Cerebrospinal fluid vasopressin in neurological and psychiatric disorders.

Sørensen, Per Soelberg; Gjerris, Annette; Hammer, Muriel

doi:10.1136/jnnp.48.1.50

Cited by 105 publications

(43 citation statements)

References 39 publications

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“…In addition, this obser vation corroborates the finding of similar plasma levels of AVP in MS patients and controls [24]. Two types of CRH neurons can be distinguished: (1) neurons that release their peptides into the capillary loops of the pituitary portal system [25] and (2) neurons that transport their peptides to other parts of the brain where they act as neurotransmitters or neuromodulators [26].…”

Section: Discussionsupporting

confidence: 66%

Increased Number of Corticotropin-Releasing Hormone Expressing Neurons in the Hypothalamic Paraventricular Nucleus of Patients with Multiple Sclerosis

et al. 1995

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Observations in experimental allergic encephalomyelitis (EAE), a model for multiple sclerosis (MS), have indicated that a low activity of the hypothalamo-pituitary-adrenal (HPA) system is accompanied by a high susceptibility for EAE in rat strains and that elevated corticosteroid levels are necessary for spontaneous recovery from EAE. The HPA axis activity is regulated by both corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). Both types of neurons are localized in the paraventricular nucleus (PVN) of the hypothalamus. We determined the number of immunocytochemically identified CRH-immunoreactive (CRH-IR) and AVP-immunoreactive (AVP-IR) neurons in the PVN of the human hypothalamus of 8 MS patients, aged 34–63 years, and 8 age-matched control subjects without any primary neurological or psychiatric disorders, aged 30–59 years. In addition, the number of oxytocin (OXT) immunoreactive (OXT-IR) neurons was determined, since these neurons innervate brain stem nuclei and might thus be related to autonomic disturbances in MS. In MS the staining intensity for AVP was clearly lower and for OXT slightly lower. For CRH, the staining intensity was similar in both groups, and, moreover, in MS patients the number of CRH-IR cells in the PVN was found to be about 2.4 times higher than that in the control group. The number of OXT-IR or AVP-IR cells in the PVN of MS patients was not significantly different from that of the control group. Our results point to an activation of the neuroendocrine HPA axis which may be compatible with the idea that the HPA axis is involved in recovery from MS. In addition, increased CRH activity might be causally related to depression which has high prevalence rates in MS patients.

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Section: Discussionsupporting

confidence: 66%

Increased Number of Corticotropin-Releasing Hormone Expressing Neurons in the Hypothalamic Paraventricular Nucleus of Patients with Multiple Sclerosis

et al. 1995

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“…In depressed patients, the CSF AVP concentration has been reported to be low during the depressed state 37,38 and elevated during the manic state. 39 While this suggests a role for central vasopressin in mood regulation, studies of nondepressed subjects 40,41 do not confirm this. In this study, no relationship was noted between the CSF AVP concentration and history of mood disorder or between the CSF AVP concentration and the severity of current depressive symptoms, if present.…”

Section: Discussionmentioning

confidence: 88%

Cerebrospinal Fluid Vasopressin Levels

Coccaro¹,

Kavoussi²,

Hauger³

et al. 1998

Arch Gen Psychiatry

367

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“…There is good evidence, however, that hypoxia and the peptides vasopressin and endothelin, all factors present during ischemia, stimulate activity of the BBB cotransporter. We have found that vasopressin, which is centrally released during ischemia (Dóczi 1993;Landgraf 1992;Ostrowski et al, 1992;Sorensen et al, 1985) and promotes edema formation (Dickinson and Betz, 1992;Dóczi, 1993;Dóczi et al, 1982Dóczi et al, , 1984Hertz et al, 2000;Rosenberg et al, 1990), is also a potent stimulator of the brain microvascular Na-K-Cl cotransporter (O'Donnell et al, 1995a), as is endothelin, which is also released during ischemia (Barone et al, 1994;Kawai et al, 1996bKawai et al, , 1997Spatz et al, 1997). We have shown that vasopressin stimulates the brain endothelial cotransporter by a V1 vasopressin receptor in a manner involving elevation of intracellular [Ca 2+ ] (O'Donnell et al, 1999).…”

Section: Discussionmentioning

confidence: 95%

Bumetanide Inhibition of the Blood-Brain Barrier Na-K-Cl Cotransporter Reduces Edema Formation in the Rat Middle Cerebral Artery Occlusion Model of Stroke

O’Donnell

Tran

Lam

et al. 2004

J Cereb Blood Flow Metab

222

258

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Summary:Increased transport of Na + across an intact bloodbrain barrier (BBB) participates in edema formation during the early hours of cerebral ischemia. In previous studies, the authors showed that the BBB Na-K-Cl cotransporter is stimulated by factors present during ischemia, suggesting that the cotransporter may contribute to the increased brain Na + uptake in edema. The present study was conducted to determine (1) whether the Na-K-Cl cotransporter is located in the luminal membrane of the BBB, and (2) whether inhibition of the BBB cotransporter reduces brain edema formation. Perfusion-fixed rat brains were examined for cotransporter distribution by immunoelectron microscopy. Cerebral edema was evaluated in rats subjected to permanent middle cerebral artery occlusion (MCAO) by magnetic resonance diffusion-weighted imaging and calculation of apparent diffusion coefficients (ADC). The immunoelectron microscopy studies revealed a predominant (80%) luminal membrane distribution of the cotransporter. Magnetic resonance imaging studies showed ADC ratios (ipsilateral MCAO/contralateral control) ranging from 0.577 to 0.637 in cortex and striatum, indicating substantial edema formation. Intravenous bumetanide (7.6-30.4 mg/kg) given immediately before occlusion attenuated the decrease in ADC ratios for both cortex and striatum (by 40-67%), indicating reduced edema formation. Bumetanide also reduced infarct size, determined by TTC staining. These findings suggest that a luminal BBB Na-K-Cl cotransporter contributes to edema formation during cerebral ischemia. Key Words: Cotransport-Blood-brain barrier-Stroke, Cerebral ischemiaCerebral edema-Bumetanide.Brain edema that forms during the early hours of ischemic stroke involves a net uptake of Na + and water from blood into brain across an intact blood-brain barrier

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Cerebrospinal fluid vasopressin in neurological and psychiatric disorders.

Cited by 105 publications

References 39 publications

Increased Number of Corticotropin-Releasing Hormone Expressing Neurons in the Hypothalamic Paraventricular Nucleus of Patients with Multiple Sclerosis

Increased Number of Corticotropin-Releasing Hormone Expressing Neurons in the Hypothalamic Paraventricular Nucleus of Patients with Multiple Sclerosis

Cerebrospinal Fluid Vasopressin Levels

Bumetanide Inhibition of the Blood-Brain Barrier Na-K-Cl Cotransporter Reduces Edema Formation in the Rat Middle Cerebral Artery Occlusion Model of Stroke

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