Caldera resurgence during the 2018 eruption of Sierra Negra volcano, Galápagos Islands.

Recent large basaltic eruptions began after only minor surface uplift and seismicity, and resulted in caldera subsidence. In contrast, some eruptions at Galápagos Island volcanoes are preceded by prolonged, large amplitude uplift and elevated seismicity. These systems also display long-term intra-caldera uplift, or resurgence. However, a scarcity of observations has obscured the mechanisms underpinning such behaviour. Here we combine a unique multiparametric dataset to show how the 2018 eruption of Sierra Negra contributed to caldera resurgence. Magma supply to a shallow reservoir drove 6.5 m of pre-eruptive uplift and seismicity over thirteen years, including an Mw5.4 earthquake that triggered the eruption. Although co-eruptive magma withdrawal resulted in 8.5 m of subsidence, net uplift of the inner-caldera on a trapdoor fault resulted in 1.5 m of permanent resurgence. These observations reveal the importance of intra-caldera faulting in affecting resurgence, and the mechanisms of eruption in the absence of well-developed rift systems.

Cryptic evolved melts beneath monotonous basaltic shield volcanoes in the Galápagos Archipelago.

Many volcanoes erupt compositionally homogeneous magmas over timescales ranging from decades to millennia. This monotonous activity is thought to reflect a high degree of chemical homogeneity in their magmatic systems, leading to predictable eruptive behaviour. We combine petrological analyses of erupted crystals with new thermodynamic models to characterise the diversity of melts in magmatic systems beneath monotonous shield volcanoes in the Galápagos Archipelago (Wolf and Fernandina). In contrast with the uniform basaltic magmas erupted at the surface over long timescales, we find that the sub-volcanic systems contain extreme heterogeneity, with melts extending to rhyolitic compositions. Evolved melts are in low abundance and large volumes of basalt flushing through the crust from depth overprint their chemical signatures. This process will only maintain monotonous activity while the volume of melt entering the crust is high, raising the possibility of transitions to more silicic activity given a decrease in the crustal melt flux.

Magma chambers versus mush zones: constraining the architecture of sub-volcanic plumbing systems from microstructural analysis of crystalline enclaves.

There are clear microstructural differences between mafic plutonic rocks that formed in a dynamic liquid-rich environment, in which crystals can be moved and re-arranged by magmatic currents, and those in which crystal nucleation and growth are essentially in situ and static. Crystalline enclaves, derived from deep crustal mushy zones and erupted in many volcanic settings, afford a unique opportunity to use the understanding of microstructural development, established from the study of intrusive plutons, to place constraints on the architecture of sub-volcanic systems. Here, we review the relevant microstructural literature, before applying these techniques to interrogate the crystallization environments of enclaves from the Kameni Islands of Santorini and Rábida Volcano in the Galápagos. Crystals in samples of deep-sourced material from both case studies preserve evidence of at least some time spent in a liquid-rich environment. The Kameni enclaves appear to record an early stage of crystallization during which crystals were free to move, with the bulk of crystallization occurring in a static, mushy environment. By contrast, the Rábida enclaves were sourced from an environment in which hydrodynamic sorting and re-arrangement by magmatic currents were common, consistent with a liquid-rich magma chamber. While presently active volcanoes are thought to be underlain by extensive regions rich in crystal mush, these examples preserve robust evidence for the presence of liquid-rich magma chambers in the geological record. This article is part of the Theo Murphy meeting issue 'Magma reservoir architecture and dynamics'.

Some fluid mechanical constraints on crystallization and recharge within sills.

The injection of hot magma into a sill can lead to heating and melting of the walls and roof of the reservoir while the injected magma cools and crystallizes. If the crystals are relatively dense, they will try to sediment from the injected magma to form a cumulate layer. In this cumulate layer, the crystals form a porous framework which traps the melt as it is built up. As the melt within the sill continually cools and precipitates dense crystals, there will be a gradual reduction in the density of the remaining silicate liquid. As a result, the melt which is progressively trapped in the pore space of the cumulate layer will become stably stratified in density. Using an idealized model of the fluid mechanical and thermodynamical principles, we explore some of the controls on the thickness and density stratification of cumulate layers following replenishment of a sill-like magma chamber. We show the balance between jamming of the crystal laden melt to form a homogeneous layer and the formation of a stratified cumulate zone depends on the cooling time scale compared to the sedimentation time scale. A key finding is that the composition and stratification in a packed crystal-melt suspension and the associated cumulate layer formed by cooling an intrusion of hot melt injected into the crust may have considerable variability, depending on the properties of the overlying roof melt and the size and hence fall speed of crystals which form in the melt. This article is part of the Theo Murphy meeting issue 'Magma reservoir architecture and dynamics'.

Triggering of major eruptions recorded by actively forming cumulates.

Major overturn within a magma chamber can bring together felsic and mafic magmas, prompting de-volatilisation and acting as the driver for Plinian eruptions. Until now identification of mixing has been limited to analysis of lavas or individual crystals ejected during eruptions. We have recovered partially developed cumulate material ('live' cumulate mush) from pyroclastic deposits of major eruptions on Tenerife. These samples represent "frozen" clumps of diverse crystalline deposits from all levels in the developing reservoir, which are permeated with the final magma immediately before eruptions. Such events therefore record the complete disintegration of the magma chamber, leading to caldera collapse. Chemical variation across developing cumulus crystals records changes in melt composition. Apart from fluctuations reflecting periodic influxes of mafic melt, crystal edges consistently record the presence of more felsic magmas. The prevalence of this felsic liquid implies it was able to infiltrate the entire cumulate pile immediately before each eruption.

Pharmacological characterisation of the thermogenic effect of bupropion.

The pharmacological mechanism of bupropion's thermogenic effect has been investigated in female Wistar rats by measuring oxygen consumption at thermoneutrality (29 degrees C). Bupropion (30 mg/kg) rapidly increased oxygen consumption (VO2) with a maximum effect at 30 min, and VO2 remained elevated throughout the 4-h experimental period. The nonselective 5-hydroxytryptamine (5-HT or serotonin) receptor antagonist, metergoline (1 mg/kg), and the alpha1-adrenoceptor antagonist, prazosin (1 mg/kg), had no effect on the VO2 response to bupropion, whereas the alpha2-adrenoceptor antagonist, RS79948 [(8aR, 12aS, 13aS)-5,8,8a,9,10,11,12,12a,13,13a-decahydro-3-methoxy-12-(ethylsulphonyl)-6H-isoquino[2,1-g][1,6]-naphthyridine hydrochloride] (1 mg/kg), potentiated the response. The VO2 response to bupropion during the first 60 min was significantly inhibited by a high dose of the nonselective beta-adrenoceptor antagonist, propranolol (20 mg/kg), but it had no effect at a low dose (1 mg/kg). Pretreatment with the dopamine D2/D1 receptor antagonist, (+)butaclamol (200 microg/kg), caused a partial, but significant, inhibition (P<0.01) of the VO2 response to bupropion during the first 60 min, and this antagonist abolished the effect of bupropion between 90 and 240 min. Pretreatment with a combination of a high dose of propranolol (20 mg/kg) and (+)butaclamol (200 microg/kg) prevented any increase in VO2 induced by bupropion. It is concluded that the beta3-adrenoceptor subtype, as well as dopamine D2/D1 receptors, is responsible for the increase in oxygen consumption induced by bupropion. We have previously demonstrated that bupropion did not significantly reduce food intake in rats. Hence, in this species, its weight-reducing action predominantly results from thermogenesis mediated via activation of beta3-adrenergic and dopamine D2/D1 receptors. Because bupropion has also been reported not to alter food intake in the clinic, thermogenesis may also contribute to its antiobesity effect in man.

Anorectic actions of prolactin-releasing peptide are mediated by corticotropin-releasing hormone receptors.

Prolactin-releasing peptide (PrRP) reduces food intake and body weight and modifies body temperature when administered centrally in rats, suggesting a role in energy homeostasis. However, the mediators of PrRP's actions are unknown. The present study, therefore, first examined the possible involvement of the anorectic neuropeptides corticotropin-releasing hormone (CRH) and the melanocortins (e.g., alpha-melanocyte-stimulating hormone) in PrRP's effects on food intake and core body temperature and, second, determined if PrRP affects energy expenditure by measuring oxygen consumption (Vo2). Intracerebroventricular injection of PrRP (4 nmol) to 24-h-fasted male Sprague-Dawley rats decreased food intake and modified body temperature. Blockade of central CRH receptors by intracerebroventricular coadministration of the CRH receptor antagonist astressin (20 microg) reversed the PrRP-induced reduction in feeding. However, astressin's effect on PrRP-induced changes in body temperature was complicated because the antagonist itself caused a slight rise in body temperature. In contrast, intracerebroventricular coadministration of the melanocortin receptor-3/4 antagonist SHU-9119 (0.1 nmol) had no effect on any of PrRP's actions. Finally, intracerebroventricular injection of PrRP (4 nmol) caused a significantly greater Vo2 over a 3-h test period compared with vehicle-treated rats. These results show that the anorectic actions of PrRP are mediated by central CRH receptors but not by melanocortin receptors-3/4 and that PrRP can modify Vo2.

Comparison of the thermogenic and hypophagic effects of sibutramine's metabolite 2 and other monoamine reuptake inhibitors.

The thermogenic and hypophagic effects of sibutramine's metabolite (metabolite 2), a 5-hydroxytryptamine (5-HT) and noradrenaline reuptake inhibitor, were investigated in rats and compared with duloxetine and bupropion. Metabolite 2 increased colonic temperature for 2.5-4.5 h. Duloxetine was also thermogenic but was less effective than metabolite 2. Bupropion similarly increased colonic temperature and was as efficacious, but less potent, than metabolite 2. At -8 degrees C, metabolite 2, duloxetine and bupropion all decreased response to heat reinforcement and reduced colonic temperature. Metabolite 2 produced a sustained increase in oxygen consumption (VO(2)) at 29 degrees C from 90 to 240 min, whereas duloxetine was far less effective. Bupropion rapidly enhanced VO(2), but its effect was less prolonged than that of metabolite 2. Metabolite 2 markedly reduced 24-h food intake. Duloxetine decreased feeding although its effect was shorter-lived, but bupropion was without effect. Thus, sibutramine's antiobesity action is probably attributable to effects on energy intake and expenditure. Duloxetine shares these properties, but is generally less efficacious. Any potential weight-reducing effect of bupropion is probably due to thermogenesis.

Leptin directly stimulates thermogenesis in skeletal muscle.

Using a method involving repeated oxygen uptake (MO(2)) determinations in skeletal muscle ex vivo, the addition of leptin was found to increase MO(2) in soleus muscles from lean mice. These effects were found to be inhibited by phosphatidylinositol 3-kinase inhibitors, absent in muscles from obese Lepr(db) mice which have the dysfunctional long form of leptin receptor, and blunted in muscles from diet-induced obese mice in the fed state but not during fasting. These findings indicate that leptin has direct thermogenic effects in skeletal muscle, and that these effects require both the long form of leptin receptors and phosphatidylinositol 3-kinase signalling.