Endothelin acts at the subfornical organ to influence the activity of putative vasopressin and oxytocin-secreting neurons

Wall, Katharine M.; Ferguson, Alastair V.

doi:10.1016/0006-8993(92)91378-r

Cited by 45 publications

(27 citation statements)

References 16 publications

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“…Although the present experiment does not identify the locus of the presynaptic excitatory neurons, most likely targets are the local glutamatergic interneurons around the SON (Boudaba et al, 1997). An excitatory action would be consistent with observations of excitatory actions of endothelin in the anteroventral third ventricular region (Yamamoto et al, 1993) and in the subfornical organ (Wall and Ferguson, 1992). The different responses of OT and VP neurons to ET-1 thus appear to be due to the fact that they activate different receptors (ET A vs ET B ) and the fact that these receptors are on different cells.…”

Section: Discussionsupporting

confidence: 86%

“…Studies examining the link between endothelin and neuroendocrine output have revealed that ET-1 induces VP secretion both in vitro (Shichiri et al, 1989;Ritz et al, 1992;Chen, 2002, 2006;Rossi, 2004) and in vivo (Rossi et al, 1997a(Rossi et al, ,b, 2008, while intracerebroventricular administration of endothelin stimulates the release of OT (Samson et al, 1991). Furthermore, ET-1 activates both OT and VP MNCs through an action at the subfornical organ (Wall and Ferguson, 1992).…”

Section: Introductionmentioning

confidence: 98%

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Opposing Actions of Endothelin-1 on Glutamatergic Transmission onto Vasopressin and Oxytocin Neurons in the Supraoptic Nucleus

Zampronio¹,

Kuzmiski²,

Florence³

et al. 2010

J. Neurosci.

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Endothelin (ET-1) given centrally has many reported actions on hormonal and autonomic outputs from the CNS. However, it is unclear whether these effects are due to local ischemia via its vasoconstrictor properties or to a direct neuromodulatory action. ET-1 stimulates the release of oxytocin (OT) and vasopressin (VP) from supraoptic magnocellular (MNCs) neurons in vivo; therefore, we asked whether ET-1 modulates the excitatory inputs onto MNCs that are critical in sculpting the activity of these neurons. To investigate whether ET-1 modulates excitatory synaptic transmission, we obtained whole-cell recordings and analyzed quantal glutamate release onto MNCs in the supraoptic nucleus (SON). Neurons identified as VP-containing neurosecretory cells displayed a decrease in quantal frequency in response to ET-1 (10 -100 pM). This decrease was mediated by ET A receptor activation and production of a retrograde messenger that targets presynaptic cannabinoid-1 receptors. In contrast, neurons identified as OT-containing MNCs displayed a transient increase in quantal glutamate release in response to ET-1 application via ET B receptor activation. Application of TTX to block action potentialdependent glutamate release inhibited the excitatory action of ET-1 in OT neurons. There were no changes in quantal amplitude in either MNC type, suggesting that the effects of ET-1 were via presynaptic mechanisms. A gliotransmitter does not appear to be involved as ET-1 failed to elevate astrocytic calcium in the SON. Our results demonstrate that ET-1 differentially modulates glutamate release onto VPversus OT-containing MNCs, thus implicating it in the selective regulation of neuroendocrine output from the SON.

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Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 98%

Opposing Actions of Endothelin-1 on Glutamatergic Transmission onto Vasopressin and Oxytocin Neurons in the Supraoptic Nucleus

Zampronio¹,

Kuzmiski²,

Florence³

et al. 2010

J. Neurosci.

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show abstract

“…ET-1 may stimulate the release of VP by acting indirectly via stimulation of the catecholaminergic or renin-angiotensinergic system, as was suggested by Yamamoto et al [21], or via activation of neurons of the subfornical organ [23]. It is noteworthy that ET can interact with VP also at the level of the kidney: both peptides increase [Na]+i in the glomerular mesangial cells in the rat [24], whereas ET-1 inhibits VP-dependent cyclic adenosine monophosphate accumulation [25] and VP-stimulated osmotic water permeability [26] in rat collecting ducts.…”

Section: Discussionmentioning

confidence: 90%

Immunoreactive Endothelin-1 in the Neural Lobe of the Rat Pituitary following Hemorrhage and Dehydration.

Uemura

Naruse²,

Nakamura

et al. 1994

Endocr J

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Abstract. Previously we found intragranular colocalization of immunoreactive endothelin-1 and neurohypophysial hormones in the axon terminals of the rat neural lobe. To investigate the function of endothelin-1 in the rat neural lobe, immunoreactive endothelin-1 in plasma and the neural lobe was measured by enzyme immunoassay in rats subjected to hemorrhage and in other rats who were deprived of water for 2 days to induce dehydration. Changes in plasma arginine vasopressin were determined by radioimmunoassay.In addition, morphometric analysis was performed in the neural lobe of rats exposed to these stresses. Plasma concentrations of immunoreactive endothelin-1 were unchanged following hemorrhage or dehydration, whereas those of immunoreactive vasopressin were remarkably increased. In the neural lobe, immunoreactive endothelin-1 content and the number of neurosecretory granules decreased significantly after dehydration.However, immunoreactive endothelin-1 in tissue increased nearly three-fold in hemorrhaged rats, whereas the endothelin-1-immunolabeling in the axon terminals was unchanged. These results suggest that endothelin-1 in the hypothalamo-hypophysial system may be involved in the local modulation of vasopressin secretion when an animal is exposed to hypovolemic and/or osmotic stress.

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“…Moreover, the origin of endogenous ET binding at these regions cannot be distinguished as to whether it is a peripherally circulating or central nervous one. Wall and Ferguson [21] reported that intravenously administered (i.e. peripherally circulating) ET acted on subfornical organ to influence the vasopressin and oxytocin neurons, but not on their neurons directly.…”

Section: And Cholecystokininmentioning

confidence: 99%

Endothelin-Induced c-fos Expression in the Rat Forebrain.

Kurokawa

Yamada

Ochi

1997

Acta Histochem. Cytochem

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Endothelin acts at the subfornical organ to influence the activity of putative vasopressin and oxytocin-secreting neurons

Cited by 45 publications

References 16 publications

Opposing Actions of Endothelin-1 on Glutamatergic Transmission onto Vasopressin and Oxytocin Neurons in the Supraoptic Nucleus

Opposing Actions of Endothelin-1 on Glutamatergic Transmission onto Vasopressin and Oxytocin Neurons in the Supraoptic Nucleus

Immunoreactive Endothelin-1 in the Neural Lobe of the Rat Pituitary following Hemorrhage and Dehydration.

Endothelin-Induced c-fos Expression in the Rat Forebrain.

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