Retrograde Carbon Monoxide Is Required for Induction of Long-Term Potentiation in Rat Superior Cervical Ganglion

Alkadhi, Karim A.; Al-Hijailan, Reem S.; Malik, Kahkashan; Hogan, Yvonne H.

doi:10.1523/jneurosci.21-10-03515.2001

Cited by 48 publications

(47 citation statements)

References 43 publications

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“…No apparent action of CO on basal hepatic vascular tone in the present study might be attributed possibly to perfusate free Hb released through hemolysis. It is reported that oxyhemoglobin, oxygenated Hb, inhibits the action of CO (1,9,26,29). The Masterflex roller pump used in the present study should have caused inevitable hemolysis, resulting in release of free Hb in the perfusate.…”

Section: Discussionmentioning

confidence: 70%

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

Ruan¹,

Shibamoto²,

Shimo³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Ruan, Zonghai, Toshishige Shibamoto, Tomohiro Shimo, Hideaki Tsuchida, Tomonobu Koizumi, and Matomo Nishio. NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver. Am J Physiol Regul Integr Comp Physiol 286: R94-R100, 2004. First published October 2, 2003 10.1152/ ajpregu.00648.2002The pathophysiology of the hepatic vascular response to anaphylaxis in guinea pig is not known. We studied effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused livers derived from guinea pigs sensitized with ovalbumin. We also determined whether nitric oxide (NO) or carbon monoxide (CO) modulates the hepatic anaphylaxis. The livers were perfused portally and recirculatingly at constant flow with diluted blood. With the use of the double-occlusion technique to estimate the hepatic sinusoidal pressure (P do), portal venous resistance (Rpv) and hepatic venous resistance (Rhv) were calculated. An antigen injection caused venoconstriction characterized by an increase in R pv greater than Rhv and was accompanied by a large liver weight gain. Pretreatment with the NO synthase inhibitor N G -nitro-L-arginine methyl ester, but not the heme oxygenase inhibitor zinc protoporphyrin IX, potentiated the antigen-induced venoconstriction by increasing both R pv and Rhv (2.2-and 1.2-fold increase, respectively). In conclusion, anaphylaxis causes both pre-and postsinusoidal constriction in isolated guinea pig livers. However, the increases in postsinusoidal resistance and Pdo cause hepatic congestion. Endogenously produced NO, but not CO, modulates these responses. hepatic circulation; antigen; double occlusion pressure; hepatic vascular resistance ANAPHYLAXIS IS AN immediate, type-1 hypersensitivity reaction that occurs after exposure of sensitized organisms and tissues to sensitizing antigen. The most common life-threatening feature of acute anaphylaxis is cardiovascular collapse and shock, although there are other life-threatening effects, including bronchospasm, angioedema, and pulmonary edema (24). Cardiovascular manifestation includes a rapid and precipitous decrease in systemic arterial pressure with a concomitant decrease in cardiac output (5). Anaphylactic hypotension is primarily caused by alterations in the systemic circulation that influence blood flow to the heart because left ventricular function is relatively well preserved during anaphylactic shock (5). Peripheral circulatory collapse is ascribed to hypovolemia, which results from a plasma volume loss. The latter could be the result of vasodilation with the peripheral pooling in largecapacity splanchnic venous beds and increased vascular permeability with a shift of intravascular fluid to the extravascular space.In canine experimental models of anaphylactic shock, congestion of livers and the upstream splanchnic organs is important in the pathogenesis of circulatory collapse. Actually, eviscerated dogs did not develop anaphylactic shock (17). Enjeti et al. (5) reported that the severity of th...

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Section: Discussionmentioning

confidence: 70%

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

Ruan¹,

Shibamoto²,

Shimo³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Liu et al (38) reported that in the hippocampus, nanomolar concentrations of A␤40 and A␤42 block the response of ␣7-containing nicotinic receptors, which are thought to mediate synaptic currents (39,40) and modulate transmitter release (41,42), thereby contributing to spatial memory and working memory formation. In addition, the ␤-APP holoprotein inhibits heme oxygenase-produced carbon monoxide (7), which has been reported to alter long-term potentiation (43)(44)(45). The role of ␤-APP holoprotein is supported also by findings showing increased mRNA for ␤-APP 751 and ␤-APP 770 in the brains of aged rats with spatial memory deficit but not in rats without impairments (46).…”

Section: Discussionmentioning

confidence: 99%

Specific spatial learning deficits become severe with age in β-amyloid precursor protein transgenic mice that harbor diffuse β-amyloid deposits but do not form plaques

Koistinaho

Ort

Cimadevilla

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

153

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Memory impairment progressing to dementia is the main clinical symptom of Alzheimer's disease (AD). AD is characterized histologically by the presence of ␤-amyloid (A␤) plaques and neurofibrillary tangles in specific brain regions. Although A␤ derived from the A␤ precursor protein (␤-APP) is believed to play a central etiological role in AD, it is not clear whether soluble and͞or fibrillar forms are responsible for the memory deficit. We have generated and previously described mice expressing human wild-type ␤-APP751 isoform in neurons. These transgenic mice recapitulate early histopathological features of AD and form A␤ deposits but no plaques. Here we describe a specific and progressive learning and memory impairment in these animals. In the Morris water maze, a spatial memory task sensitive to hippocampal damage, one pedigree already showed significant differences in acquisition in 3-month-old mice that increased in severity with age and were expressed clearly in 6-month-and 2-year-old animals. The second transgenic pedigree displayed a milder impairment with a later age of onset. Performance deficits significantly decreased during the 6 days of training in young but not in aged transgenic animals. Both pedigrees of the transgenic mice differed from wild-type mice by less expressed increase of escape latencies after the platform position had been changed in the reversal experiment and by failure to prefer the goal quadrant in probe trials. Both pedigrees performed at wild-type level in a number of other tests (open field exploration and passive and active place avoidance). The results suggest that plaque formation is not a necessary condition for the neuronal ␤-APP751 transgene-induced memory impairment, which may be caused by ␤-APP overexpression, isoform misexpression, or elevated soluble A␤.

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“…In that it is a gas, carbon monoxide can travel freely through intracellular and extracellular compartments. The CO literature is vast and complex with many controversies that have yet to be resolved [58][59][60][61][62][63] . CO is better known to be toxic at high levels.…”

Section: Carbon Monoxidementioning

confidence: 99%

Unique Properties of Polyphenol Stilbenes in the Brain: More than Direct Antioxidant Actions; Gene/Protein Regulatory Activity

Doré

2005

Neurosignals

102

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The ‘French Paradox’ has been typically associated with moderate consumption of wine, especially red wine. A polyphenol 3,4’,5-trihydroxy-trans-stilbene (a member of the non-flavonoids family), better known as resveratrol, has been purported to have many health benefits. A number of these valuable properties have been attributed to its intrinsic antioxidant capabilities, although the potential level of resveratrol in the circulation is likely not enough to neutralize free radical scavenging. The brain and the heart are uniquely vulnerable to hypoxic conditions and oxidative stress injuries. Recently, evidence suggests that resveratrol could act as a signaling molecule within tissues and cells to modulate the expression of genes and proteins. Stimulation of such proteins and enzymes could explain some the intracellular antioxidative properties. The modulation of genes could suffice as an explanation of some of resveratrol’s cytoprotective actions, as well as its influence on blood flow, cell death, and inflammatory cascades. Resveratrol stimulation of the expression of heme oxygenase is one example. Increased heme oxygenase activity has led to significant protection against models of in vitro and in vivo oxidative stress injury. Resveratrol could provide cellular resistance against insults; although more work is necessary before it is prescribed as a potential prophylactic in models of either acute or chronic conditions, such as stroke, amyotrophic lateral sclerosis, Parkinson, Alzheimer, and a variety of age-related vascular disorders.

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Retrograde Carbon Monoxide Is Required for Induction of Long-Term Potentiation in Rat Superior Cervical Ganglion

Cited by 48 publications

References 43 publications

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

Specific spatial learning deficits become severe with age in β-amyloid precursor protein transgenic mice that harbor diffuse β-amyloid deposits but do not form plaques

Unique Properties of Polyphenol Stilbenes in the Brain: More than Direct Antioxidant Actions; Gene/Protein Regulatory Activity

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