The Roles of Ca2+ and cAMP in the Nematocyst Discharge of the Sea Anemone Tentacle

The phylum Cnidarians are aquatic animals, including jellyfish, hydra, sea anemones, and corals. They are the simplest metazoans having a nervous system and are diploblastic. Cnidarians are obligate predators that capture prey using specialized stinging cells called cnidocytes. The cnidocyte contains a nematocyst, which is a capsule containing an inverted, hollow tubule. Prey contacting the tentacle triggers the nematocyst tubule to rapidly evert; a process called discharge. The everting tubule penetrates and envenomates the prey, which is carried to the mouth by tentacle movements. Generally both chemical and mechanical stimuli are needed to trigger discharge. The cnidocytes, in sea anemones, are surrounded by two or more supporting cells that have chemoreceptors and possibly contact-sensitive mechanoreceptors (CSMs). Therefore, the cnidocyte/supporting cell complex (CSCC) controls nematocyst discharge. This project explores the chemoreceptor signaling pathway controlling nematocyst discharge from tentacles of the sea anemone, Aiptasia pallida. Chemoreceptors respond to N-acetylated sugars, such as N-acetylneuraminic acid (NANA), which occur on prey surfaces. When stimulated, this chemosensory pathway sensitizes CSMs to trigger nematocyst discharge in response to physical contact. Indirect evidence suggested that the NANA chemosensory pathway acts through the intracellular second-messenger, cyclic-AMP (cAMP). We now show that NANA dose-dependently increases in situ cAMP levels in the ectodermal layer of tentacles from A. pallida, but has no effect on the endodermal cAMP content. In addition, NANA activates cAMP-dependent protein kinase (PKA) in whole tentacle homogenates. High levels of extracellular Mg2+ are commonly used to anesthetize excised tentacles and to block discharge. We find that high levels of Mg2+ block the NANAstimulated cAMP increase. This supports the fact that high Mg2+ levels inhibit nematocyst discharge, but calls into question published findings in which NANAinduced changes in stereociliary bundle length of excised, Mg2+ -anesthetized tentacles are attributed to cAMP. We also find that NANA stimulates calcium influx into isolated tentacle ectodermal cells and that the influx is sensitive to various L-type calcium channel blockers, including dihydropyridines. The coincidence of the desensitization region of the nematocyst discharge curve with those NANA concentrations that most stimulate calcium influx, suggests a role of NANA-stimulated calcium influx in desensitization

Seismic Behaviour of Cable-Stayed Bridges: A Review

Cable-stayed bridges represent backbones in the infrastructure networks and their adequate seismic response must be ensured. These structures present complex interactions between the deck, the cables, the towers and their foundation. This, in combination with the reduced damping and the outstanding slenderness of cable-stayed bridges, renders a unique dynamic response. A complete review on the state of knowledge about the seismic behaviour of cable-stayed bridges is presented here, with special attention to the analysis techniques. The current design trends in the seismic design and control of cable-stayed bridges are also presented

Global Socioeconomic Impact of Cystic Echinococcosis

Because the human and economic losses of cystic echinococcosis are substantial, global prevention and control measures should be increased

Mediterranean Jellyfish Venoms: A Review on Scyphomedusae

The production of natural toxins is an interesting aspect, which characterizes the physiology and the ecology of a number of marine species that use them for defence/offence purposes. Cnidarians are of particular concern from this point of view; their venoms are contained in specialized structures–the nematocysts–which, after mechanical or chemical stimulation, inject the venom in the prey or in the attacker. Cnidarian stinging is a serious health problem for humans in the zones where extremely venomous jellyfish or anemones are common, such as in temperate and tropical oceanic waters and particularly along several Pacific coasts, and severe cases of envenomation, including also lethal cases mainly induced by cubomedusae, were reported. On the contrary, in the Mediterranean region the problem of jellyfish stings is quite modest, even though they can have anyhow an impact on public health and be of importance from the ecological and economic point of view owing to the implications on ecosystems and on some human activities such as tourism, bathing and fishing. This paper reviews the knowledge about the various aspects related to the occurrence and the stinging of the Mediterranean scyphozoan jellyfish as well as the activity of their venoms

Mechanisms of Estrogens’ Dose-Dependent Neuroprotective and Neurodamaging Effects in Experimental Models of Cerebral Ischemia

Ever since the hypothesis was put forward that estrogens could protect against cerebral ischemia, numerous studies have investigated the mechanisms of their effects. Despite initial studies showing ameliorating effects, later trials in both humans and animals have yielded contrasting results regarding the fundamental issue of whether estrogens are neuroprotective or neurodamaging. Therefore, investigations of the possible mechanisms of estrogen actions in brain ischemia have been difficult to assess. A recently published systematic review from our laboratory indicates that the dichotomy in experimental rat studies may be caused by the use of insufficiently validated estrogen administration methods resulting in serum hormone concentrations far from those intended, and that physiological estrogen concentrations are neuroprotective while supraphysiological concentrations augment the damage from cerebral ischemia. This evidence offers a new perspective on the mechanisms of estrogens’ actions in cerebral ischemia, and also has a direct bearing on the hormone replacement therapy debate. Estrogens affect their target organs by several different pathways and receptors, and the mechanisms proposed for their effects on stroke probably prevail in different concentration ranges. In the current article, previously suggested neuroprotective and neurodamaging mechanisms are reviewed in a hormone concentration perspective in an effort to provide a mechanistic framework for the dose-dependent paradoxical effects of estrogens in stroke. It is concluded that five protective mechanisms, namely decreased apoptosis, growth factor regulation, vascular modulation, indirect antioxidant properties and decreased inflammation, and the proposed damaging mechanism of increased inflammation, are currently supported by experiments performed in optimal biological settings

Neuroprotective Efficacy of the Peroxisome Proliferator-Activated Receptor-gamma Ligand in Chronic Cerebral Hypoperfusion

WOS: 000294411200002PubMed: 21675957Chronic cerebral hypoperfusion can cause learning and memory impairment and neuronal damage resembling the effects observed in vascular dementia. PPAR-gamma agonists were shown to modulate inflammatory response and neuronal death following cerebral ischemia. The present study was designed to evaluate possible neuroprotective effects of rosiglitazone, a PPAR-gamma agonist, in rat model of chronic cerebral hypoperfusion. Cerebral hypoperfusion was induced by permanent bilateral occlusion of the common carotid arteries. Oral administration of rosiglitazone (1.5, 3, and 6 mg/kg/day) or vehicle was carried out for 5 weeks, starting one week before the surgery. Cognitive performance was assessed using the Morris water maze. The density of S100B protein-immunoreactive astrocytes and the OX-42-labeled microglial activation were estimated. Synaptogenesis was also evaluated by the measurement of synaptophysin, the pre-synaptic vesicular protein, level via western blotting technique. Cerebral hypoperfusion for 30 days induced a significant cognitive impairment along with hyperactivation of both microglial and astroglial cells, and reduction of synaptophysin level. Rosiglitazone treatment (3 and 6 mg/kg) not only suppressed the activation of astrocytes and microglia markedly but also alleviated the impairment of memory and increased the synaptophysin level. In conclusion, our results suggest that the chronic administration of rosiglitazone significantly prevents chronic cerebral hypoperfusion-induced brain damage, at least, partly through suppressing glial activation and preserving synaptic plasticity. Thus, it appears that rosiglitazone may be a promising pharmacological agent in the development of therapeutic approaches for the prevention or treatment of cerebrovascular diseases.Turkish Scientific Research Council (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [108S114, SBAG-HD-303]We have gratefully acknowledged the Research Projects Fund of Turkish Scientific Research Council (TUBITAK) for providing financial support that made the present study possible (the grant # 108S114, SBAG-HD-303)