No abstract

Landscape ecology has evolved rapidly as a terrestrial discipline over the past centuries due to an increased concern over habitat loss and fragmentation. Proceedings in the marine realm have been comparatively scarce, even though many key habitats in marine ecosystems are becoming equally fragmented. We sampled the macrofauna associated with blue mussel beds in naturally patchy landscapes of islands and reefs in the non-tidal Baltic Sea and tested for the effect of island area, isolation and reef depth on local species richness and composition. The fauna was also compared among islands and reefs. Contrary to expectations, species richness did not increase with island size, and species diversity was higher on deep reefs compared to shallow reefs and islands protruding from the water. Region and depth also had an effect on species assemblage. Geographical distance to nearest island or reef showed no correlation with species richness but correlated positively with faunal density, i.e. a higher degree of isolation increased density. In accordance with other marine studies, our data, therefore, supports the nearest refuge hypothesis, postulating that mobile invertebrates disperse over areas of non-habitat and then concentrate in isolated habitats because habitats in isolation are the nearest available refuge. We show that terrestrial landscape approaches cannot be directly applied to the study system. This has important implications for the planning of marine protected areas and their management.

No abstract

Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a master regulator of mitochondria biogenesis and cell stress playing a role in metabolic and degenerative diseases. In the brain PGC-1α expression has been localized mainly to GABAergic interneurons but its overall role is not fully understood. We observed here that the protein levels of γ-aminobutyric acid (GABA) type A receptor-α2 subunit (GABARα2) were increased in hippocampus and brain cortex in transgenic (Tg) mice overexpressing PGC-1α in neurons. Along with this, GABARα2 expression was enhanced in the hippocampus of the PGC-1α Tg mice, as shown by quantitative PCR. Double immunostaining revealed that GABARα2 co-localized with the synaptic protein gephyrin in higher amounts in the striatum radiatum layer of the hippocampal CA1 region in the Tg compared with Wt mice. Electrophysiology revealed that the frequency of spontaneous and miniature inhibitory postsynaptic currents (mIPSCs) was increased in the CA1 region in the Tg mice, indicative of an augmented GABAergic transmission. Behavioral tests revealed an increase for anxiety-like behavior in the PGC-1α Tg mice compared with controls. To study whether drugs acting on PPARγ can affect GABARα2, we employed pioglitazone that elevated GABARα2 expression in primary cultured neurons. Similar results were obtained using the specific PPARγ agonist, N-(2-benzoylphenyl)-O-[2-(methyl-2-pyridinylamino) ethyl]-L-tyrosine hydrate (GW1929). These results demonstrate that PGC-1α regulates GABARα2 subunits and GABAergic neurotransmission in the hippocampus with behavioral consequences. This indicates further that drugs like pioglitazone, widely used in the treatment of type 2 diabetes, can influence GABARα2 expression via the PPARγ/PGC-1α system.