Activation of Hypothalamic Neurons by Intraovarian Pressure Signals in a Teleost Fish, Clams batrachus: Role of Mechanosensitive Channels

1996 ◽  
Vol 47 (4) ◽  
pp. 179-184 ◽  
Author(s):  
Nishikant Subhedar ◽  
Makrand K. Deshmukh ◽  
Mukul R. Jain ◽  
Firdos Alam Khan ◽  
N.S. Rama Krishna
Aquaculture ◽  
2008 ◽  
Vol 280 (1-4) ◽  
pp. 21-34 ◽  
Author(s):  
Douglas R. Tocher ◽  
Eldar Å. Bendiksen ◽  
Patrick J. Campbell ◽  
J. Gordon Bell
Keyword(s):  

2010 ◽  
Vol 298 (4) ◽  
pp. R870-R876 ◽  
Author(s):  
Christopher A. Cooper ◽  
Jonathan M. Whittamore ◽  
Rod W. Wilson

Marine teleost fish continuously ingest seawater to prevent dehydration and their intestines absorb fluid by mechanisms linked to three separate driving forces: 1) cotransport of NaCl from the gut fluid; 2) bicarbonate (HCO3−) secretion and Cl− absorption via Cl−/HCO3− exchange fueled by metabolic CO2; and 3) alkaline precipitation of Ca2+ as insoluble CaCO3, which aids H2O absorption). The latter two processes involve high rates of epithelial HCO3− secretion stimulated by intestinal Ca2+ and can drive a major portion of water absorption. At higher salinities and ambient Ca2+ concentrations the osmoregulatory role of intestinal HCO3− secretion is amplified, but this has repercussions for other physiological processes, in particular, respiratory gas transport (as it is fueled by metabolic CO2) and acid-base regulation (as intestinal cells must export H+ into the blood to balance apical HCO3− secretion). The flounder intestine was perfused in vivo with salines containing 10, 40, or 90 mM Ca2+. Increasing the luminal Ca2+ concentration caused a large elevation in intestinal HCO3− production and excretion. Additionally, blood pH decreased (−0.13 pH units) and plasma partial pressure of CO2 (Pco2) levels were elevated (+1.16 mmHg) at the highest Ca perfusate level after 3 days of perfusion. Increasing the perfusate [Ca2+] also produced proportional increases in net acid excretion via the gills. When the net intestinal flux of all ions across the intestine was calculated, there was a greater absorption of anions than cations. This missing cation flux was assumed to be protons, which vary with an almost 1:1 relationship with net acid excretion via the gill. This study illustrates the intimate link between intestinal HCO3− production and osmoregulation with acid-base balance and respiratory gas exchange and the specific controlling role of ingested Ca2+ independent of any other ion or overall osmolality in marine teleost fish.


Author(s):  
Christopher Paul Cutler ◽  
Anne-Sophie Martinez ◽  
Gordon Cramb
Keyword(s):  

Author(s):  
Changjun Guo ◽  
Jian He ◽  
Zhi-Min Li ◽  
Yuanyuan Wang ◽  
Chen nan nan ◽  
...  

Exosomes are associated with cancer progression, pregnancy, cardiovascular diseases, central nervous system–related diseases, immune responses and viral pathogenicity. However, study on the role of exosomes in the immune response of teleost fish, especially antiviral immunity, is limited. Herein, serum-derived exosomes from mandarin fish were used to investigate antiviral effect for the exosomes of teleost fish. Exosomes were isolated from mandarin fish serum by ultracentrifugation could internalize into Mandarin fish fry (MFF-1) cells and inhibited Infectious spleen and kidney necrosis virus (ISKNV) infection. To further investigated the underlying mechanisms of exosomes in inhibiting ISKNV infection. The protein composition of serum-derived exosomes was by analysis mass spectrometry and found that myxovirus resistance 1 (Mx1) was incorporated in the exosomes. Furthermore, the scMx1 protein was proved transferred to the recipient cells though the exosomes. Our results found that the serum-derived exosomes from mandarin fish could inhibit ISKNV replication and suggested an underlying mechanism of the serum-derived exosomes antivirus is that serum-derived exosomes incorporation of the Mx1 protein into exosomes and delivery into recipient cells. This study provided an evidence for the important antiviral role of exosomes in the immune system of teleost fish.


1994 ◽  
Vol 193 (1) ◽  
pp. 79-95 ◽  
Author(s):  
J Claiborne ◽  
J Walton ◽  
D Compton-Mccullough

A number of studies have implied a linkage between acid­base and ion exchanges in both freshwater and seawater fish, although little is known about the branchial and renal acid­base transfers involved as the animals move between different salinities. To investigate the role of these transfers in a marine teleost fish as it is exposed to a dilute environment, we measured plasma acid­base values and net movements from fish to water of NH4+, HCO3- and H+ in long-horned sculpin (Myoxocephalus octodecimspinosus) placed in 100 %, 20 %, 8 % or 4 % sea water for 24­48 h. Renal excretion of H+ was also monitored in fish exposed to 4 % sea water. Sculpin proved to be somewhat euryhaline for they were able to maintain plasma ion and acid­base transfers in hypo-osmotic (20 %) sea water, but could not tolerate greater dilutions for more than several days. Plasma pH and carbon dioxide concentration (CCO2) increased in the 20 % and 8 % dilution groups, with CCO2 nearly doubling (control, 4.56 mmol l-1; 8 % group, 8.56 mmol l-1) as a result of a combined increase in the partial pressure of plasma CO2 (PCO2) and [HCO3-]. During a 44­46 h exposure, HCO3- transfers increased progressively in the most dilute water, with animals in the 8 % and 4 % groups exhibiting a net H+ loss that was smaller than that of seawater fish (control, 5.1 mmol kg-1; 8 %, 0.9 mmol kg-1; 4 %, -2.9 mmol kg-1). Animals exposed to 4 % sea water for 24 h and then returned to normal sea water had a variable plasma pH, an elevated CCO2 and a net efflux of H+ that effectively stopped (control, 0.10 mmol kg-1 h-1; 4 %, 0.02 mmol kg-1 h-1; seawater recovery, 0.20 mmol kg-1 h-1) during the low-salinity period. Renal acid excretion remained relatively constant throughout the experiment but only made up a significant portion (approximately 40 %) of the total acid transfers during the 4 % dilution period (control rate approximately 3 µmol kg-1 h-1: 3 % of branchial rate). We postulate that the increase in plasma CCO2 during exposure to low salinity may be due to mobilization of base from the intracellular bone compartment. The decrease in external salinity could induce base loss by alteration of gill ion exchanges (Na+/H+, Cl-/HCO3-) and/or changes in branchial HCO3- permeability. For the first time, we have shown that the effects of a dilute environment on acid­base transfers may be an important limitation to the survival of a euryhaline species in brackish or fresh water.


2001 ◽  
Vol 281 (4) ◽  
pp. E649-E654 ◽  
Author(s):  
Charles V. Mobbs ◽  
Lee-Ming Kow ◽  
Xue-Jun Yang

Interest in brain glucose-sensing mechanisms is motivated by two distinct neuronal responses to changes in glucose concentrations. One mechanism is global and ubiquitous in response to profound hypoglycemia, whereas the other mechanism is largely confined to specific hypothalamic neurons that respond to changes in glucose concentrations in the physiological range. Although both mechanisms use intracellular metabolism as an indicator of extracellular glucose concentration, the two mechanisms differ in key respects. Global hyperpolarization (inhibition) in response to 0 mM glucose can be reversed by pyruvate, implying that the reduction in ATP levels acting through ATP-dependent potassium (K-ATP) channels is the key metabolic signal for the global silencing in response to 0 mM glucose. In contrast, neuroendocrine hypothalamic responses in glucoresponsive and glucose-sensitive neurons (either excitation or inhibition, respectively) to physiological changes in glucose concentration appear to depend on glucokinase; neuroendocrine responses also depend on K-ATP channels, although the role of ATP itself is less clear. Lactate can substitute for glucose to produce these neuroendocrine effects, but pyruvate cannot, implying that NADH (possibly leading to anaplerotic production of malonyl-CoA) is a key metabolic signal for effects of glucose on glucoresponsive and glucose-sensitive hypothalamic neurons.


2015 ◽  
Vol 223 ◽  
pp. 87-107 ◽  
Author(s):  
Frank Pfennig ◽  
Andrea Standke ◽  
Herwig O. Gutzeit

2021 ◽  
Vol 15 ◽  
Author(s):  
Chiara Berteotti ◽  
Viviana Lo Martire ◽  
Sara Alvente ◽  
Stefano Bastianini ◽  
Cristiano Bombardi ◽  
...  

The loss of hypothalamic neurons that produce wake-promoting orexin (hypocretin) neuropeptides is responsible for narcolepsy type 1 (NT1). While the number of histamine neurons is increased in patients with NT1, results on orexin-deficient mouse models of NT1 are inconsistent. On the other hand, the effect of histamine deficiency on orexin neuron number has never been tested on mammals, even though histamine has been reported to be essential for the development of a functional orexin system in zebrafish. The aim of this study was to test whether histamine neurons are increased in number in orexin-deficient mice and whether orexin neurons are decreased in number in histamine-deficient mice. The hypothalamic neurons expressing L-histidine decarboxylase (HDC), the histamine synthesis enzyme, and those expressing orexin A were counted in four orexin knock-out mice, four histamine-deficient HDC knock-out mice, and four wild-type C57BL/6J mice. The number of HDC-positive neurons was significantly higher in orexin knock-out than in wild-type mice (2,502 ± 77 vs. 1,800 ± 213, respectively, one-tailed t-test, P = 0.011). Conversely, the number of orexin neurons was not significantly lower in HDC knock-out than in wild-type mice (2,306 ± 56 vs. 2,320 ± 120, respectively, one-tailed t-test, P = 0.459). These data support the view that orexin peptide deficiency is sufficient to increase histamine neuron number, supporting the involvement of the histamine waking system in the pathophysiology of NT1. Conversely, these data do not support a significant role of histamine in orexin neuron development in mammals.


Sign in / Sign up

Export Citation Format

Share Document