Nitric Oxide Signals That Aplysia Have Attempted to Eat, a Necessary Component of Memory Formation After Learning That Food Is Inedible

2006 ◽  
Vol 96 (3) ◽  
pp. 1247-1257 ◽  
Author(s):  
Ayelet Katzoff ◽  
Tziona Ben-Gedalya ◽  
Itay Hurwitz ◽  
Nimrod Miller ◽  
Yehoshua Z. Susswein ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Rejection Rate ◽  
Memory Formation ◽  
Critical Component ◽  
No Donor ◽  
Ad Libitum ◽  
Ad Libitum Feeding ◽  
Insight Into ◽  
Stimulation Of

Inhibiting nitric oxide (NO) synthesis during learning that food is inedible in Aplysia blocks subsequent memory formation. To gain insight into the function of NO transmission during learning we tested whether blocking NO synthesis affects aspects of feeding that are expressed both in a nonlearning context and during learning. Inhibiting NO synthesis with L-NAME and blocking guanylyl cyclase with methylene blue decreased the efficacy of ad libitum feeding. D-NAME had no effect. L-NAME also decreased rejection responses frequency, but did not affect rejection amplitude. The effect of L-NAME was explained by a decreased signaling that efforts to swallow are not successful, leading to a decreased rejection rate, and a decreased ability to reposition and subsequently consume food in ad libitum feeding. Signaling that animals have made an effort to swallow is a critical component of learning that food is inedible. Stimulation of the lips with food alone did not produce memory, but stimulation combined with the NO donor SNAP did produce memory. Exogenous NO at a concentration causing memory also excited a key neuron responding to NO, the MCC. Block of the cGMP second-messenger cascade during training by methylene blue also blocked memory formation after learning. Our data indicate that memory arises from the contingency of three events during learning that food is inedible. One of the events is efforts to swallow, which are signaled by NO by cGMP.

scholarly journals Modulation of rat peripheral polymorphonuclear leukocyte response by nitric oxide and arginine

Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2741-2748 ◽  
Author(s):  
P Seth ◽  
R Kumari ◽  
M Dikshit ◽  
RC Srimal
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Methylene Blue ◽  
Polymorphonuclear Leukocytes ◽  
Reactive Oxygen Species Generation ◽  
Oxygen Species ◽  
Superoxide Generation ◽  
No Donor ◽  
Radical Generation ◽  
Leukocyte Response

The effect of nitric oxide (NO) on the luminol-dependent chemiluminescence (LCL) response of rat polymorphonuclear leukocytes (PMNLs) was analyzed by using sodium nitroprusside (SNP), a NO donor, and L-arginine (L-arg), a NO precursor. A significant reduction in the LCL intensity was observed in presence of SNP (100 mumol/L) or L-arg (5 or 10 mmol/L) in arachidonic acid (AA) phorbol ester (PMA) and formyl- methionyl-leucyl-phenylalanine stimulated PMNLs. However, opsonized zymosan-induced LCL was not attenuated significantly. Reduction in hydroxyl radical and superoxide generation was also observed in SNP- or L-arg-pretreated cells. D-Arg (10 mmol/L) pretreatment did not inhibit PMNLs' LCL response. Furthermore, methylene blue (5 mumol/L) and L-NG- mono methyl-L-arginine (100 or 300 mumol/L) significantly attenuated the LCL response, as induced by various agonists. Cyclic GMP did not alter the reactive oxygen species generation from rat PMNLs. In addition, AA-induced release of myeloperoxidase, a marker of azurophilic granules, was found to be enhanced in L-arg- (10 mmol/L) pretreated PMNLs. The results suggest that NO inhibits free radical generation from rat PMNLs.

scholarly journals Angiotensin II-mediated hypertension impairs nitric oxide-induced NKCC2 inhibition in thick ascending limbs

2016 ◽  
Vol 310 (8) ◽  
pp. F748-F754 ◽  
Author(s):  
Vanesa D. Ramseyer ◽  
Pablo A. Ortiz ◽  
Oscar A. Carretero ◽  
Jeffrey L. Garvin
Keyword(s):  
Nitric Oxide ◽  
Pde5 Inhibitor ◽  
Cell Types ◽  
No Production ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
No Donor ◽  
Induced Hypertension ◽  
Stimulation Of

In thick ascending limbs (THALs), nitric oxide (NO) decreases NaCl reabsorption via cGMP-mediated inhibition of Na-K-2Cl cotransporter (NKCC2). In angiotensin (ANG II)-induced hypertension, endothelin-1 (ET-1)-induced NO production by THALs is impaired. However, whether this alters NO's natriuretic effects and the mechanisms involved are unknown. In other cell types, ANG II augments phosphodiesterase 5 (PDE5)-mediated cGMP degradation. We hypothesized that NO-mediated inhibition of NKCC2 activity and stimulation of cGMP synthesis are blunted via PDE5 in ANG II-induced hypertension. Sprague-Dawley rats were infused with vehicle or ANG II (200 ng·kg−1·min−1) for 5 days. ET-1 reduced NKCC2 activity by 38 ± 13% ( P < 0.05) in THALs from vehicle-treated rats but not from ANG II-hypertensive rats (Δ: −9 ± 13%). A NO donor yielded similar results as ET-1. In contrast, dibutyryl-cGMP significantly decreased NKCC2 activity in both vehicle-treated and ANG II-hypertensive rats (control: Δ−44 ± 15% vs. ANG II: Δ−41 ± 10%). NO increased cGMP by 2.08 ± 0.36 fmol/μg protein in THALs from vehicle-treated rats but only 1.06 ± 0.25 fmol/μg protein in ANG II-hypertensive rats ( P < 0.04). Vardenafil (25 nM), a PDE5 inhibitor, restored NO's ability to inhibit NKCC2 activity in THALs from ANG II-hypertensive rats (Δ: −60 ± 9%, P < 0.003). Similarly, NO's stimulation of cGMP was also restored by vardenafil (vehicle-treated: 1.89 ± 0.71 vs. ANG II-hypertensive: 2.02 ± 0.32 fmol/μg protein). PDE5 expression did not differ between vehicle-treated and ANG II-hypertensive rats. We conclude that NO-induced inhibition of NKCC2 and increases in cGMP are blunted in ANG II-hypertensive rats due to PDE5 activation. Defects in the response of THALs to NO may enhance NaCl retention in ANG II-induced hypertension.

Nitric oxide modulates elicitation of reflex swallowing from the pharynx in rats

2006 ◽  
Vol 291 (3) ◽  
pp. R651-R656 ◽  
Author(s):  
Hiroshi Kijima ◽  
Tomio Shingai ◽  
Yoshihiro Takahashi ◽  
Yuka Kajii ◽  
Shin-ichi Fukushima ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Intraperitoneal Administration ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Electromyographic Activity ◽  
No Donor ◽  
Pharyngeal Branch ◽  
Prolonged Latency ◽  
Stimulation Of

The pharynx is very important for elicitation of reflex swallowing. The region of the pharynx is innervated by the pharyngeal branch of the glossopharyngeal nerve (GPN-ph). Nitric oxide (NO) plays an important role in various physiological functions. The purpose of this study is to investigate the contribution of NO to reflex swallowing evoked by electrical stimulation of the GPN-ph. Swallowing was evoked in urethane-anesthetized rats by application of repetitive electrical stimulation (10- to 20-μA amplitude, 10- to 20-Hz frequency, 1.0-ms duration) to the central cut end of the GPN-ph or superior laryngeal nerve. Swallowing was identified by electromyographic activity of the mylohyoid muscle. Latency to the first swallow and the interval between swallows were measured. Intravenous administration of NG-nitro-l-arginine (l-NNA, 0.6 mg/kg), a nonselective inhibitor of NO synthase (NOS), extremely prolonged latency to the first swallow and the interval between swallows evoked by the GPN-ph. Intraperitoneal administration of 7-nitroindazole (5.0 mg/kg), a selective inhibitor of neuronal NOS, significantly prolonged latency to the first swallow and the interval between swallows evoked by the GPN-ph. Administration of l-arginine (an NO donor, 500 mg/kg) and sodium nitroprusside (an NO releaser, 0.6 mg/kg) restored the suppression of swallowing induced by the NOS inhibitor. Superior laryngeal nerve-evoked swallowing was suppressed by administration of a higher dose of l-NNA (6.0 mg/kg). Swallowing evoked by water stimulation of the pharynx was also suppressed by l-NNA (0.6 mg/kg). These results suggest that NO plays an important role in signal processing for initiation of reflex swallowing from the pharynx.

Suppression and stimulation of TSH and thyroid hormones in bulls during starvation and refeeding

1983 ◽  
Vol 103 (2) ◽  
pp. 223-226 ◽  
Author(s):  
Borghild Tveit ◽  
Flemming Larsen
Keyword(s):  
Half Life ◽  
Experimental Period ◽  
Starvation Period ◽  
Disappearance Rate ◽  
Fasting Period ◽  
Blood Samples ◽  
Bull Calves ◽  
Ad Libitum ◽  
Ad Libitum Feeding ◽  
Stimulation Of

Abstract. Sixteen bull calves were fasted during two periods, 3½ and 7 months old. Blood samples were taken every 6 h during an experimental period of 9 days: 2 control days, 5 fasting days and 2 refeeding days. During the control days with ad libitum feeding, T3, T4 and TSH increased during the day. During the fasting period, T4 decreased with a half-life of 3.5 days and T3 with a half-life of 3 days. TSH decreased in a less regularly way to a mean of 60% of control mean. Six h after refeeding, TSH had increased to 300% of control mean. T3 and T4 had a maximum 12 h after refeeding. As the T4 decreased with a rate nearly similar to the T4 disappearance rate in starving bulls, the secretion of T4 from the thyroid gland must have been almost stopped during the starvation period. The morning values were below normal for all three hormones after 2 days of refeeding.

Regulation of VIP release from rat enteric nerve terminals: evidence for a stimulatory effect of NO

1996 ◽  
Vol 271 (4) ◽  
pp. G568-G574 ◽  
Author(s):  
H. D. Allescher ◽  
M. Kurjak ◽  
A. Huber ◽  
P. Trudrung ◽  
V. Schusdziarra
Keyword(s):  
Nitric Oxide ◽  
No Synthase ◽  
Nerve Terminals ◽  
No Donor ◽  
Cyclic Monophosphate ◽  
A 23187 ◽  
Basal Release ◽  
Significant Release ◽  
Synthase Inhibitor ◽  
Stimulation Of

The basal release of vasoactive intestinal polypeptide (VIP) from freshly prepared enriched synaptosomes was 159.1 +/- 17.3 fmol/mg protein (100%), which constituted 2.5% of the total VIP content. Basal VIP release was reduced by 65% by removal of external Ca2+. Release of VIP was stimulated by depolarization with KCl (65 mM, 143%) and in the presence of veratridine (10(-6) M, 184%), monensin (10(-5) M, 131%), and the Ca2+ ionophore A-23187 (10(-6) M, 160%). Stimulation of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent mechanisms using isoproterenol (10(-6)-10(-4) M) and forskolin (10(-6) and 10(-5) M) had no stimulatory influence on VIP release. In contrast, sodium nitroprusside (10(-4) M, 198%), the nitric oxide (NO) donor 3-(morpholino)sydnonimine (10(-4) M, 155%), and the guanosine 3',5'-cyclic monophosphate (cGMP) analogue 8-bromo cGMP (10(-4) M, 196%) caused a significant release of VIP. L-Arginine (10(-3) M, 246%) also caused a significant increase of VIP release that was antagonized by the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (5 x 10(-4) M, 131%), which had no effect when given alone. The results demonstrate that VIP can be released from enriched synaptosomes by Ca(2+)-dependent mechanisms by NO agonists or NO-dependent mechanisms. It is speculated that this VIP release is induced by a presynaptic stimulatory mechanism of NO and this effect could enhance or contribute to the action of NO.

Inhibition of guanylate cyclase stimulation by NO and bovine arterial relaxation to peroxynitrite and H2O2

1999 ◽  
Vol 277 (3) ◽  
pp. H978-H985 ◽  
Author(s):  
Takafumi Iesaki ◽  
Sachin A. Gupte ◽  
Pawel M. Kaminski ◽  
Michael S. Wolin
Keyword(s):  
Nitric Oxide ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Superoxide Production ◽  
No Donor ◽  
Arterial Relaxation ◽  
Stimulation Of

The inhibitor of soluble guanylate cyclase (sGC) stimulation by nitric oxide (NO), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), was examined for its effects on the prolonged relaxation of endothelium-removed bovine coronary (BCA) and pulmonary (BPA) arteries to peroxynitrite (ONOO−) and on H2O2-elicited relaxation and sGC stimulation. Our previous studies suggest that ONOO− causes a prolonged relaxation of BPA by regenerating NO and that a 2-min exposure of BCA or BPA to 50 nM NO causes an ONOO−-elicited relaxation. The relaxation of K+-precontracted BCA to 50 nM NO or 100 μM ONOO− was essentially eliminated by 10 μM ODQ. ODQ also eliminated relaxation to 0.1 nM-10 μM of NO donor S-nitroso- N-acetyl-penicillamine (SNAP), but it did not alter relaxation to 1–300 μM H2O2. Similar responses were also observed in BPA. ODQ did not increase lucigenin-detectable superoxide production in BCA, and it did not alter luminol-detectable endogenous ONOO− formation observed during a 2-min exposure of BCA to 50 nM NO. In addition, ODQ did not affect tissue release of NO after 2 min exposure of BCA to 50 nM NO. The activity of sGC in BPA homogenate that is stimulated by endogenous H2O2was not altered by ODQ, whereas sGC activity in the presence of 10 μM SNAP (+fungal catalase) was reduced by ODQ. Thus relaxation of K+-precontracted BCA and BPA to ONOO− appears to be completely mediated by NO stimulation of sGC, whereas the actions of ODQ suggest that NO is not involved in H2O2-elicited relaxation and sGC stimulation. This study did not detect evidence for the participation of additional mechanisms potentially activated by ONOO− in the responses studied.

scholarly journals Nitric oxide increases carbon monoxide production by piglet cerebral microvessels

2005 ◽  
Vol 289 (4) ◽  
pp. H1442-H1447 ◽  
Author(s):  
Charles W. Leffler ◽  
Liliya Balabanova ◽  
Alexander L. Fedinec ◽  
Helena Parfenova
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Catalytic Activity ◽  
Excitatory Amino Acid ◽  
Gas Chromatography Mass Spectrometry ◽  
No Production ◽  
No Donor ◽  
Cerebral Microvessels ◽  
Stimulation Of

Carbon monoxide (CO) and nitric oxide (NO) can be involved in the regulation of cerebral circulation. Inhibition of production of either one of these gaseous intercellular messengers inhibits newborn pig cerebral arteriolar dilation to the excitatory amino acid glutamate. Glutamate can increase NO production. Therefore, the present study tests the hypothesis that NO, which is increased by glutamate, stimulates the production of CO by cerebral microvessels. Experiments used freshly isolated cerebral microvessels from piglets that express only heme oxygenase-2 (HO-2). CO production was measured by gas chromatography-mass spectrometry. Although inhibition of nitric oxide synthase (NOS) with Nω-nitro-l-arginine (l-NNA) did not alter basal HO-2 catalytic activity or CO production, l-NNA blocked glutamate stimulation of HO-2 activity and CO production. Furthermore, the NO donor sodium nitroprusside mimicked the actions of glutamate on HO-2 and CO production. The action of NO appears to be via cGMP because 8-bromo-cGMP mimics and 1 H-[1,2,4]oxadiazole-[4,3- a]quinoxalin-1-one (ODQ) blocks glutamate stimulation of CO production and HO-2 catalytic activity. Inhibitors of neither casein kinase nor phosphotidylinositol 3-kinase altered HO-2 catalytic activity. Conversely, inhibition of calmodulin with calmidazolium chloride blocked glutamate stimulation of CO production and reduced HO-2 catalytic activity. These data suggest that glutamate may activate NOS producing NO that leads to CO synthesis via a cGMP-dependent elevation of HO-2 catalytic activity. These results are consistent with the findings in vivo that either HO or NOS inhibition blocks cerebrovascular dilation to glutamate in piglets.

Modulation of mitochondrial Ca2+ by nitric oxide in cultured bovine vascular endothelial cells

2005 ◽  
Vol 289 (4) ◽  
pp. C836-C845 ◽  
Author(s):  
Elena N. Dedkova ◽  
Lothar A. Blatter
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Membrane Potential ◽  
Pulmonary Artery ◽  
Laser Scanning ◽  
Mitochondrial Permeability Transition ◽  
No Production ◽  
No Donor ◽  
Negative Feedback Regulation ◽  
Stimulation Of

In the present study, we used laser scanning confocal microscopy in combination with fluorescent indicator dyes to investigate the effects of nitric oxide (NO) produced endogenously by stimulation of the mitochondria-specific NO synthase (mtNOS) or applied exogenously through a NO donor, on mitochondrial Ca2+ uptake, membrane potential, and gating of mitochondrial permeability transition pore (PTP) in permeabilized cultured calf pulmonary artery endothelial (CPAE) cells. Higher concentrations (100–500 μM) of the NO donor spermine NONOate (Sper/NO) significantly reduced mitochondrial Ca2+ uptake and Ca2+ extrusion rates, whereas low concentrations of Sper/NO (<100 μM) had no effect on mitochondrial Ca2+ levels ([Ca2+]mt). Stimulation of mitochondrial NO production by incubating cells with 1 mM l-arginine also decreased mitochondrial Ca2+ uptake, whereas inhibition of mtNOS with 10 μM l- N5-(1-iminoethyl)ornithine resulted in a significant increase of [Ca2+]mt. Sper/NO application caused a dose-dependent sustained mitochondrial depolarization as revealed with the voltage-sensitive dye tetramethylrhodamine ethyl ester (TMRE). Blocking mtNOS hyperpolarized basal mitochondrial membrane potential and partially prevented Ca2+-induced decrease in TMRE fluorescence. Higher concentrations of Sper/NO (100–500 μM) induced PTP opening, whereas lower concentrations (<100 μM) had no effect. The data demonstrate that in calf pulmonary artery endothelial cells, stimulation of mitochondrial Ca2+ uptake can activate NO production in mitochondria that in turn can modulate mitochondrial Ca2+ uptake and efflux, demonstrating a negative feedback regulation. This mechanism may be particularly important to protect against mitochondrial Ca2+ overload under pathological conditions where cellular [NO] can reach very high levels.

Inhibition of basal and reflex-mediated sympathetic activity in the RVLM by nitric oxide

1995 ◽  
Vol 268 (4) ◽  
pp. R958-R962 ◽  
Author(s):  
J. Zanzinger ◽  
J. Czachurski ◽  
H. Seller
Keyword(s):  
Nitric Oxide ◽  
Intercostal Nerve ◽  
Ventrolateral Medulla ◽  
Nervous Control ◽  
No Donor ◽  
Functional Roles ◽  
Arterial Blood ◽  
Somatosympathetic Reflex ◽  
Higher Doses ◽  
Stimulation Of

We examined possible functional roles for nitric oxide (NO) in the rostral ventrolateral medulla (RVLM), which is the final area for integration of sympathetic nerve activity (SNA) within the brain stem. Chloralose-anesthetized cats were completely baro- and chemoreceptor denervated, the RVLM was exposed for microinjections, and preganglionic SNA was recorded from the white ramus of the 3rd thoracic segment. Injections of NG-nitro-L-arginine (L-NNA), an inhibitor of NO synthase, but not of NG-nitro-D-arginine, caused distinct increases in SNA and arterial blood pressure (BP). Excitatory somatosympathetic reflex amplitudes evoked by electrical stimulation of the 4th intercostal nerve were significantly increased by L-NNA whereas inhibitory responses to baroreflex activation by stimulation of the carotid sinus nerve were not affected. The effects of L-NNA were counteracted by the NO-donor compounds glyceryltrinitrate and S-nitroso-N-acetylpenicillamine, which decreased BP and SNA below control values at higher doses. These results suggest that endogenous NO, in addition to its peripheral actions, modulates the central nervous control of cardiovascular functions by reduction of basal sympathetic tone and by attenuation of excitatory reflex responses.

scholarly journals N-acetyl ornithine deacetylase is a moonlighting protein and is involved in the adaptation of Entamoeba histolytica to nitrosative stress

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Preeti Shahi ◽  
Meirav Trebicz-Geffen ◽  
Shruti Nagaraja ◽  
Rivka Hertz ◽  
Sharon Alterzon-Baumel ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Entamoeba Histolytica ◽  
Detrimental Effect ◽  
Nitrosative Stress ◽  
Metabolic Enzyme ◽  
Rna Seq ◽  
No Donor ◽  
Moonlighting Protein ◽  
Insight Into

Abstract Adaptation of the Entamoeba histolytica parasite to toxic levels of nitric oxide (NO) that are produced by phagocytes may be essential for the establishment of chronic amebiasis and the parasite’s survival in its host. In order to obtain insight into the mechanism of E. histolytica’s adaptation to NO, E. histolytica trophozoites were progressively adapted to increasing concentrations of the NO donor drug, S-nitrosoglutathione (GSNO) up to a concentration of 110 μM. The transcriptome of NO adapted trophozoites (NAT) was investigated by RNA sequencing (RNA-seq). N-acetyl ornithine deacetylase (NAOD) was among the 208 genes that were upregulated in NAT. NAOD catalyzes the deacetylation of N-acetyl-L-ornithine to yield ornithine and acetate. Here, we report that NAOD contributes to the better adaptation of the parasite to nitrosative stress (NS) and that this function does not depend on NAOD catalytic activity. We also demonstrated that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is detrimental to E. histolytica exposed to NS and that this detrimental effect is neutralized by NAOD or by a catalytically inactive NAOD (mNAOD). These results establish NAOD as a moonlighting protein, and highlight the unexpected role of this metabolic enzyme in the adaptation of the parasite to NS.

Sign in / Sign up

Export Citation Format

Share Document