Rhythmic aftereffects in the osmotic stimulation-induced spike activity of thermosensitive neurons of the preoptic region

AbstractThe aim of this study was to correlate three commercially available copeptin assays and their diagnostic accuracy in the differential diagnosis of the polyuria-polydipsia syndrome. Analyzed data include repeated copeptin measures of 8 healthy volunteers and 40 patients with polyuria-polydipsia syndrome undergoing osmotic stimulation and of 40 patients hospitalized with pneumonia. Copeptin was measured using the automated Brahms KRYPTOR, the manual Brahms LIA and the manual Cloud Clone ELISA assay. Primary outcome was the interrater correlation coefficient (ICC) and diagnostic accuracy in the polyuria-polydipsia syndrome of the three assays. In healthy volunteers, there was a moderate correlation for the KRYPTOR and LIA (ICC 0.74; 95% CI 0.07 to 0.91), and a poor correlation for the KRYPTOR and ELISA (ICC 0.07; 95% CI − 0.06 to 0.29), as for the LIA and ELISA (ICC 0.04; 95% CI − 0.04 to 0.17). The KRYPTOR had the highest diagnostic accuracy (98% (95% CI 83 to100)), comparable to the LIA (88% (95% CI 74 to 100)), while the ELISA had a poor diagnostic accuracy (55% (95% CI 34 to 68)) in the differential diagnosis of the polyuria-polydipsia syndrome. The KRYPTOR and LIA yield comparable copeptin concentrations and high diagnostic accuracy, while the ELISA correlates poorly with the other two assays and shows a poor diagnostic accuracy for polyuria-polydipsia patients. The current copeptin cut-off is valid for the KRYPTOR and LIA assay. Our results indicate that interpretation with other assays should be performed with caution and separate validation studies are required before their use in differentiating patients with polyuria-polydipsia syndrome.Trial registration: NCT02647736 January 6, 2016/NCT01940614 September 12, 2013/NCT00973154 September 9, 2009.

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Lipopolysaccharide Endotoxin Potentiates the Effect of Osmotic Stimulation on Vasopressin Synthesis and Secretion in the Rat Hypothalamus

Journal of Neuroendocrinology ◽

10.1046/j.1365-2826.2003.00967.x ◽

2003 ◽

Vol 15 (2) ◽

pp. 141-149 ◽

Cited By ~ 18

Author(s):

V. Grinevich ◽

X.-M. Ma ◽

G Jirikowski ◽

J. Verbalis ◽

G. Aguilera

Keyword(s):

Rat Hypothalamus ◽

Lipopolysaccharide Endotoxin ◽

Osmotic Stimulation ◽

Vasopressin Synthesis

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Mitral and Tufted Cells Differ in the Decoding Manner of Odor Maps in the Rat Olfactory Bulb

Journal of Neurophysiology ◽

10.1152/jn.01266.2003 ◽

2004 ◽

Vol 91 (6) ◽

pp. 2532-2540 ◽

Cited By ~ 122

Author(s):

Shin Nagayama ◽

Yuji K. Takahashi ◽

Yoshihiro Yoshihara ◽

Kensaku Mori

Keyword(s):

Olfactory Bulb ◽

Spike Activity ◽

Homologous Series ◽

Morphological Difference ◽

Aliphatic Acid ◽

Mitral Cells ◽

Firing Rates ◽

Aliphatic Acids ◽

Projection Pattern ◽

Tufted Cells

Mitral and tufted cells in the mammalian olfactory bulb are principal neurons, each type having distinct projection pattern of their dendrites and axons. The morphological difference suggests that mitral and tufted cells are functionally distinct and may process different aspects of olfactory information. To examine this possibility, we recorded odorant-evoked spike responses from mitral and middle tufted cells in the aliphatic acid- and aldehyde-responsive cluster at the dorsomedial part of the rat olfactory bulb. Homologous series of aliphatic acids and aldehydes were used for odorant stimulation. In response to adequate odorants, mitral cells showed spike responses with relatively low firing rates, whereas middle tufted cells responded with higher firing rates. Examination of the molecular receptive range (MRR) indicated that most mitral cells exhibited a robust inhibitory MRR, whereas a majority of middle tufted cells showed no or only a weak inhibitory MRR. In addition, structurally different odorants that activated neighboring clusters inhibited the spike activity of mitral cells, whereas they caused no or only a weak inhibition in the middle tufted cells. Furthermore, responses of mitral cells to an adequate excitatory odorant were greatly inhibited by mixing the odorant with other odorants that activated neighboring glomeruli. In contrast, odorants that activated neighboring glomeruli did not significantly inhibit the responses of middle tufted cells to the adequate excitatory odorant. These results indicate a clear difference between mitral and middle tufted cells in the manner of decoding the glomerular odor maps.

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