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The implementation of the UN’s Sustainable Development Goals in the urban centres of the world is one of the most consequential and ambitious projects that the nations of the world have undertaken. Guidance for achieving the goals in an integrated way that creates true sustainability is currently lacking because of the wicked nature of the problem. However, its wickedness highlights the critical importance of governance and decision-making processes for such integration, including the relationship between governments and their citizens. In particular, there is strong evidence to suggest that managing wicked problems like the SDGs is best done through forms of democracy that are deliberative, representative and influential. Called “deliberative democracy”, we draw on an existing body of research and case studies of deliberative democracy in action to apply its principles to a step-by-step process for the implementation and integration of the Goals in Cities. The paper concludes with the beginnings of a framework based on deliberative democratic principles, and an outline of methods for the scaling and expansion of the implementation process to cope with the global nature of the problem.

High levels of trust in government are important in addressing complex issues, including the realization of the mainstream sustainability agenda. However, trust in government has been declining for decades across the western world, undermining legitimacy and hampering policy implementation and planning for long-term sustainability. We hypothesize that an important factor in this decline is citizen disappointment with the current types of public participation in governance and that this could be reversed through a change from informing/consulting to a relationship of partnership. Using case studies from Western Australia, the paper investigates whether an intervention targeted at establishing a partnership relationship through mini-public, deliberative, participatory budgeting would improve trust and help the implementation of sustainability. These results show evidence of improvements in trust and provide conceptual and practical tools for government administrations wishing to close the detrimental trust gap that may hamper the implementation of a sustainability agenda.

BACKGROUND AND PURPOSEIonotropic GABA receptors are evolutionarily conserved proteins that mediate cellular and network inhibition in both vertebrates and invertebrates. A unique class of excitatory GABA receptors has been identified in several nematode species. Despite wellcharacterized functions in Caenorhabditis elegans, little is known about the pharmacology of the excitatory GABA receptors EXP-1 and LGC-35. Using a panel of compounds that differentially activate and modulate ionotropic GABA receptors, we investigated the agonist binding site and allosteric modulation of EXP-1 and LGC-35. EXPERIMENTAL APPROACHWe used two-electrode voltage clamp recordings to characterize the pharmacological profile of EXP-1 and LGC-35 receptors expressed in Xenopus laevis oocytes. KEY RESULTSThe pharmacology of EXP-1 and LGC-35 is different from that of GABA A and GABA A -ρ receptors. Both nematode receptors are resistant to the competitive orthosteric antagonist bicuculline and to classical ionotropic receptor pore blockers. The GABA A -ρ specific antagonist, TPMPA, was the only compound tested that potently inhibited EXP-1 and LGC-35. Neurosteroids have minimal effects on GABA-induced currents, but ethanol selectively potentiates LGC-35. CONCLUSIONS AND IMPLICATIONSThe pharmacological properties of EXP-1 and LGC-35 more closely resemble the ionotropic GABA A -ρ family. However, EXP-1 and LGC-35 exhibit a unique profile that differs from vertebrate GABA A and GABA A -ρ receptors, insect GABA receptors and nematode GABA receptors. As a pair, EXP-1 and LGC-35 may be utilized to further understand the differential molecular mechanisms of agonist, antagonist and allosteric modulation at ionotropic GABA receptors and may aid in the design of new and more specific anthelmintics that target GABA neurotransmission. AbbreviationsEXP-1, expulsion defective; LGC-35, ligand-gated ion channel

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