Independent effects of seawater pH and high PCO2 on olfactory sensitivity in fish: possible role of carbonic anhydrase

Ocean acidification may alter olfactory-driven behaviour in fish by direct effects on the peripheral olfactory system; olfactory sensitivity is reduced in CO2-acidified seawater. The current study tested whether this is due to elevated PCO2 or the consequent reduction in seawater pH and, if the former, investigate the possible involvement of carbonic anhydrase, the enzyme responsible for the hydration of CO2 and production of carbonic acid. Olfactory sensitivity to amino acids was assessed by extracellular multi-unit recording from the olfactory nerve of the gilthead seabream (Sparus auratus L,) in normal seawater (pH ∼8.2), and after acute exposure to acidified seawater (pH ∼7.7, but normal PCO2; ∼340 µatm) and high PCO2 seawater (∼1400 µatm) at normal pH (∼8.2). Reduced pH in the absence of elevated PCO2 caused reduction in olfactory sensitivity to L-serine, L-leucine, L-arginine and L-glutamine, but not L-glutamic acid. Increased PCO2 in the absence of changes in pH caused reduced olfactory sensitivity to L-serine, L-leucine and L-arginine, including increases in their thresholds of detection, but had no effect on sensitivity to L-glutamine and L-glutamic acid. Inclusion of 1 mM acetazolamide (a membrane-permeant inhibitor of carbonic anhydrase) in the seawater reversed the inhibition of olfactory sensitivity to L-serine caused by high PCO2. Ocean acidification may reduce olfactory sensitivity by reduction in seawater pH and intracellular pH (of olfactory receptor neurones); the former by reducing odorant-receptor affinity, and the latter by reducing the efficiency of olfactory transduction. The physiological role of carbonic anhydrase in the olfactory receptor neurones remains to be explored.

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Simulated CO2-induced ocean acidification for ocean in the East China: historical conditions since preindustrial time and future scenarios

Scientific Reports ◽

10.1038/s41598-019-54861-0 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 1

Author(s):

Han Zhang ◽

Kuo Wang

Keyword(s):

Ocean Acidification ◽

Inorganic Carbon ◽

Dissolved Inorganic Carbon ◽

Reduction Rate ◽

System Model ◽

East China ◽

Seawater Ph ◽

The Individual ◽

Induced Changes

AbstractSince preindustrial times, as atmospheric CO2 concentration increases, the ocean continuously absorbs anthropogenic CO2, reducing seawater pH and $$[{{\rm{C}}{\rm{O}}}_{3}^{2-}]$$[CO32−], which is termed ocean acidification. We perform Earth system model simulations to assess CO2-induced acidification for ocean in the East China, one of the most vulnerable areas to ocean acidification. By year 2017, ocean surface pH in the East China drops from the preindustrial level of 8.20 to 8.06, corresponding to a 35% rise in [H+], and reduction rate of pH becomes faster in the last two decades. Changes in surface seawater acidity largely result from CO2-induced changes in surface dissolved inorganic carbon (DIC), alkalinity (ALK), salinity and temperature, among which DIC plays the most important role. By year 2300, simulated reduction in sea surface $$[{{\rm{C}}{\rm{O}}}_{3}^{2-}]$$[CO32−] is 13% under RCP2.6, contrasted to 72% under RCP8.5. Furthermore, simulated results show that CO2-induced warming acts to mitigate reductions in $$[{{\rm{C}}{\rm{O}}}_{3}^{2-}]$$[CO32−], but the individual effect of oceanic CO2 uptake is much greater than the effect of CO2-induced warming on ocean acidification. Our study quantifies ocean acidification induced by anthropogenic CO2, and indicates the potentially important role of accelerated CO2 emissions in projections of future changes in biogeochemistry and ecosystem of ocean in the East China.

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Short- and Medium-Term Exposure to Ocean Acidification Reduces Olfactory Sensitivity in Gilthead Seabream

Frontiers in Physiology ◽

10.3389/fphys.2019.00731 ◽

2019 ◽

Vol 10 ◽

Cited By ~ 3

Author(s):

Zélia Velez ◽

Christina C. Roggatz ◽

David M. Benoit ◽

Jörg D. Hardege ◽

Peter C. Hubbard

Keyword(s):

Ocean Acidification ◽

Gilthead Seabream ◽

Olfactory Sensitivity ◽

Medium Term

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Resilience to ocean acidification: decreased carbonic anhydrase activity in sea anemones under high pCO2 conditions

Marine Ecology Progress Series ◽

10.3354/meps11916 ◽

2016 ◽

Vol 559 ◽

pp. 257-263 ◽

Cited By ~ 15

Author(s):

P Ventura ◽

MD Jarrold ◽

PL Merle ◽

S Barnay-Verdier ◽

T Zamoum ◽

...

Keyword(s):

Carbonic Anhydrase ◽

Ocean Acidification ◽

Carbonic Anhydrase Activity ◽

High Pco2 ◽

Sea Anemones

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Dynamics of carotid body responses in vitro in the presence of CO2-HCO3-: role of carbonic anhydrase

Journal of Applied Physiology ◽

10.1152/jappl.1993.75.4.1587 ◽

1993 ◽

Vol 75 (4) ◽

pp. 1587-1594 ◽

Cited By ~ 34

Author(s):

R. Iturriaga ◽

A. Mokashi ◽

S. Lahiri

Keyword(s):

Carbonic Anhydrase ◽

Carotid Body ◽

High Pco2 ◽

Relative Contribution ◽

Baseline Activity ◽

Perfusate Flow ◽

Steady State Responses ◽

Co2 Flow

The role of carbonic anhydrase (CNA) in the dynamics of carotid body (CB) function was tested by studying the effects of the membrane-permeable CNA inhibitor methazolamide on the chemosensory responses of the cat CB, perfused and superfused in vitro with cell-free and modified Tyrode solution at 36.5 +/- 0.5 degrees C in the presence of CO2-HCO3- (PO2 = 120 Torr, PCO2 = 32 Torr, pH = 7.40). The bulk of CO2 flow to the CB from the external milieu was overwhelmingly large relative to the metabolic production of CO2 in the CB. Accordingly, the relative contribution of the endogenous CO2 to the CB responses was small. The chemosensory nerve discharges were recorded from the whole desheathed carotid sinus nerve. The responses to acidic hypercapnia (PCO2 = 50–60 Torr, pH = 7.20–7.10), hypoxia (PO2 = 25 and 50 Torr), perfusate flow interruption, and bolus injections of sodium cyanide (20–40 nmol) were tested. To contrast, we also measured the effects of nicotine (2–4 nmol), which may act at sites other than those for O2 and CO2. Methazolamide (30 mg/l) in the perfusate at constant PCO2 and pH reduced the baseline activity and delayed the responses to step changes in PCO2 (and concomitantly pH) and PO2 and to cyanide but not to nicotine. The steady-state responses to these stimuli, measured as differences from control, were reduced, but not significantly. The initial overshoots seen with step changes in both high PCO2 and low PO2 were eliminated.(ABSTRACT TRUNCATED AT 250 WORDS)

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Coral resistance to ocean acidification linked to increased calcium at the site of calcification

Proceedings of The Royal Society B Biological Sciences ◽

10.1098/rspb.2018.0564 ◽

2018 ◽

Vol 285 (1878) ◽

pp. 20180564 ◽

Cited By ~ 43

Author(s):

T. M. DeCarlo ◽

S. Comeau ◽

C. E. Cornwall ◽

M. T. McCulloch

Keyword(s):

Raman Spectroscopy ◽

Calcium Carbonate ◽

Coral Reefs ◽

Ocean Acidification ◽

Pocillopora Damicornis ◽

Seawater Ph ◽

Ph Conditions

Ocean acidification threatens the persistence of biogenic calcium carbonate (CaCO 3 ) production on coral reefs. However, some coral genera show resistance to declines in seawater pH, potentially achieved by modulating the chemistry of the fluid where calcification occurs. We use two novel geochemical techniques based on boron systematics and Raman spectroscopy, which together provide the first constraints on the sensitivity of coral calcifying fluid calcium concentrations ( ) to changing seawater pH. In response to simulated end-of-century pH conditions, Pocillopora damicornis increased to as much as 25% above that of seawater and maintained constant calcification rates. Conversely, Acropora youngei displayed less control over , and its calcification rates strongly declined at lower seawater pH. Although the role of in driving calcification has often been neglected, increasing may be a key mechanism enabling more resistant corals to cope with ocean acidification and continue to build CaCO 3 skeletons in a high-CO 2 world.

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Silicon Substitution for Calcium in the Shell of the Fingernail Clam, Musculium Transversum Studied By X-Ray Analysis

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s1431927600002488 ◽

1980 ◽

Vol 38 ◽

pp. 560-561

Author(s):

Judith A. Murphy ◽

Anthony Paparo ◽

Richard Sparks

Keyword(s):

Carbonic Anhydrase ◽

River Water ◽

Food Chains ◽

Well Water ◽

Shell Formation ◽

X Ray ◽

Molluscan Shell ◽

Fingernail Clams

Fingernail clams (Muscu1ium transversum) are dominant bottom-dwelling animals in some waters of the midwest U.S. These organisms are key links in food chains leading from nutrients in water and mud to fish and ducks which are utilized by man. In the mid-1950’s, fingernail clams disappeared from a 100-mile section of the Illinois R., a tributary of the Mississippi R. Some factor(s) in the river and/or sediment currently prevent clams from recolonizing areas where they were formerly abundant. Recently, clams developed shell deformities and died without reproducing. The greatest mortality and highest incidence of shell deformities appeared in test chambers containing the highest proportion of river water to well water. The molluscan shell consists of CaCO3, and the tissue concerned in its secretion is the mantle. The source of the carbonate is probably from metabolic CO2 and the maintenance of ionized Ca concentration in the mantle is controlled by carbonic anhydrase. The Ca is stored in extracellular concentric spherical granules(0.6-5.5μm) which represent a large amount of inertCa in the mantle. The purpose of this investigation was to examine the role of raw river water and well water on shell formation in the fingernail clam.

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The role of the glutamic acid receptors in the micturition center in pons of the rat.

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)36693-4 ◽

1996 ◽

Vol 71 ◽

pp. 113

Author(s):

Takahiro Nakai ◽

Hitoshi Kontani

Keyword(s):

Glutamic Acid

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CHOP-Dependent Stress-Inducible Expression of a Novel Form of Carbonic Anhydrase VI

Molecular and Cellular Biology ◽

10.1128/mcb.19.1.495 ◽

1999 ◽

Vol 19 (1) ◽

pp. 495-504 ◽

Cited By ~ 102

Author(s):

John Sok ◽

Xiao-Zhong Wang ◽

Nikoleta Batchvarova ◽

Masahiko Kuroda ◽

Heather Harding ◽

...

Keyword(s):

Carbonic Anhydrase ◽

Target Gene ◽

Target Genes ◽

Direct Evidence ◽

Nuclear Protein ◽

Intracellular Form ◽

Carbonic Anhydrase Vi ◽

Responsive Element

ABSTRACT CHOP (also called GADD153) is a stress-inducible nuclear protein that dimerizes with members of the C/EBP family of transcription factors and was initially identified as an inhibitor of C/EBP binding to classic C/EBP target genes. Subsequent experiments suggested a role for CHOP-C/EBP heterodimers in positively regulating gene expression; however, direct evidence that this is the case has so far not been uncovered. Here we describe the identification of a positively regulated direct CHOP-C/EBP target gene, that encoding murine carbonic anhydrase VI (CA-VI). The stress-inducible form of the gene is expressed from an internal promoter and encodes a novel intracellular form of what is normally a secreted protein. Stress-induced expression of CA-VI is both CHOP and C/EBPβ dependent in that it does not occur in cells deficient in either gene. A CHOP-responsive element was mapped to the inducibleCA-VI promoter, and in vitro footprinting revealed binding of CHOP-C/EBP heterodimers to that site. Rescue of CA-VIexpression in c/ebpβ−/− cells by exogenous C/EBPβ and a shorter, normally inhibitory isoform of the protein known as LIP suggests that the role of the C/EBP partner is limited to targeting the CHOP-containing heterodimer to the response element and points to a preeminent role for CHOP in CA-VI induction during stress.

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