Penetration of neurohypophyseal hormones from plasma into cerebrospinal fluid (CSF): Half-times of disappearance of these neuropeptides from CSF

Mens, Wim B.J.; Witter, A.; Greidanus, T.B. van Wimersma

doi:10.1016/0006-8993(83)90478-x

Cited by 329 publications

(229 citation statements)

References 22 publications

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“…(Rivier and Shen 1994)] are much higher than those that have a central inhibitory effect. Interestingly, very large peripheral doses of oxytocin (1 mg/kg, s.c.) have been reported to have a biphasic action on the HPA axis, acutely increasing corticosterone but subsequently causing suppression (Petersson et al, 1999), and this latter effect may be attributable to the low level of oxytocin that penetrates the ventricular system from the circulation (Mens et al, 1983). Strong support for a central site for oxytocin suppression of HPA activity also comes from the present observation of near-total suppression of the PVN response to stress, as measured by c-fos and CRF mRNA levels.…”

Section: Discussionsupporting

confidence: 53%

Oxytocin Attenuates Stress-Induced c-fosmRNA Expression in Specific Forebrain Regions Associated with Modulation of Hypothalamo–Pituitary–Adrenal Activity

Windle¹,

Kershaw²,

Shanks³

et al. 2004

J. Neurosci.

377

288

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We reported previously that the neuropeptide oxytocin attenuates stress-induced hypothalamo-pituitary-adrenal (HPA) activity and anxiety behavior. This study sought to identify forebrain target sites through which oxytocin may mediate its anti-stress effects. Ovariectomized, estradiol-treated rats received intracerebroventricular infusions of oxytocin (1 or 10 ng/hr) or vasopressin (10 ng/hr), and the patterns of neuronal activation after restraint stress were determined by semiquantitative mapping of c-fos mRNA expression. Oxytocin administration significantly attenuated the release of ACTH and corticosterone and the increase in corticotropin-releasing factor mRNA expression in the hypothalamic paraventricular nucleus (PVN) in response to 30 min restraint. Restraint also induced the expression of c-fos mRNA in selective regions of the forebrain, including the PVN, paraventricular thalamic nucleus, habenula, medial amygdala, ventrolateral septum (LSV), most subfields of the dorsal and ventral hippocampus, and piriform and endopiriform cortices. In most cases, this level of gene expression was unaffected by concomitant administration of oxytocin. However, in the PVN, LSV, and throughout all subfields of the dorsal hippocampus, restraint evoked no detectable increase in c-fos mRNA in animals treated with either dose of oxytocin. Vasopressin had no effects on either HPA axis responses or neuronal activation in response to restraint, indicating that the effects were highly peptide selective. These data show that central oxytocin attenuates both the stress-induced neuroendocrine and molecular responses of the HPA axis and that the dorsal hippocampus, LSV, and PVN constitute an oxytocin-sensitive forebrain stress circuit.

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Section: Discussionsupporting

confidence: 53%

Oxytocin Attenuates Stress-Induced c-fosmRNA Expression in Specific Forebrain Regions Associated with Modulation of Hypothalamo–Pituitary–Adrenal Activity

Windle¹,

Kershaw²,

Shanks³

et al. 2004

J. Neurosci.

377

288

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“…It can be argued that these gradual and prolonged responses might be related to the half-life of AVP in the brain, which is ϳ20 min (18). This considerable half-life suggests that AVP could interact with neighboring synapses to facilitate long- ) and salt-loaded animals (solid bars; n ϭ 6) after ganglionic blockade with HX.…”

Section: Discussionmentioning

confidence: 99%

Salt-induced sympathoexcitation involves vasopressin V_1a receptor activation in the paraventricular nucleus of the hypothalamus

Ribeiro

Panizza

Santos

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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-A high-salt diet can lead to hydromineral imbalance and increases in plasma sodium and osmolality. It is recognized as one of the major contributing factors for cardiovascular diseases such as hypertension. The paraventricular nucleus (PVN) plays a pivotal role in osmotically driven sympathoexcitation and high blood pressure, the precise mechanisms of which are not fully understood. Recent evidence indicates that AVP released from magnocellular neurons might be involved in this process. Using a combination of in vivo and in situ studies, we sought to investigate whether AVP, acting on PVN neurons, can change mean arterial pressure (MAP) and sympathetic nerve activity (SNA) in euhydrated male rats. Furthermore, we wanted to determine whether V 1a receptors on PVN neurons would be involved in saltinduced sympathoexcitation and hypertension. In rats, 4 days of salt loading (NaCl 2%) elicited a significant increase in plasma osmolality (39 Ϯ 7 mosmol/kgH 2O), an increase in MAP (26 Ϯ 2 mmHg, P Ͻ 0.001), and sympathoexcitation compared with euhydrated rats. Microinjection of AVP into the PVN of conscious euhydrated animals (100 nl, 3 M) elicited a pressor response (14 Ϯ 2 mmHg) and a significant increase in lumbar SNA (100 nl, 1 mM) (19 Ϯ 5%). Pretreatment with a V 1a receptor antagonist, microinjected bilaterally into the PVN of salt-loaded animals, elicited a decrease in lumbar SNA (Ϫ14 Ϯ 5%) and MAP (Ϫ19 Ϯ 5 mmHg), when compared with the euhydrated group. Our findings show that AVP plays an important role in modulating the salt-induced sympathoexcitation and high blood pressure, via V 1a receptors, within the PVN of male rats. As such, V 1a receptors in the PVN might contribute to neurogenic hypertension in individuals consuming a high-salt diet.vasopressin; paraventricular nucleus of the hypothalamus; salt loading; sympathoexcitation; hypertension A HIGH DIETARY INTAKE OF SALT is one of the major contributing factors to cardiovascular diseases, such as hypertension (11,12,32). High-salt diets can lead to a hydromineral imbalance and increases the plasma sodium concentrations and osmolality. This, in turn, can activate central hypothalamic nuclei that elevate sympathetic outflow and arterial blood pressure (BP), leading to a disorder referred to as salt-sensitive neurogenic hypertension (33).Osmotic perturbations are primarily sensed by osmosensing neurons located in brain regions that lack a blood-brain barrier termed circumventricular organs (CVOs). Under systemic hyperosmotic conditions, the CVOs are activated and send excitatory inputs to the paraventricular nucleus of the hypothalamus (PVN), an important integrative center involved in the autonomic and neuroendocrine functions to maintain body fluids and cardiovascular homeostasis (14,19,28). The PVN lies adjacent to the third ventricle in the anterior hypothalamus, and it is composed of magnocellular neurons (MCNs) and parvocellular neurons (PCN). The PCN send projections to autonomic nuclei, such as the rostral ventrolateral medulla (RVLM) and intermediola...

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“…It cannot be ex and OT in the plasma, whereas the concentrations in the CSF remained unchanged (Landgraf and Gunther, 1983). In contrast, following peripheral application of high pharmacological doses, exoge nous VP and OT were found to cross the blood CSF barrier in amounts that, though minute, were sufficient to trigger central effects (Mens et a!., 1983).…”

Section: Minal [3h]tyrosyl Residue Of the Enkephalin Mole Cule Was CLmentioning

confidence: 98%

Blood—Brain Barrier and Peptides

Ermisch

Rühle

Landgraf

et al. 1985

J Cereb Blood Flow Metab

181

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Summary: The brain is both the source and the recipient of peptide signals, The question is: Do endogenous, blood-borne peptide molecules influence brain function?Brain regions with the tight capillaries of the blood-brain barrier (BBB) extract low but measurable amounts of la beled peptide molecules from an intracarotid bolus injec tion, In the rat, the extraction fractions of f3-casomor phin-5, DesGlyNH2-arginine-vasopressin, arginine-vaso pressin, lysine-vasopressin, oxytocin, gonadoliberin, substance P, and f3-endorphin, studied in this laboratory, range from 0.5% (substance P) to 2.4% (arginine-vaso pressin). Extraction varies little among the 15 examined brain regions. As shown for arginine-vasopressin, the ex tracted peptides may be bound in part to specific binding sites located on the luminal membrane of the tight en dothelial cells. Tr ansport of peptide molecules across the BBB cannot be ruled out, but it is unlikely that endoge nous peptides pass the BBB in physiologically significant amounts. In contrast, in brain regions with leaky capil- BRAIN AND PEPTIDESNeurons process information. The process in cludes the release of chemical signals such as ace tylcholine, catecholamines, indolamines, amino acids, and peptides [for review, see Ganong (1982)]. There is evidence that numerous neuronal cell pop ulations produce and release peptides [for review, see Swaab (1982)J. Certain peptides including va sopressin (VP) and oxytocin (OT) trigger events in the brain itself as well as in the periphery of the body (Sterba et aI., 1981). Thus, the neuropeptides may serve in at least two lines of communication (Ermisch, 1980). First, they may trigger events within the brain when released into the synaptic cleft, or second, they may trigger events within the 350laries, e.g., selected circumventricular organs including the pineal gland, neurohypophysis, and choroid plexus, the peptide fraction extracted approaches that of water.Within the circumventricular organs, the peptide mole cules actually reach the cellular elements of the tissue.However, no studies definitively show that pep tides reach neurons in the deeper layers of the brain. On the other hand, blood-borne peptides influence the BBB per meability by altering the transport of essential sub stances. The effect may be mediated by specific peptide binding sites located at the luminal membrane of the en dothelium. It is possible that the effect of peptides on the BBB is necessary for proper brain function. There is some evidence that peptides, released centrally into the synaptic clefts as well as peripherally into the blood stream, support complex brain performances by both of these pathways.

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Penetration of neurohypophyseal hormones from plasma into cerebrospinal fluid (CSF): Half-times of disappearance of these neuropeptides from CSF

Cited by 329 publications

References 22 publications

Oxytocin Attenuates Stress-Induced c-fosmRNA Expression in Specific Forebrain Regions Associated with Modulation of Hypothalamo–Pituitary–Adrenal Activity

Oxytocin Attenuates Stress-Induced c-fosmRNA Expression in Specific Forebrain Regions Associated with Modulation of Hypothalamo–Pituitary–Adrenal Activity

Salt-induced sympathoexcitation involves vasopressin V_1a receptor activation in the paraventricular nucleus of the hypothalamus

Blood—Brain Barrier and Peptides

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Penetration of neurohypophyseal hormones from plasma into cerebrospinal fluid (CSF): Half-times of disappearance of these neuropeptides from CSF

Cited by 329 publications

References 22 publications

Oxytocin Attenuates Stress-Induced c-fosmRNA Expression in Specific Forebrain Regions Associated with Modulation of Hypothalamo–Pituitary–Adrenal Activity

Oxytocin Attenuates Stress-Induced c-fosmRNA Expression in Specific Forebrain Regions Associated with Modulation of Hypothalamo–Pituitary–Adrenal Activity

Salt-induced sympathoexcitation involves vasopressin V1a receptor activation in the paraventricular nucleus of the hypothalamus

Blood—Brain Barrier and Peptides

Contact Info

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Salt-induced sympathoexcitation involves vasopressin V_1a receptor activation in the paraventricular nucleus of the hypothalamus