Non-indigenous species refined national baseline inventories: A synthesis in the context of the European Union's Marine Strategy Framework Directive.

Refined baseline inventories of non-indigenous species (NIS) are set per European Union Member State (MS), in the context of the Marine Strategy Framework Directive (MSFD). The inventories are based on the initial assessment of the MSFD (2012) and the updated data of the European Alien Species Information Network, in collaboration with NIS experts appointed by the MSs. The analysis revealed that a large number of NIS was not reported from the initial assessments. Moreover, several NIS initially listed are currently considered as native in Europe or were proven to be historical misreportings. The refined baseline inventories constitute a milestone for the MSFD Descriptor 2 implementation, providing an improved basis for reporting new NIS introductions, facilitating the MSFD D2 assessment. In addition, the inventories can help MSs in the establishment of monitoring systems of targeted NIS, and foster cooperation on monitoring of NIS across or within shared marine subregions.

Liver transcriptome analysis in gilthead sea bream upon exposure to low temperature.

BACKGROUND: Water temperature greatly influences the physiology and behaviour of teleost fish as other aquatic organisms. While fish are able to cope with seasonal temperature variations, thermal excursions outside their normal thermal range might exceed their ability to respond leading to severe diseases and death.Profound differences exist in thermal tolerance across fish species living in the same geographical areas, promoting for investigating the molecular mechanisms involved in susceptibility and resistance to low and high temperatures toward a better understanding of adaptation to environmental challenges. The gilthead sea bream, Sparus aurata, is particularly sensitive to cold and the prolonged exposure to low temperatures may lead to the "winter disease", a metabolic disorder that significantly affects the aquaculture productions along the Northern Mediterranean coasts during winter-spring season. While sea bream susceptibility to low temperatures has been extensively investigated, the cascade of molecular events under such stressful condition is not fully elucidated. RESULTS: In the present study two groups of wild sea bream were exposed for 21 days to two temperature regimes: 16 ± 0.3°C (control group) and 6.8 ± 0.3°C (cold-exposed group) and DNA microarray analysis of liver transcriptome was carried out at different time points during cold exposure.A large set of genes was found to be differentially expressed upon cold-exposure with increasingly relevant effects being observed after three weeks at low temperature. All major known responses to cold (i.e. anti-oxidant response, increased mitochondrial function, membrane compositional changes) were found to be conserved in the gilthead sea bream, while, evidence for a key role of unfolded protein response (UPR) to endoplasmic reticulum (ER) stress, during short- and long-term exposure to cold is reported here for the first time. CONCLUSIONS: Transcriptome data suggest a scenario where oxidative stress, altered lipid metabolism, ATP depletion and protein denaturation converge to induce ER stress. The resulting UPR activation further promotes conditions for cell damage, and the inability to resolve ER stress leads to severe liver dysfunction and potentially to death.

4-methyl benzylamine stimulates food consumption and counteracts the hypophagic effects of amphetamine acting on brain Shaker-like Kv1.1 channels.

1.--4-methyl benzylamine (4-MBZ; 28 microg, 231 nmol) elicits a hyperphagic response in starved mice in contrast to the hypophagia induced by the parent compound benzylamine (BZ; 33 microg, 231 nmol) or by amphetamine (AMPH, 2 mug). 2.--In mice starved for only 4 h, and therefore with little stimulation to eat, the maximal increase in food consumption induced by intracerebroventricular (i.c.v.)-injected 4-MBZ was 190% over that of the controls (ED(50) 8.3+/-2.7 microg mouse(-1); 68+/-22 nmol mouse(-1)), whereas after i.p. administration, these values were 160% and approximately 129 mg kg(-1), respectively. 3.--The hyperphagic effect of 4-MBZ was reduced by more than 60% in mice pretreated with antisense oligodeoxyribonucleotide (aODN(1)) previously found to selectively inhibit (over 50%) the expression of Shaker-like Kv1.1 channels. 4.--In mice highly stimulated to eat after 12-h fasting, 4-MBZ (28 microg) significantly reduced (to about 70%) the hypophagic response by AMPH (2 microg) or BZ (33 microg). Conversely, these two compounds reduced (respectively, by 69 and 44%) the hyperphagic response of 4-MBZ in 4-h fasting mice. 5.--4-MBZ (28 microg) also reduced the hypermotility and the stimulation of inspection activity elicited by AMPH in mice and the release of DA stimulated by AMPH (2 microg) from the nucleus accumbens of rats. We hypothesize that 4-MBZ elicits hyperphagic effects probably by opening Shaker-like Kv1.1 subtypes in the brain, whereas AMPH and BZ are hypophagic by blocking these channels.

Antisense knockdown of the Shaker-like Kv1.1 gene abolishes the central stimulatory effects of amphetamines in mice and rats.

Amphetamine (AMPH) is an indirect sympathomimetic compound classified as a substrate-type releaser that distinguishes it from other stimulants that act as uptake 1 blockers, such as cocaine (COC). In mammals, AMPH elicits central stimulation, hypermotility, anorexia, analgesia and analeptic activity, mainly through the increase of extracellular brain dopamine (DA). The inversion of vesicular transporters and/or intravesicular alkalinization is assumed to have a role in AMPH-induced exocytosis. However, the action mechanism of this compound has not yet been completely clarified. Recent evidence on the action of AMPHs indicates potassium channel-blocking properties in peripheral tissues. We investigated the possible involvement of a Shaker-like Kv1.1 channel subtype in the central effects of AMPH, using an antisense oligodeoxyribonucleotide (aODN) that specifically and reversibly inhibits the expression of these channels in the brain. The effect of aODN pretreatments was studied by evaluating the modification of behavioral effects induced in mice through the intracerebroventricular administration of AMPH, COC, or other compounds. The aODN in mice almost completely blocked the stimulatory effects of AMPH and other releasers but was ineffective in reducing the central activity of COC. In aODN-pretreated rats a strong reduction of the AMPH, but not of the COC-stimulated DA efflux from nucleus accumbens was observed. Our results suggest that the stimulant effects of AMPH and chemically related compounds, but not COC, require the presence of functionally active Kv1.1 channels in the brain.