through direct projections to GnRH neurons and tuberoinfundibular dopaminergic neurons.

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“…In regard to the activity of neurones within the MnPO, electrophysiological recordings from MnPO neurones in anaesthetized sheep and rats showed their firing rate to increase as a result of systemic doses of hypertonic saline or direct microinjection of angiotensin II into the subfornical organ (Tanaka et al . , , Tanaka & Nomura , McAllen et al . ).…”

Section: Fluid Homeostasismentioning

confidence: 99%

The median preoptic nucleus: front and centre for the regulation of body fluid, sodium, temperature, sleep and cardiovascular homeostasis

et al. 2015

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Located in the midline anterior wall of the third cerebral ventricle (i.e. the lamina terminalis), the median preoptic nucleus (MnPO) receives a unique set of afferent neural inputs from fore-, mid- and hindbrain. These afferent connections enable it to receive neural signals related to several important aspects of homeostasis. Included in these afferent projections are (i) neural inputs from two adjacent circumventricular organs, the subfornical organ and organum vasculosum laminae terminalis, that respond to hypertonicity, circulating angiotensin II or other humoural factors, (ii) signals from cutaneous warm and cold receptors that are relayed to MnPO, respectively, via different subnuclei in the lateral parabrachial nucleus and (iii) input from the medulla associated with baroreceptor and vagal afferents. These afferent signals reach appropriate neurones within the MnPO that enable relevant neural outputs, both excitatory and inhibitory, to be activated or inhibited. The efferent neural pathways that proceed from the MnPO terminate on (i) neuroendocrine cells in the hypothalamic supraoptic and paraventricular nuclei to regulate vasopressin release, while polysynaptic pathways from MnPO to cortical sites may drive thirst and water intake, (ii) thermoregulatory pathways to the dorsomedial hypothalamic nucleus and medullary raphé to regulate shivering, brown adipose tissue and skin vasoconstriction, (iii) parvocellular neurones in the hypothalamic paraventricular nucleus that drive autonomic pathways influencing cardiovascular function. As well, (iv) other efferent pathways from the MnPO to sites in the ventrolateral pre-optic nucleus, perifornical region of the lateral hypothalamic area and midbrain influence sleep mechanisms.

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Responses of median preoptic neurons projecting to the hypothalamic paraventricular nucleus to osmotic stimulation in Wistar-Kyoto and spontaneously hypertensive rats

Cited by 17 publications

References 19 publications

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

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

Projections of the sexually dimorphic anteroventral periventricular nucleus in the female rat

The median preoptic nucleus: front and centre for the regulation of body fluid, sodium, temperature, sleep and cardiovascular homeostasis

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