Despite growing interplay between ecological and evolutionary studies, the question of how biodiversity influences evolutionary dynamics within species remains understudied. Here, using a classical model of phenotypic evolution in species occupying a patchy environment, but introducing global change affecting patch conditions, we show that biodiversity can inhibit species’ evolution during global change. The presence of several species increases the chance that one or more species are pre‐adapted to new conditions, which restricts the ecological opportunity for evolutionary responses in all the species. Consequently, environmental change tends to select for changes in species abundances rather than for changing phenotypes within each species. The buffering effects of species diversity that we describe might be one important but neglected explanation for widely observed niche conservatism in natural systems. Furthermore, the results show that attempts to understand biotic responses to environmental change need to consider both ecological and evolutionary processes in a realistically diverse setting.

Foundation species enhance biodiversity and multifunctionality across many systems; however, whether foundation species patch configuration mediates their ecological effects is unknown. In a 6-month field experiment, we test which attributes of foundation species patch configuration - i.e. patch size, total patch area, perimeter, area-perimeter ratio, or connectivity - control biodiversity, stability and multifunctionality by adding a standardised density of mussel foundation species in patches of 1, 5, 10, 30, 60, 90 or 180 individuals to a southeastern US salt marsh. Over 67% of response variables increased with clustering of mussels, responses that were driven by increases in area-perimeter ratio (33%), decreases in perimeter (29%), or increases in patch size (5%), suggesting sensitivity to external stressors and/or dependence on foundation species-derived niche availability and segregation. Thus, mussel configuration - by controlling the relative distribution of multidimensional patch interior and edge niche space - critically modulates this foundation species' effects on ecosystem structure, stability and function.

µ-Opioid receptor activation underpins clinical analgesia and is the central event in the abuse of narcotics. Continued opioid use produces tolerance to the acute effects of the drug and adaptations that lead to physical and psychological dependence. Continued µ-receptor signaling provides the engine for these adaptations, with most evidence suggesting that chronic agonist treatment produces only limited alterations in primary µ-opioid receptor signaling. Here we examine agonist regulation of µ-opioid receptor function, and whether this is altered by chronic treatment. Receptor phosphorylation is thought to be the key initial event in agonist regulation of the µ-opioid receptor, providing a signal for acute receptor desensitization and also subsequent receptor resensitization. Morphine appears to produce qualitatively and quantitatively different µ-receptor phosphorylation than other agonists, but the consequences of this remain obscure, at least in neurons. There is no evidence that agonist-induced µ-opioid receptor phosphorylation changes in chronically morphine-treated animals, although receptor regulation appears to be altered. Thus, as receptor phosphorylation and resensitization appear to maintain continued signaling through the µ-opioid receptor, these two events are crucial in facilitating adaptations to chronic opioid treatment, and the possibility that agonist-specific phosphorylation can contribute to the development of different adaptations remains open.

Background: There is evidence to suggest that the midbrain periaqueductal grey (PAG) has a role in migraine and the actions of the anti-migraine drug sumatriptan. In the present study we examined the serotonergic modulation of GABAergic and glutamatergic synaptic transmission in rat midbrain PAG slices in vitro.