A Dysfunctional Sense of Smell: The Irreversibility of Olfactory Evolution in Free-Living Pigs

Artificial selection began to override natural selection in domesticated wild boar and other species about 10,000 years ago. The intentional selection of a desired phenotypic trait is a complex process, and comes along with unexpected or even unwanted changes in other traits, because of epistatic gene effects, and ontogenetic constraints. The loss of brain mass in domestic ungulates is related to selection for reduced reaction to external stimuli. Evolutionary losses in body structures and genes were once considered mostly irreversible, in keeping with Dollo’s law. Here we studied the biochemical and the histological functioning of the free-living pigs (FLPs) olfactory system, to see if and to what extent does FLPs regain a full sense of smell, as compared to the domestic pigs and wild boar Sus scrofa. In our samples both wild boars and FLPs have significantly larger brain per unit mass than domestic pigs, and FLPs’ brains are not significantly smaller than wild boar’s. Similarly, both wild boars and FLPs have significantly higher cell density than domestic pigs in the olfactory mucosa. Yet, at the functional level, olfactory marker protein and neuropeptide Y, both of which are important to the correct functioning of the sense of smell, are fully expressed only in wild boar. These results suggest that FLPs reacquired structural, but not the biochemical capability in their olfactory system.     

Cobalt staining of Actinia equina nematocysts.

Nematocysts of Actinia equina are stained black by incubation in 2% CoCl2 followed by an aqueous wash and H2S treatment. They are also stained positively by morin. Nematocysts isolated from the acrorhage were found to have a high concentration of calcium of which only 30% was "free." It is suggested that the high concentration of calcium in the nematocysts accounts for their staining by cobalt and morin. Cobalt staining offers a simple and effective technique for investigation of nemotocysts.     

Adaptation morphologique de l'acrorrhage chez Actinia equina L.

Résumé L'analyse ultra-structurale de l'acrorrhage d'Actinia equina L. a permis de montrer une adaptation histologique au décollement de l'ectoderme lors de la réponse de l'actinie à une agression. La zone basale et digitée des cellules ectodermiques est très vacuolisée. La turgescence de l'acrorrhage provoque une extension de la mésoglée; on observe un écartement des bases cellulaires et la rupture des vésicules facilite la séparation de l'ectoderme et de la mésoglée. Celle-ci a lieu après ancrage des nématocystes atriches dans les tissus de l'agresseur, et retrait de l'Actinie.

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Morphological adaptation of the acrorhagi of Actinia equina L.

Summary The ultrastructural analysis of the acrorhagi of Actinia equina reveals histological adaptations to the specific detachment of this brightly colored strip of ectoderm in case of being attached. The basal zone of the ectoderm cells is highly vacuolated. The turgidity of the acrorhagous provokes an extension of the mesoglea. The separation of the ectoderm is facilitated by rupture of the vacuoles and the specific arrangement of the filament containing branched bases of the cells. When the ectoderm, which contains numerous nematocysts, is fixed in the tissue of a agressor, this one detaches.

     

Experimental habituation of aggression in the sea anemone Actinia equina

Behavioural plasticity in Actinia equina (L.) was examined in experimental contests using a range of pedal disc colour phenotypes, which characterize 3 known, ecologically distinct morphs. With repeated pairing of individuals in auto-phenotypic encounters, habituation was easily induced in the 2 mid-shore morphs, but was not obvious in the less aggressive, low-shore form. Subsequent pairing with a different partner revealed that anemones remained aggressive towards a novel opponent. Following novel contact, repairing of the dark red pedal phenotype with the original partner provided some evidence of retention of habituation to a previous opponent, and thus of a specific inducible memory.     

Laceration,knospung und heteromorphose bei Actinia equina L.

Ohne Zusammenfassung     

Actions of adenylyl compounds in the pedal disc of the cnidarian Actinia equina

1. The actions of adenylyl compounds were investigated in the circular muscle of the pedal disc of the sea anenome Actinia equina.2. Adenosine, adenosine 5'-diphosphate and adenosine 5'-triphosphate (ATP), but not adenosine 5'-monophosphate or the analogues of ATP, α,β-methylene ATP, and 2-methylthio ATP, caused concentration-dependent contractions.3. Neurogenic contractions in response to electrical field stimulation were not consistently affected by any of the adenylyl compounds and could be either potentiated or almost abolished by them.4. Reactive Blue 2, a vertebrate P₂-purinoceptor antagonist, caused concentration-dependent contractions which were mediated by nerves, being blocked by the anaesthetic chlorobutanol.5. The pharmacological profile of the adenylyl compounds in the pedal disc of Actinia equina is different from that observed in other invertebrate species and adds to the greater diversity of such profiles in invertebrates than in vertebrates.     

The First Finding of the Actinia Synandwakia hozawai in the Sea of Okhotsk

The finding of the actinia Synandwakia hozawai in the coastal waters of northern Sakhalin (Sea of Okhotsk) suggests a wider range of this species, which was previously only known to inhabit the coastal waters of eastern Japan. Data are presented on the morphology of the S. hozawai specimen from the Sea of Okhotsk and the types of its nematocysts.     

Cathepsin S and cruzipain are inhibited by equistatin from Actinia equina.

Cathepsin S has been isolated for the first time from human tissue. It has a molecular mass of 24 kDa and an isoelectric point in the range of 8.2 to 8.6. The enzyme is inhibited by equistatin, which belongs to the thyropins, a new family of protein inhibitors, with an inhibition constant of Ki = 0.40 +/- 0.07 nM. Cruzipain, a cathepsin L-like enzyme sharing a 130 amino acid long C-terminal extension, is also strongly inhibited by equistatin (Ki = 0.028 +/- 0.006 nM). Together with previously reported data, these results further indicate that a functional heterogeneity exists among thyropin inhibitors, as demonstrated by their interaction with cathepsin S and cruzipain.     

On the pathogenesis of galactosamine hepatitis. Indications of extrahepatocellular mechanisms responsible for liver cell death.

In order to evaluate the pathogenesis of galactosamine hepatitis, the action of galactosamine on mast cells, and alteration in the complement system suring the course of this experimental injury were studied. It has been previously demonstrated that rat livers after colectomy are refractory to galactosamine-induced liver cell necrosis and inflammation. For this reason colectomized animals were used to see whether the biochemical alterations produced by this aminosugar and thought to be responsible for cell death developed. Results showed: 1. galactosamine potently degranulates mast cells in vivo and in vitro, 2. the complement system is a) activated during the course of galactosamine hepatitis, probably by circulating endotoxins, and b) is essential for liver cell death in galactosamine hepatitis, and 3. colectomy does not prevent biochemical changes known to occur during galactosamine metabolism. It is concluded that death of galactosamine-injured liver cells is triggered by extrahepatocellular mechanisms, which lead ultimately to an activated complement system by endotoxins. It is postulated that related mechanism may also occur in viral hepatitis and in fulminant hepatic failure in man.