Abstract. Questions: This paper examines the long‐term change in the herbaceous layer of semi‐arid vegetation since grazing ceased. We asked whether (1) there were differences in the temporal trends of abundance among growth forms of plants; (2) season of rainfall affected the growth form response; (3) the presence of an invasive species influenced the abundance and species richness of native plants relative to non‐invaded plots, and (4) abundance of native plants and/or species richness was related to the time it took for an invasive species to invade a plot. Location: Alice Springs, Central Australia. Methods: Long‐term changes in the semi‐arid vegetation of Central Australia were measured over 28 years (1976–2004) to partition the effects of rainfall and an invasive perennial grass. The relative abundance (biomass) of all species was assessed 25 times in each of 24 plots (8 m × 1 m) across two sites that traversed floodplains and adjacent foot slopes. Photo‐points, starting in 1972, were also used to provide a broader overview of a landscape that had been intensively grazed by cattle and rabbits prior to the 1970s. Species’abundance data were amalgamated into growth forms to examine their relationship with environmental variation in space and time. Environmental variables included season and amount of rainfall, fire history, soil variability and the colonization of the plots by the exotic perennial grass Cenchrus ciliaris (Buffel grass). Results: Constrained ordination showed that season of rainfall and landscape variables relating to soil depth strongly influenced vegetation composition when Cenchrus was used as a covariate. When Cenchrus was included in constrained ordination, it was strongly related to the decline of all native growth forms over time. Univariate comparisons of non‐invaded vs impacted plots over time revealed unequivocal evidence that Cenchrus had caused the decline of all native growth form groups and species richness. They also revealed a contrasting response of native plants to season of rainfall, with a strong response of native grasses to summer rainfall and forbs to winter rainfall. In the presence of Cenchrus these responses were strongly attenuated. Discussion: Pronounced changes in the composition of vegetation were interpreted as a response to removal of grazing pressure, fluctuations in rainfall and, most importantly, invasion of an exotic grass. Declines in herbaceous species abundance and richness in the presence of Cenchrus appear to be directly related to competition for resources. Indirect effects may also be causing the declines of some woody species from changed fire regimes as a result of increased fuel loads. We predict that Cenchrus will begin to alter landscape level processes as a result of the direct and indirect effects of Cenchrus on the demography of native plants when there is a switch from resource limited (rainfall) establishment of native plants to seed limited recruitment.

Australia’s 2019–2020 ‘Black Summer’ bushfires burnt more than 8 million hectares of vegetation across the south-east of the continent, an event unprecedented in the last 200 years. Here we report the impacts of these fires on vascular plant species and communities. Using a map of the fires generated from remotely sensed hotspot data we show that, across 11 Australian bioregions, 17 major native vegetation groups were severely burnt, and up to 67–83% of globally significant rainforests and eucalypt forests and woodlands. Based on geocoded species occurrence data we estimate that >50% of known populations or ranges of 816 native vascular plant species were burnt during the fires, including more than 100 species with geographic ranges more than 500 km across. Habitat and fire response data show that most affected species are resilient to fire. However, the massive biogeographic, demographic and taxonomic breadth of impacts of the 2019–2020 fires may leave some ecosystems, particularly relictual Gondwanan rainforests, susceptible to regeneration failure and landscape-scale decline.

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Nicotinic synapses in the autonomous nervous system display use-dependent plasticity but the contribution of cellular environment, as well as the presynaptic mechanisms implicated in this process remain to be determined. To address these questions synaptic function was assayed in rat superior cervical ganglion (SCG) neurons microcultured in isolation from any other cell type and compared to those microcultured in the presence of Schwann cells of ganglionar origin. Schwann cells were not required for synapse formation in vitro because functional cholinergic autaptic synapses were established in both experimental conditions. The number of synapses was comparable between the two culture conditions but the frequency of spontaneous miniature excitatory postsynaptic currents was enhanced in those neurons grown in direct contact with glial cells. Autapses displayed facilitation and depression, both processes being determined by the fraction of vesicles from the readily releasable pool discharged by an action potential. At high release probabilities vesicles were more efficiently mobilized, thus promoting depression, whilst low release probabilities made facilitation likely to occur. Schwann cells did not modify significantly facilitation but increased synaptic depression. In single cell microcultures, paired pulse stimuli showed a monoexponential recovery from depression with a time constant of ∼60 ms, while in microcultures developed together with glial cells, recovery was bi-exponential with a significantly slower time course. Altogether these results show that Schwann cells from sympathetic ganglia directly modulate use-dependent plasticity of nicotinic synapses in vitro by enhancing short-term depression.

GABAA receptor (GABAAR) pentamers are assembled from a pool of 19 subunits, and variety in subunit combinations diversifies GABAAR functions to tune brain activity. Pentamers with distinct subunit compositions localize differentially at synaptic and non-synaptic sites to mediate phasic and tonic inhibition, respectively. Despite multitudes of theoretical permutations, limited subunit combinations have been identified in the brain. Currently, no molecular model exists for combinatorial GABAAR assembly in vivo. Here, we reveal assembly rules of native GABAAR complexes that explain GABAAR subunit subcellular distributions using mice and Xenopus laevis oocytes. First, α subunits possess intrinsic signals to segregate into distinct pentamers. Second, γ2 is essential for GABAAR assembly with Neuroligin-2 (NL2) and GARLHs, which localize GABAARs at synapses. Third, δ suppresses α6 synaptic localization by preventing assembly with GARLHs/NL2. These findings establish the first molecular model for combinatorial GABAAR assembly in vivo and reveal an assembly pathway regulating GABAAR synaptic localization.

Kcc2 plays a critical role in determining the efficacy of synaptic inhibition, however, the cellular mechanisms neurons use to regulate its membrane trafficking, stability and activity are ill-defined. To address these issues, we used affinity purification to isolate stable multi-protein complexes of K-Cl Co-transporter 2 (Kcc2) from the plasma membrane of murine forebrain. We resolved these using blue-native polyacrylamide gel electrophoresis (BN-PAGE) coupled to LC-MS/MS and label-free quantification. Data are available via ProteomeXchange with identifier PXD021368. Purified Kcc2 migrated as distinct molecular species of 300, 600, and 800 kDa following BN-PAGE. In excess of 90% coverage of the soluble N-and C-termini of Kcc2 was obtained. In total we identified 246 proteins significantly associated with Kcc2. The 300 kDa species largely contained Kcc2, which is consistent with a dimeric quaternary structure for this transporter. The 600 and 800 kDa species represented stable multi-protein complexes of Kcc2. We identified a set of novel structural, ion transporting, immune related and signaling protein interactors, that are present at both excitatory and inhibitory synapses, consistent with the proposed localization of Kcc2. These included spectrins, C1qa/b/c and the IP3 receptor. We also identified interactors more directly associated with phosphorylation; Akap5, Akap13, and Lmtk3. Finally, we used LC-MS/MS on the same purified endogenous plasma membrane Kcc2 to detect phosphorylation sites. We detected 11 sites with high confidence, including known and novel sites. Collectively our experiments demonstrate that Kcc2 is associated with components of the neuronal cytoskeleton and signaling molecules that may act to regulate transporter membrane trafficking, stability, and activity.

HTLV-1-associated myelopathy/tropical spastic paraparesis (TSP/HAM) is a chronic CNS disease characterized by axomyelinic degeneration of the long axons of corticospinal tracts. Levels of NGF, NT-3, NT-4/5, BDNF, GDNF, CNTF, and FGF-2 were measured in the cerebrospinal fluid (CSF) of 21 TSP/HAM patients and 20 controls. NGF, BDNF, and FGF-2 levels were also determined in 19 patients with HIV motor cognitive motor syndrome, and in 21 subjects diagnosed with Creutzfeldt Jakob disease (CJD). No significant differences were detected in the concentrations of NGF, BDNF, NT-3, NT-4/5, GDNF, and CNTF in the CSF between TSP/HAM patients and controls. FGF-2 was significantly lower in the CSF of the three groups of patients compared with controls; the HIV group exhibited the lowest values. HIV patients differed from TSP/HAM in their significantly higher levels of NGF and lower levels of BDNF and FGF-2, whereas CJD patients differed only in their higher levels of NGF. Immunohistochemical studies were done of trophic factors (NGF and FGF-2) and neurotrophin receptors (trkA and p75) in spinal cord and motor cortical areas from anatomopathological cases of TSP/HAM. Results indicated that NGF is expressed in motoneurons and oligodendrocytes of the posterior column of the spinal cord. FGF-2 was detected in motoneurons and spinal cord vessels. p75 receptor was detected in cortical neurons. The absence of a significant change in the trophic factor levels in TSP/HAM may be attributed to a selective axonal lesion in a slow process.