Author Correction: Forearc carbon sink reduces long-term volatile recycling into the mantle.

An Amendment to this paper has been published and can be accessed via a link at the top of the paper.

Author Correction: Forearc carbon sink reduces long-term volatile recycling into the mantle.

Change history: In this Article, the original affiliation 2 was not applicable and has been removed. In addition, in the Acknowledgements there was a statement missing and an error in a name. These errors have been corrected online.

Forearc carbon sink reduces long-term volatile recycling into the mantle.

Carbon and other volatiles in the form of gases, fluids or mineral phases are transported from Earth's surface into the mantle at convergent margins, where the oceanic crust subducts beneath the continental crust. The efficiency of this transfer has profound implications for the nature and scale of geochemical heterogeneities in Earth's deep mantle and shallow crustal reservoirs, as well as Earth's oxidation state. However, the proportions of volatiles released from the forearc and backarc are not well constrained compared to fluxes from the volcanic arc front. Here we use helium and carbon isotope data from deeply sourced springs along two cross-arc transects to show that about 91 per cent of carbon released from the slab and mantle beneath the Costa Rican forearc is sequestered within the crust by calcite deposition. Around an additional three per cent is incorporated into the biomass through microbial chemolithoautotrophy, whereby microbes assimilate inorganic carbon into biomass. We estimate that between 1.2 × 108 and 1.3 × 1010 moles of carbon dioxide per year are released from the slab beneath the forearc, and thus up to about 19 per cent less carbon is being transferred into Earth's deep mantle than previously estimated.

Identifying and Understanding Microbial Methanogenesis in CO2 Storage.

Carbon capture and storage (CCS) is an important component in many national net-zero strategies. Ensuring that CO2 can be safely and economically stored in geological systems is critical. To date, CCS research has focused on the physiochemical behavior of CO2, yet there has been little consideration of the subsurface microbial impact on CO2 storage. However, recent discoveries have shown that microbial processes (e.g., methanogenesis) can be significant. Importantly, methanogenesis may modify the fluid composition and the fluid dynamics within the storage reservoir. Such changes may subsequently reduce the volume of CO2 that can be stored and change the mobility and future trapping systematics of the evolved supercritical fluid. Here, we review the current knowledge of how microbial methanogenesis could impact CO2 storage, including the potential scale of methanogenesis and the range of geologic settings under which this process operates. We find that methanogenesis is possible in all storage target types; however, the kinetics and energetics of methanogenesis will likely be limited by H2 generation. We expect that the bioavailability of H2 (and thus potential of microbial methanogenesis) will be greatest in depleted hydrocarbon fields and least within saline aquifers. We propose that additional integrated monitoring requirements are needed for CO2 storage to trace any biogeochemical processes including baseline, temporal, and spatial studies. Finally, we suggest areas where further research should be targeted in order to fully understand microbial methanogenesis in CO2 storage sites and its potential impact.

Complex Microbial Communities Drive Iron and Sulfur Cycling in Arctic Fjord Sediments.

Glacial retreat is changing biogeochemical cycling in the Arctic, where glacial runoff contributes iron for oceanic shelf primary production. We hypothesize that in Svalbard fjords, microbes catalyze intense iron and sulfur cycling in low-organic-matter sediments. This is because low organic matter limits sulfide generation, allowing iron mobility to the water column instead of precipitation as iron monosulfides. In this study, we tested this with high-depth-resolution 16S rRNA gene libraries in the upper 20 cm at two sites in Van Keulenfjorden, Svalbard. At the site closer to the glaciers, iron-reducing Desulfuromonadales, iron-oxidizing Gallionella and Mariprofundus, and sulfur-oxidizing Thiotrichales and Epsilonproteobacteria were abundant above a 12-cm depth. Below this depth, the relative abundances of sequences for sulfate-reducing Desulfobacteraceae and Desulfobulbaceae increased. At the outer station, the switch from iron-cycling clades to sulfate reducers occurred at shallower depths (∼5 cm), corresponding to higher sulfate reduction rates. Relatively labile organic matter (shown by δ13C and C/N ratios) was more abundant at this outer site, and ordination analysis suggested that this affected microbial community structure in surface sediments. Network analysis revealed more correlations between predicted iron- and sulfur-cycling taxa and with uncultured clades proximal to the glacier. Together, these results suggest that complex microbial communities catalyze redox cycling of iron and sulfur, especially closer to the glacier, where sulfate reduction is limited due to low availability of organic matter. Diminished sulfate reduction in upper sediments enables iron to flux into the overlying water, where it may be transported to the shelf.IMPORTANCE Glacial runoff is a key source of iron for primary production in the Arctic. In the fjords of the Svalbard archipelago, glacial retreat is predicted to stimulate phytoplankton blooms that were previously restricted to outer margins. Decreased sediment delivery and enhanced primary production have been hypothesized to alter sediment biogeochemistry, wherein any free reduced iron that could potentially be delivered to the shelf will instead become buried with sulfide generated through microbial sulfate reduction. We support this hypothesis with sequencing data that showed increases in the relative abundance of sulfate reducing taxa and sulfate reduction rates with increasing distance from the glaciers in Van Keulenfjorden, Svalbard. Community structure was driven by organic geochemistry, suggesting that enhanced input of organic material will stimulate sulfate reduction in interior fjord sediments as glaciers continue to recede.

[3H]GABA binding in brains from Huntington's chorea patients: altered regulation by phospholipids?

Binding sites for tritum-labeled gamma-aminobutyric acid (GABA) in cerebellar cortex of Huntington's chorea patients have an increased affinity but unaltered maximum capacity as compared to binding sites in tissue from control patients. A similar binding pattern is produced in control membranes by treatment with Triton X-100, phospholipase C, or glycerophosphoethanolamine. Thus, it is likely that phospholipids or their metabolites regulate the accessibility of the GABA binding site and that this regulation is abnormal in Huntington's chorea.

Cortical and subcortical projected foci in cats: inhibitory action of taurine.

The effects of local application of taurine and isethionic acid on the propagation of the epileptic activity to the mirror area in cats have been studied. Cortical and amygdaloid acute foci were induced by local administration of conjugated estrogens. Taurine proved to be effective in reducing and sometimes in abolishing the appearance of the epileptic propagated elements in the mirror area. When this agent was applied 30 minutes before the induction of the primary focus, the single spike transmission was reduced or prevented; however, the transmission of a seizure was not blocked. No changes in the transmitted phenomena were observed when isethionic acid was administered with the same technique as that used for taurine. The present study stresses the clear antiepileptic activity of taurine in this experimental model, ruling out the possibility of an unspecific interaction with the epileptogenic agents. Moreover, it is suggested that the deamination of taurine is not important for its antiepileptic action.

Catecholamine and octopamine concentrations in brains of patients with Reye syndrome.

Dopamine, norepinephrine, and octopamine levels were estimated in regions of brains obtained postmortem from children who died with Reye syndrome and from age-matched controls. Hypothalamic norepinephrine levels were greatly decreased (to 30 percent of control, p less than 0.02) and octopamine levels were increased (to 700 percent of control, p less than 0.01). Levodopa had little effect on the physiologic condition of the patients. However, CNS dopamine and homovanillic concentrations were not elevated by levodopa, indicating that in the present cases levodopa was not metabolized to its catecholamine products. The findings indicate that the encephalopathy of Reye syndrome (as in other types of hepatic coma) may be linked to the presence of false transmitters in the brain and that levodopa is a rational therapy if administered before irreversible CNS changes occur.

New anticonvulsants: Schiff bases of gamma-aminobutyric acid and gamma-aminobutyramide.

Schiff bases of gamma-aminobutyric acid (gammaAbu) and gamma-aminobutyramide (gammaAbuNH2) were prepared and tested for anticonvulsant and gammaAbu mimetic activity. 4-[[(4-Chlorophenyl)(5-fluoro-2-hydroxyphenyl)methylene]amino]butanoic acid monosodium salt (4) and 4-[[(4-chlorophenyl)(5-fluoro-2-hydroxyphenyl)methylene]amino]butanamide (5) blocked bicuculline-induced lethality and convulsions and displaced [3H]gammaAbu from its membrane binding sites. In the rat dorsal root sensory ganglion, compound 4 exhibited gammaAbu agonist properties. Compounds 4 and 5 are thus anticonvulsants and directly acting gammaAbu mimetics.

Sulphasalazine and PhCL28A inhibit the formation of ethanol- and phenylbutazone-induced rat gastric ulcers: lack of involvement of endogenous prostaglandins?

1. The effects of sulphasalazine (SZP) and PhCL28A on macroscopic lesion formation and ex vivo prostaglandin inactivation were studied in the ethanol (ETOH) and phenylbutazone (PBT) models of gastric ulcers in the rat. Prostaglandin 'synthesis' during homogenisation of the stomachs was also studied in the latter model. 2. Both PhCL28A and SZP when injected i.p. prevented the formation of ETOH- and PBT-induced gastric ulcers with ED50 values of 13 and 41 mgkg-1 (vs ETOH) and 3 and 32 mgkg-1 (vs PBT) for PhCL28A and SZP respectively. However, neither compound was active orally in the dose ranges used (up to 30 mg kg-1 for PhCL28A and 100 mg kg-1 for SZP). 3. Irrespective of the route of administration, SZP (100 mg kg-1) and PhCL28A (30 mg kg-1) produced slight but statistically significant decreases in ex vivo prostaglandin inactivation by 100,000 g cytosolic supernatants prepared from stomachs not receiving ulcerogen. When tested in vitro, PhCL28A (IC50 = 230 nM) was approximatively 480 times mor potent than SZP (IC50 = 110 microM) against rat stomach cytosolic prostaglandin inactivation. 4. Both ETOH (50%, 5 ml kg-1, orally) and PBT (200 mg kg-1, orally) significantly decreased ex vivo gastric cytosolic prostaglandin inactivation. PhCL28A (30 mg kg-1, orally or i.p.) decreased prostaglandin inactivation still further after ulcerogen treatment except when given i.p. before ETOH treatment. SZP (100 mg kg-1) had a similar effect when given orally before PBT treatment. 5. When the prostaglandin content of the stomach homogenates was used as a measure of ex vivo prostaglandin synthesis in the PBT experiments, PhCL28A 30 mg kg-' orally (but not i.p.) produced an 88% increase in prostaglandin E2 (PGE2) levels, but had no effect on 6-keto-PGF,, or thromboxane B2 formation during homogenization. SZP (100mg kg' i.p. or orally) was without effect. 6. We conclude from these results that the anti gastric ulcer activity of SZP and PhCL28A is independent of prostaglandin inactivation and endogenous prostaglandin formation is probably not involved.

Anti-apomorphine effects of phenothiazine drug metabolites.

The potencies in producing muscle relaxation, and in antagonizing apomorphine-induced climbing and hypothermia in mice, were examined for chlorpromazine, levomepromazine and their main metabolites, and for fluphenazine and 7-hydroxy fluphenazine. 3-Hydroxy chlorpromazine was more potent than chlorpromazine in antagonizing apomorphine-induced climbing, while levomepromazine and 3-hydroxy levomepromazine were equipotent in this test. The 3-hydroxy metabolites of chlorpromazine and levomepromazine were more potent than the parent compounds in antagonizing hypothermia, and had significantly weaker muscle relaxant effects than the parent compounds. The 7-hydroxy and N-monodesmethyl metabolites were generally less potent that the parent compounds in antagonizing apomorphine-induced effects. N-Monodesmethyl levomepromazine had a pronounced muscle relaxant effect, like levomepromazine itself. The sulphoxide metabolites of chlorpromazine and levomepromazine were inactive in all tests. Their potencies in these tests indicate that among the metabolites 7-hydroxy chlorpromazine, N-monodesmethyl chlorpromazine and 3-hydroxy levomepromazine, which have all been identified in plasma from patients, may contribute to the antipsychotic effects of the drugs, and furthermore that N-monodesmethyl levomepromazine may contribute to the sedative effects of levomepromazine.

Involvement of the amygdala in the effect of antidepressants on the passive avoidance deficit in bulbectomised rats.

In the present study the role of the amygdala is demonstrated in the effect of antidepressant drugs on passive avoidance learning in bulbectomised rats. Imipramine, amitriptyline, or fluoxetine injected bilaterally (2 X 10 microgram) into the medial part of the amygdala improves passive avoidance learning by bulbectomised rats. Systemic pretreatment with metergoline attenuates the effect of local imipramine or fluoxetine injection. Microinjection of serotonin but not noradrenaline into the amygdala improves passive avoidance learning by bulbectomised rats. The relevance of the amygdala in the behavioral effects of antidepressants in animals is discussed.

The comparative effects of benzodiazepines, progabide and PK 9084 on acquisition of passive avoidance in mice.

Acquisition of passive avoidance following aversive conditioning to a dark compartment was measured in mice under the influence of one of seven benzodiazepines, the GABA-mimetic drug progabide or PK 9084, a nonbenzodiazepine ligand on benzodiazepine receptors. The drugs were administered prior to the training trial and retention was measured in the absence of the drug 24 h later. Oral administration (dose in mg/kg in parentheses) of flunitrazepam (0.1), lorazepam (1.0), nitrazepam (3.0), diazepam (10), flurazepam (10) and chlordiazepoxide (30), all prevented retention whereas progabide (100-800) and PPK 9084 (10-100) were ineffective. In comparison to effects on motor capacity none of the benzodiazepines was outstanding in its acquisition interfering effects.

An analysis of [3H]gamma-aminobutyric acid (GABA) binding in the human brain.

The binding of [3H]GABA to membranes prepared from human brains obtained post morten was examined. This binding was independent of patient sex, age (16--80 years), postmortem interval (4--33 h) or storage time when frozen (0-64 months). In preparations from cerebellar cortex various compounds displaced [3H]GABA binding with the following order of potency: muscimol greater than 3-aminopropanesulfonic acid greater than GABA greater than imidazoleacet acid greater than delta-amino-n-valeric acid greater than 3-hydroxyGABA greater than bicuculline. Other compounds active 'in vitro' included strychnine, homocarnosine and some (e.g. clozapine, thioridazine, pimozide) but not all (chlorpromazine, haloperiodol) neuroleptics. Compounds inactive 'in vitro' included aminooxyacetic acid, baclofen, picrotoxin, anticholinergics, metrazole, anticonvulsants and naloxone. Triton X-100 augmented the [3H]GABA binding (25 nM) by about 10--20-fold in most brain regions. [3H]GABA binding (IC50) was altered in Huntington's chorea and Reye's syndrome, but not in schizophrenics (4-neuroleptic-treated patients) or sudden infant death syndrome. The data presented strongly support the proposal that the measurement of [3H]GABA binding in postmortem human brain offers a reflection of the state of the physiologically relevant GABA receptor.

Enhancing GABAergic transmission reverses the aversive state in rats induced by electrical stimulation of the periaqueductal grey region.

In a proposed rat model for anxiety (electrical stimulation of the periaqueductal grey region), progabide (a GABA agonist) and diazepam both increased the latency to escape to a safe compartment and also the current needed to induce the escape response (escape threshold). Furthermore, the effects of progabide and diazepam were greater than additive in their actions on the escape response as when given together in normally subliminal doses, the combination exerted a marked anti-aversive effect. These actions of the drugs alone or in combination could not be explained by non-specific motor effects. Blockade of GABA receptors by bicuculline greatly reduced or abolished the action of progabide and diazepam (single administration). Sodium valproate, which indirectly augments GABAergic transmission, also increased the escape latency and escape threshold whereas, in contrast, diphenylhydantoin accentuated the aversive effects of stimulation of the periaqueductal grey. Haloperidol increased the escape latency and threshold but not other signs of distress following central stimulation (vocalization, jumping) which were effectively blocked by progabide and diazepam. The action of haloperidol was completely explicable by an interference with motor mechanisms. These results are interpreted as an indication that GABA agonists have an anti-aversive action in this proposed rat model for anxiety and, furthermore, that GABA receptors at least partially mediate the actions of benzodiazepines in this model.

Subchronic administration of GABAergic agonists elevates [3H]GABA binding and produces tolerance in striatal dopamine catabolism.

Directly and indirectly acting GABAergic agonists were assessed for their ability to alter striatal dopamine catabolism after subchronic administration (7-14 days) via subcutaneously implanted osmotic minipumps. THIP, kojic amine and baclofen failed to alter striatal DOPAC and HVA concentrations, but THIP and kojic amine were effective after a single acute dose. Striatal GABA levels proved difficult to elevate when inhibitors of GABA transaminase were released from minipumps, but a high dose of gamma-vinyl GABA increased GABA by 44% of control, although striatal dopamine and DOPAC levels were unaltered. [3H]GABA binding studies revealed that THIP and kojic amine, but not baclofen or gamma-acetylenic GABA, produced large increases in [3H]GABA 'A' binding (150 and 228% of control respectively) which were attributable to altered densities of binding sites without changes in affinity. Despite alterations in GABAergic function, nigrostriatal dopaminergic neurones seem to develop tolerance to the effects of GABAergic drugs.

Cortical modulation of striatal function.

The effect of bilateral section of the corticostriatal projections or of selective bilateral ablation of the frontal cortex on behavioral and biochemical parameters related to striatal function were investigated in the rat. Either lesion almost completely prevented the cataleptogenic action of haloperidol: this effect was observed as soon as 3 days and lasted for at least 3 months after surgery, paralleling a reduction in striatal glutamate uptake. Also, such lesions enhanced the apomorphine-induced stereotyped behavior (as measured 21 days after surgery). In the striatum, dopamine, dihydroxyphenylacetic acid, acetylcholine and substance P levels as well as choline acetyltransferase and glutamic acid decarboxylase activities were unaffected 10 or 21 days after either type of lesion. In the substantia nigra, substance P levels were unchanged 10 days following suction of the frontal cortex, but glutamic acid decarboxylase was reduced at 21 days postsurgery. Cortical lesions only partially prevented the reduction in striatal acetylcholine concentrations and did not affect the increase in striatal dihydroxyphenylacetic acid caused by haloperidol. Finally, lesions of the corticostriatal pathways failed to affect the apomorphine-induced increase in striatal acetylcholine levels, reduction of the potassium (20 mM) evoked [3H]acetylcholine release in striatal slices preloaded with [3H]choline and decrease of striatal dihydroxyphenylacetic acid concentrations. These findings indicate that the frontal cortex influences extrapyramidal function by a mechanism which--in behavioral terms--is antagonistic to dopamine-mediated events. As indicated by the biochemical data, this mechanism does not involve changes in striatal dopaminergic and cholinergic neuron activity. This mechanism may utilize: (1) corticostriatal glutamatergic neurons as suggested by the reduction in striatal glutamate uptake following lesions; and (2) GABAergic pathways as suggested by the reduction of nigral glutamic acid decarboxylase activity as well as by the finding that GABA receptor agonists reinstate haloperidol-induced catalepsy.

Effects of pharmacological manipulation on neurotransmitter and other amino acid levels in the CSF of the Senegalese baboon Papio papio.

The concentrations of GABA, glutamate, aspartate, glycine, taurine, glutamine, asparagine and alanine were determined in the CSF of 10 Senegalese baboons (Papio papio) following initial ketamine anaesthesia and subsequent administration (4 h later) of different compounds known to alter either inhibitory or excitatory neurotransmission. Ketamine itself was apparently without effect as the administration of a second dose of ketamine did not significantly alter the levels of any of the amino acids studied, although GABA levels tended to decrease. The presence of haemolysed material in occasional samples was associated with high GABA, glutamate, aspartate, taurine and asparagine levels. Therefore only haemolysate-free samples were included for analysis. Of the compounds administered, gamma-vinyl GABA had the most evident effect on CSF amino acid levels, increasing GABA (greater than 5-fold) and decreasing glutamate (greater than 50%), aspartate (40-50%), asparagine (20%) and alanine (30-35%) levels. The changes in GABA, glutamate and aspartate were still apparent 24 h post-gamma-vinyl GABA administration. In contrast, sodium valproate did not significantly alter the CSF levels of any of the amino acids studied. Upon acute administration allylglycine decreased the CSF concentrations of GABA and alanine, but not glutamate. These alterations are unlikely related to the occurrence of allylglycine-induced convulsions (in 2 of 4 experiments) as electroconvulsive shock did not alter CSF amino acid levels. During the experimental period encompassing the allylglycine injection (8 weeks), basal (initial post-ketamine, pre-drug sample) amino acid levels were abnormal with large increases in glutamate, GABA, aspartate and taurine whereas asparagine levels were below the limit of detection. Diazepam administration was followed by a significant increase in taurine and a decrease in aspartate levels.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of N-methyl-D-aspartate and kainate lesions of the rat striatum on striatal ornithine decarboxylase activity and polyamine levels.

The intrastriatal injection of N-methyl-D-aspartate (NMDA) (250 nmol) produced a delayed and marked increase in striatal ornithine decarboxylase (ODC) activity and putrescine levels which peaked 6-15 h following the injection of NMDA. Striatal ODC activity subsequently returned to normal values while putrescine levels remained significantly elevated for up to 4 days following the lesion. NMDA produced an early and progressive decline in striatal spermine and spermidine levels, preceding the increase in ODC activity, with a maximum effect 2 h following injection. Spermidine levels returned to normal 6 h post-NMDA infusion, and subsequently increased to above normal levels 36 h and 4 days after the infusion of NMDA. This late increase in striatal spermidine levels paralleled an increase in the binding of the glial cell/macrophage marker [3H]PK 11195. Spermine levels tended to return to normal values 6 h after the injection of NMDA but may be further depressed at later intervals (15 h to 4 days). The intrastriatal injection of saline also resulted in a delayed increase in striatal ODC activity and putrescine levels, but these changes were minor compared to those produced by NMDA. Intrastriatal saline injection provoked no consistent change in striatal spermine or spermidine levels. The changes in polyamine metabolism produced by the intrastriatal injection of kainic acid (4 nmol) were only analysed at 6 and 15 h following injection but were qualitatively similar to those produced by NMDA although perhaps following a slightly more delayed time-course.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebrospinal fluid amino acid and monoamine metabolite levels of Papio papio: correlation with photosensitivity.

Several putative neurotransmitter amino acids and monoamine metabolites were measured in the cerebrospinal fluid of spontaneously photosensitive baboons (Papio papio) at different periods with varying degrees of photosensitivity in the same animals. At maximum photosensitivity the inhibitory amino acids gamma-aminobutyric acid and taurine were lower, and those of asparagine (metabolite of the excitatory amino acid aspartate) were higher, than when the animals were not photosensitive. Thus a decreased inhibition and perhaps increased excitation correlates with the level of photosensitivity.