Role of olfaction and vision in homing behaviour of black rockfish Sebastes inermis

How fish find their original habitat and natal home remains an unsolved riddle of animal behaviour. Despite extensive efforts to study the homing behaviour of diadromous fish, relatively little attention has been paid to that of non-diadromous marine fish. Among these, most rockfish of the genus Sebastes exhibit homing ability and/or a strong fidelity to their habitats. However, how these rockfish detect the homeward direction has not been clarified. The goal of the present research was to investigate the sensory mechanisms involved in the homing behaviour of the black rockfish Sebastes inermis, using acoustic telemetry. Vision-blocked or olfactory-ablated rockfish were released in natural waters and their homing behaviours compared with those of intact or control individuals. Blind rockfish showed homing from both inside and outside their habitat. The time taken by blind fish to reach their home habitat was not significantly different from that of the control fish. In contrast, most olfactory-ablated fish did not successfully reach their original habitat. Our results indicate that black rockfish predominantly use the olfactory sense in their homing behaviour.     

Effect of nitrous oxide on nickel deprivation in rats

Because nickel may have a biological function in a pathway in which vitamin B₁₂ is important, an experiment was performed to determine the effects of nitrous oxide exposure in rats deprived of nickel. Exposure to nitrous oxide (N₂O) causes inactivation of cobalamin and a subsequent decrease in the vitamin B₁₂-dependent enzymes methionine synthase and methylmalonyl CoA mutase. Rats were assigned to dietary groups of 12 in a factorially arranged experiment with dietary variables of nickel (0 or 1 μg/g) and vitamin B₁₂ (0 or 50 ng/g). After 6 wk, one-half of the rats from each dietary group were exposed to 50% N₂O/50% O₂ for 90 min/d for the last 28 d of the experiment. Vitamin B₁₂, N₂O, or their interaction had numerous effects; classical findings included N₂O-induced reduction in plasma vitamin B₁₂ and decreases in the vitamin B₁₂-dependent enzymes. Inactivation of vitamin B₁₂ by N₂O, however, did not exacerbate signs of nickel deprivation, possibly because the rats were able to metabolically compensate to N₂O exposure. Mention of a trademark or proprietary product in this article does not constitute a guarantee or warranty of the product by the United States Department of Agriculture and does not imply its approval to the exclusion of other products that may also be suitable.     

Induced preference for host plant chemicals in the tobacco hornworm: contribution of olfaction and taste

Many herbivorous insects induce preferences for host plants. Recent work in Manduca sexta indicates that induced preferences are mediated by a “tuning” of the peripheral taste system to chemicals within host plant foliage. We tested this hypothesis by rearing caterpillars on artificial diet or potato foliage, and then examining olfactory- and taste-mediated responses to potato foliage extract. First, we confirmed earlier reports that consumption of potato foliage tunes the peripheral taste system by reducing responsiveness to glucose and increasing responsiveness to foliage extract. Second, we offered caterpillars a choice between disks treated with foliage extract (experimental) or solvent alone (control). The foliage-reared caterpillars approached and consumed the experimental disks disproportionately, whereas the diet-reared caterpillars approached and consumed both disks indiscriminately. This indicated that induced preferences involve olfaction and taste. Third, we ran choice tests with foliage-reared caterpillars deprived of either olfactory or gustatory input. Caterpillars lacking olfactory input approached both disks indiscriminately, but fed selectively on experimental disks. In contrast, caterpillars lacking gustatory input approached experimental disks selectively, but fed indiscriminately on both types of disk. We conclude that even though olfaction helps caterpillars locate potato foliage, it is the “tuned” gustatory response that ultimately mediates the induced preference.     

The relative importance of olfaction and vision in a diurnal and a nocturnal hawkmoth

Nectar-feeding animals can use vision and olfaction to find rewarding flowers and different species may give different weight to the two sensory modalities. We have studied how a diurnal or nocturnal lifestyle affects the weight given to vision and olfaction. We tested naïve hawkmoths of two species in a wind tunnel, presenting an odour source and a visual stimulus. Although the two species belong to the same subfamily of sphingids, the Macroglossinae, their behaviour was quite different. The nocturnal Deilephila elpenor responded preferably to the odour while the diurnal Macroglossum stellatarum strongly favoured the visual stimulus. Since a nocturnal lifestyle is ancestral for sphingids, the diurnal species, M. stellatarum, has evolved from nocturnal moths that primarily used olfaction. During bright daylight visual cues may have became more important than odour.     

Function and Dysfunction of CNG Channels: Insights from Channelopathies and Mouse Models

Channels directly gated by cyclic nucleotides (CNG channels) are important cellular switches that mediate influx of Na⁺ and Ca²⁺ in response to increases in the intracellular concentration of cAMP and cGMP. In photoreceptors and olfactory receptor neurons, these channels serve as final targets for cGMP and cAMP signaling pathways that are initiated by the absorption of photons and the binding of odorants, respectively. CNG channels have been also found in other types of neurons and in non-excitable cells. However, in most of these cells, the physiological role of CNG channels has yet to be determined. CNG channels have a complex heteromeric structure. The properties of individual subunits that assemble in specific stoichiometries to the native channels have been extensively investigated in heterologous expression systems. Recently, mutations in human CNG channel genes leading to inherited diseases (so-called channelopathies) have been functionally characterized. Moreover, mouse knockout models were generated to define the role of CNG channel proteins in vivo. In this review, we will summarize recent insights into the physiological and pathophysiological role of CNG channel proteins that have emerged from genetic studies in mice and humans.     

Making sense with TRP channels: store-operated calcium entry and the ion channel Trpm5 in taste receptor cells

The sense of taste plays a critical role in the life and nutritional status of organisms. During the last decade, several molecules involved in taste detection and transduction have been identified, providing a better understanding of the molecular physiology of taste receptor cells. However, a comprehensive catalogue of the taste receptor cell signaling machinery is still unavailable. We have recently described the occurrence of calcium signaling mechanisms in taste receptor cells via apparent store-operated channels and identified Trpm5, a novel candidate taste transduction element belonging to the mammalian family of transient receptor potential channels. Trpm5 is expressed in a tissue-restricted manner, with high levels in gustatory tissue. In taste cells, Trpm5 is co-expressed with taste-signaling molecules such as alpha-gustducin, Ggamma(13), phospholipase C beta(2) and inositol 1,4,5-trisphosphate receptor type III. Biophysical studies of Trpm5 heterologously expressed in Xenopus oocytes and mammalian CHO-K1 cells indicate that it functions as a store-operated channel that mediates capacitative calcium entry. The role of store-operated channels and Trpm5 in capacitative calcium entry in taste receptor cells in response to bitter compounds is discussed.     

Beneficial role of naringin, a flavanoid on nickel induced nephrotoxicity in rats

This study was conducted to investigate the beneficial role of naringin on nickel induced nephrotoxicity. Nickel (Ni) (20 mg/kg body weight (b.w.) was administered intraperitoneally (i.p.) for 20 days. Naringin was administered orally (20, 40 and 80 mg/kg b.w.) with i.p. administration of Ni. Ni administration increased the levels of serum urea, uric acid and creatinine with a significant decrease in creatinine clearance and decreased levels of urea, uric acid and creatinine in urine. The levels of lipid peroxidation markers and nickel concentration in blood and kidney were also increased. While, the activities of enzymic and non-enzymic antioxidants were decreased. Treatment with naringin attenuated the alterations in the renal and urine markers, decreasing lipid peroxidation markers, increasing the antioxidant cascade and decreasing the nickel concentration in blood and kidney. All these changes were supported by histopathological observations. These findings demonstrate that naringin exerts a protective effect against nickel toxicity.     

Tamoxifen produces conditioned taste avoidance in male rats: An analysis of microstructural licking patterns and taste reactivity

Estrogen receptor activation has been shown to reduce body weight and produce a conditioned reduction in food intake in male rats that is putatively mediated by estradiol's suggested aversive effects. Evidence has shown that the selective estrogen receptor modulator tamoxifen used in the prevention and treatment of breast cancer may also produce changes in food intake and body weight, which are known to impact cancer development and survival. The purpose of the present study was to examine whether tamoxifen produces a conditioned reduction in intake similar to estradiol by producing a conditioned aversion. A one bottle lickometer test was used to examine conditioned changes in sucrose drinking, while the taste reactivity test was used to measure rejection reactions, which serve to index aversion in rats. A backward conditioning procedure that consisted of 3 conditioning days and one vehicle test day was used to examine conditioned changes in 0.3 M sucrose intake and taste reactivity. Our results show that tamoxifen produced a conditioned reduction in sucrose drinking in a one bottle fluid intake test that was similar to the effects produced by estradiol (positive control); however, no active rejection reactions were produced by either tamoxifen (1 and 10 mg/kg) or estradiol. The present results suggest that tamoxifen, at the doses used in the present study, acts as an estrogen receptor agonist to regulate food intake and that the conditioned reduction in intake produced by tamoxifen and estradiol reflects conditioned taste avoidance rather than conditioned taste aversion.     

Effect of monoamines on the taste buds in the mouse

Summary Mouse taste buds were investigated following administration of monoamines and their precursors by fluorescence and electron microscopy. The appearance of fluorescent cells within the taste bud and the ultrastructural changes of vesicles in the gustatory cells were due to the treatment of 5-hydroxytryptophan. Small dense-cored vesicles (30–60 nm in diameter) appeared throughout the cytoplasm and accumulated especially at the presynaptic membranes of afferent synapses. Large dense-cored vesicles (80–100 nm) increased twice in number, and electron densities of their cores became more dense as compared with untreated mice. Fluorescent cells appeared in the taste bud of l-DOPA treated mice, whereas no ultrastructural changes were observed. These results suggest that the gustatory cells of the taste bud are capable of taking up and storing monoamines, which might act as neurotransmitters from the gustatory cells to the nerves.     

Alteration of sweet taste in high-fat diet induced obese rats after 4 weeks treatment with exenatide

Exenatide, a glucagon-like peptide-1 (GLP-1) receptor agonist, is effective in inducing weight loss. The exact mechanisms are not fully understood. Reduced appetite and food intake may play important roles. Sweet taste contributes to food palatability, which promotes appetite. Interestingly, GLP-1 and its receptor are expressed in the taste buds of rodents and their interaction has an effect on mediating sweet taste sensitivity. Our aim was to investigate whether sweet taste will be changed after long term treatment with exenatide. The results showed that high-fat diet induced obese rats (HF-C) presented metabolic disorders in food intake, body weight, blood glucose and lipid metabolism compared with long term exenatide treated obese rats (EX) and normal chow fed control rats (NC). Meanwhile, greater preference for sweet taste was observed in HF-C rats but not in EX rats. Compared with NC rats, brain activities induced by sweet taste stimulation were stronger in HF-C rats, however these stronger activities were not found in EX rats. We further found reduced sweet taste receptor T1R3 in circumvallte taste buds of HF-C rats, while GLP-1 was increased. Besides, serum leptin was evaluated in HF-C rats with decreased leptin receptor expressed in taste buds. These changes were not observed in EX rats, which suggest them to be the underlying hormone and molecular mechanisms responsible for alterations in sweet taste of HF-C rats and EX rats. In summary, our results suggest that long term treatment with exenatide could benefit dietary obese rats partially by reversing sweet taste changes.     

Effect of nickel on testicular nucleic acid concentrations of rats on protein restriction

The nucleic acids (DNA and RNA) and total protein concentration in testes were estimated in male Wistar strain rats treated intraperitorally with nickel sulfate (2.0 mg/100 g body weight) on alternate days for 10 dosages. In both normal (18% casein) and protein-restricted (5% casein) experimental animals, the nucleic acids and total protein concentration were found to decrease significantly compared to the corresponding controls. Sperm count and sperm motility were also reduced in both experimental groups of animals. The results indicate that nickel influences the expression of genetic information by reducing testicular nucleic acids and protein concentration in both dietary experimental groups.     

Dietary vitamin B12, sulfur amino acids,and odd-chain fatty acids affect the response of rats to nickel deprivation

An experiment was performed to ascertain whether changing the dietary intake of two substances, cystine and margaric acid (heptadecanoic acid), that affect the flux through pathways involving the two vitamin B₁₂-depednent enzymes, methionine synthase and methylmalonyl-CoA mutase, would affect the interaction between nickel and vitamin B₁₂. Rats were assigned to treatment groups of six in a fully crossed, four-factorial arrangement. The independent variables, or factors, were: per kg of fresh diet, nickel analyzed at 25 and 850 μg; vitamin B₁₂ supplements of 0 and 50 μg; margaric acid supplements of 0 and 5 g; andl-cystine supplements of 0 and 12 g. The diet without cystine was marginally deficient in sulfur amino acids. Nickel affected growth, liver wt/body wt ratio (LB/BW), and a number of variables associated with iron, calcium, zinc, copper, and magnesium metabolism. Most of the effects of nickel were modified by the vitamin B₁₂ status of the rat. In numerous cases, the interaction between nickel and vitamin B₁₂ was dependent on, or altered by, the cystine or margaric acid content of the diet. Thus, the findings showed that the extent and the direction of changes in numerous variables in response to nickel deprivation varied greatly with changes in diet composition. These variables include those previously reported to be affected by nickel deprivation, including growth and the distribution or functioning of iron, calcium, zinc, copper, and magnesium. The findings also support the hypothesis that nickel has a biological function in a metabolic pathway in which vitamin B₁₂ is important.     

Conditioned taste avoidance induced by forced and voluntary wheel running in rats

Voluntary exercise by rats running in a freely rotating wheel (free wheel) produces conditioned taste avoidance (CTA) of a flavored solution consumed before running [e.g., Lett, B.T., Grant, V.L., 1996. Wheel running induces conditioned taste aversion in rats trained while hungry and thirsty. Physiol. Behav. 59, 699-702]. Forced exercise, swimming or running, also produces CTA in rats [e.g., Masaki, T., Nakajima, S., 2006. Taste aversion induced by forced swimming, voluntary running, forced running, and lithium chloride injection treatments. Physiol. Behav. 88, 411-416]. Energy expenditure may be the critical factor in producing such CTA. If so, forced running in a motorized running wheel should produce CTA equivalent to that produced by a similar amount of voluntary running. In two experiments, we compared forced running in a motorized wheel with voluntary running in a free wheel. Mean distance run over 30 min was equated as closely as possible in the two apparatuses. Both types of exercise produced CTA relative to sedentary, locked-wheel controls. However, voluntary running produced greater CTA than forced running. We consider differences between running in the free and motorized wheels that may account for the differences in strength of CTA.     

Biochemical studies of taste sensation XI. Isolation,characterization and taste ligand binding activity of plasma membranes from catfish taste tissue

Plasma membranes were isolated from taste receptor-containing epithelium of the channel catfish, Ictalurus punctatus. The membranes were prepared by ultracentrifugation of a sedimentable fraction in sucrose, using either a discontinous density gradient or a continous linear density gradient. The plasma membranes were characterized by their increased content of 5′-nucleotidase and by electron microscopy, as well as by a greatly diminished content of NADH-cytochrome c reductase and succinate-cytochrome c reductase. The recovery of binding activity for taste ligands was low, because of the long time-period required for ultracentrifugation, but of the recovered activity 80% occurred in the plasma-membrane preparation. Binding of seven chemostimulatory amino acids was demonstrated and found to correspond reasonably well with earlier binding data obtained using a less pure sedimentable fraction. The data provide direct evidence supporting the long-standing hypothesis that taste receptor sites are localized to the plasma membranes.     

镍对水稻离体叶片脂质过氧化作用的影响

杂交水稻离体叶片用１０－３ｍｏｌ／ＬＮｉＳＯ４处理后,镍阻抑了叶片在衰老过程中ＳＯＤ、ＣＡＴ酶活性的下降和ＡｓＡ氧化酶活性的上升,ＡｓＡ和叶绿素含量的下降得到延缓,减少了膜脂过氧化程度。     

Protective role of zinc in nickel induced hepatotoxicity in rats

This study was planned to determine the protective role of zinc, if any, in attenuating the toxicity induced by nickel sulfate in rat liver. Female Sprague Dawley (SD) rats received either nickel alone in the dose of 800 mg/l in drinking water, zinc alone in the dose of 227 mg/l in drinking water, and nickel plus zinc or drinking water alone for a total duration of eight weeks. The effects of different treatments were studied on various parameters in rat liver which include antioxidant enzymes, levels of nickel and zinc and histoarchitecture at the light microscopic level. Further, the activities of hepatic marker enzymes AST and ALT were also studied in rat serum. Nickel treatment to the normal control animals, resulted in a significant increase in lipid peroxidation and enzyme activities of catalase and glutathione-S-transferase. On the contrary, nickel treatment to normal rats caused a significant inhibition in the levels of reduced glutathione. Superoxide dismutase activity was found to be decreased which however was not significant. Interestingly, when Zn was supplemented to nickel treated rats, the activities of catalase, and glutathione-S-transferase and the levels of GSH and lipid peroxidation came back to within normal limits. Activities of serum AST and ALT were increased significantly following nickel treatment to normal rats. Simultaneous zinc administration to nickel treated rats tended to restore the altered levels of AST and ALT. Normal control and zinc treated animals revealed normal histology of liver. On the other hand, nickel treated animals showed alterations in normal hepatic histoarchitecture which comprise of vacuolization of the hepatocytes and dilatation of sinusoids as well as increase in the number of bi-nucleated cells. Administration of zinc to nickel treated rats resulted in marked improvement in the structure of hepatocytes, thus emphasizing the protective potential of zinc in restoring the altered hepatic histoarchitecture. The nickel administration to normal rats indicated increased concentrations of nickel and decreased concentrations of zinc. However, zinc effectively brought the altered levels of nickel and zinc to within normal range. The study concludes that zinc has the potential in alleviating the toxic effects of nickel in rat liver because of its property to induce metallothionein (S-rich protein) as a free radical scavenger, or its indirect action in reducing the levels of oxygen reactive species.     

Effect of dietary nickel and iron on the trace element content of rat liver

The level and/or form of dietary iron, dietary nickel, and the interaction between them affected the trace element content of rat liver. Livers were from the offspring of dams fed diets containing 10–16 ng, or 20 μg, of nickel/g. Dietary iron was supplied as ferric chloride (30 μg/g) or ferric sulfate (30 μg, or 60 μg). In nickel-deprived rats fed 60 μg of iron/g of diet as ferric sulfate, at age 35 days, levels of iron and zinc were depressed in liver and the level of copper was elevated. At age 55 days, iron was still depressed, copper was still elevated, but zinc also was elevated. In rats fed 30 μg of iron/g of diet as ferric chloride, liver iron content was higher in nickel-deprived than in nickel-supplemented rats at 30, but not at 50, days of age. Also manganese and zinc were lower in nickel-deprived than in nickel-supplemented rats at age 35 days if their dams had been on experiment for an extended period of time (i.e., since age 21 days). Thus, the levels of copper, iron, manganese, and zinc in liver were affected by nickel deprivation, but the direction and extent of the affects depended upon the iron status of the rat.     

Effect of form of iron on nickel deprivation in the rat

In three fully crossed, factorially arranged, completely randomized experiments, female weanling rats were fed a basal diet (containing about 10 ng of nickel and 2.3 μg of iron/g) supplemented with graded levels of nickel and iron. Iron was supplemented to the diet in experiment 1 at levels of 0, 25, 50, and 100 μg/g as a mixture of 40% FeSO₄·nH₂O and 60% Fe₂(SO₄)₃·nH₂O; in experiment 2 at levels of 0, 12.5, 25, 50, and 100 μg/g as Fe₂(SO₄)₃·nH₂O; in experiment 3 at levels of 0, 25, and 50 μg/g as either the mixture of ferric-ferrous sulfates, or as ferric sulfate only. Nickel as NiCl₂·3H₂O was supplemented to the diet in experiment 1 at levels of 0, 5, and 50 μg/g; in experiment 2 at levels of 0 and 50 μg/g; and in experiment 3 at levels of 0 and 5 μg/g. Regardless of dietary nickel, rats fed no supplemental iron exhibited depressed iron content and elevated copper, manganese, and zinc contents in the liver. Nickel and iron did not interact to affect iron, manganese, and zinc in liver. Liver copper was inconsistently affected by an interaction between nickel and iron. Nickel deprivation apparently accentuated the elevation of the copper level in livers of severely iron-deficient rats. Experiment 3 showed that the form of dietary iron altered the effect of nickel deprivation on the iron content of the liver. When only ferric sulfate was supplemented to the diet, liver iron content was depressed in nickel-deprived rats. On the other hand, when the ferric-ferrous mixture was supplemented to the diet, nickel deprivation apparently elevated the iron content in the liver. The findings support the views that (1) parameters that are affected by an interaction between nickel and iron are limited in factorially arranged experiments, and (2) the form and level of dietary iron markedly influence the effect of nickel deprivation in the rat.