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Expression of the N-methyl-D-aspartate receptor, particularly when containing the GluN2B subunit (NMDAR-GluN2B), varies across the prefrontal cortex (PFC). In humans, the subgenual cingulate cortex (SGC) contains among the highest levels of NMDAR-GluN2B expression, while the dorsolateral prefrontal cortex (dlPFC) exhibits a more moderate level of NMDAR-GluN2B expression. NMDAR-GluN2B are commonly associated with ionotropic synaptic function and plasticity and are essential to the neurotransmission underlying working memory in the macaque dlPFC in the layer III circuits, which in humans are afflicted in schizophrenia. However, NMDAR-GluN2B can also be found at extrasynaptic sites, where they may trigger distinct events, including some linked to neurodegenerative processes. The SGC is an early site of tau pathology in sporadic Alzheimer’s disease (sAD), which mirrors its high NMDAR-GluN2B expression. Additionally, the SGC is hyperactive in depression, which can be treated with NMDAR antagonists. Given the clinical relevance of NMDAR in the SGC and dlPFC, the current study used immunoelectron microscopy (immunoEM) to quantitatively compare the synaptic and extrasynaptic expression patterns of NMDAR-GluN2B across excitatory and inhibitory neuron dendrites in rhesus macaque layer III SGC and dlPFC. We found a larger population of extrasynaptic NMDAR-GluN2B in dendrites of putative pyramidal neurons in SGC as compared to the dlPFC, while the dlPFC had a higher proportion of synaptic NMDAR-GluN2B. In contrast, in putative inhibitory dendrites from both areas, extrasynaptic expression of NMDAR-GluN2B was far more frequently observed over synaptic expression. These findings may provide insight into varying cortical vulnerability to alterations in excitability and neurodegenerative forces. 

It is widely recognized that large‐scale topographic variation affects the distribution of tree diversity, yet the effects of topography at smaller scales are less appreciated but can be no less consequential. We evaluated how small‐scale topographic variation affects tree demography and diversity in a hyperdiverse Amazonian forest where species distributions respond strongly to elevation differences as small as 22 m. For topographically structured species distributions to arise, species should grow and survive (perform) better in the topographic habitat they are associated with, and they should outperform other species that are found, but not strongly aggregated, in that habitat. Here, we tested these demographic hypotheses using data on the growth and mortality of 79,911 trees (352 species) among three topographic habitats (valleys, slopes and ridges) in the 25‐ha Amacayacu Forest Dynamics Plot.Despite the small variation in elevation, there was significant community‐level variation in growth and mortality among topographic habitats: trees growing in valleys, where soil moisture is higher, had significantly higher growth and mortality rates than those growing on slopes and ridges. However, tree growth rates did not depend on, and mortality rates varied inconsistently with, species' habitat association. Our results partially support the resident‐advantage hypotheses for valley‐associated species, which grew best in their home habitat (valleys) than elsewhere and had lower mortality there compared to slope‐associated or generalist species (foreigners). For slope‐ and ridge‐associated species, our results did not support these hypotheses at the community level. Species‐specific analyses revealed that 73 out of the 352 species analysed at the community level supported either hypothesis. Our findings show that even small differences in elevation can lead to biologically meaningful variation in resource access that translates into significant differences in tree growth and survival. However, resource access could not fully explain the patterns of topographically driven demographic variation we observed. While certain species may still exhibit home and resident advantages in specific habitats, even when community‐level averages partially reflect this pattern, alternative hypotheses are likely driving the patterns observed at the community level. 

Abstract Alzheimer’s disease cortical tau pathology initiates in the layer II cell clusters of entorhinal cortex, but it is not known why these specific neurons are so vulnerable. Aging macaques exhibit the same qualitative pattern of tau pathology as humans, including initial pathology in layer II entorhinal cortex clusters, and thus can inform etiological factors driving selective vulnerability. Macaque data have already shown that susceptible neurons in dorsolateral prefrontal cortex express a “signature of flexibility” near glutamate synapses on spines, where cAMP-PKA magnification of calcium signaling opens nearby potassium and hyperpolarization-activated cyclic nucleotide-gated channels to dynamically alter synapse strength. This process is regulated by PDE4A/D, mGluR3, and calbindin, to prevent toxic calcium actions; regulatory actions that are lost with age/inflammation, leading to tau phosphorylation. The current study examined whether a similar “signature of flexibility” expresses in layer II entorhinal cortex, investigating the localization of PDE4D, mGluR3, and HCN1 channels. Results showed a similar pattern to dorsolateral prefrontal cortex, with PDE4D and mGluR3 positioned to regulate internal calcium release near glutamate synapses, and HCN1 channels concentrated on spines. As layer II entorhinal cortex stellate cells do not express calbindin, even when young, they may be particularly vulnerable to magnified calcium actions and ensuing tau pathology. 

ImportanceThe risk of mental disorders is consistently associated with variants inCACNA1C(L-type calcium channel Cav1.2) but it is not known why these channels are critical to cognition, and whether they affect the layer III pyramidal cells in the dorsolateral prefrontal cortex that are especially vulnerable in cognitive disorders. ObjectiveTo examine the molecular mechanisms expressed in layer III pyramidal cells in primate dorsolateral prefrontal cortices. Design, Setting, and ParticipantsThe design included transcriptomic analyses from human and macaque dorsolateral prefrontal cortex, and connectivity, protein expression, physiology, and cognitive behavior in macaques. The research was performed in academic laboratories at Yale, Harvard, Princeton, and the University of Pittsburgh. As dorsolateral prefrontal cortex only exists in primates, the work evaluated humans and macaques. Main Outcomes and MeasuresOutcome measures included transcriptomic signatures of human and macaque pyramidal cells, protein expression and interactions in layer III macaque pyramidal cells using light and electron microscopy, changes in neuronal firing during spatial working memory, and working memory performance following pharmacological treatments. ResultsLayer III pyramidal cells in dorsolateral prefrontal cortex coexpress a constellation of calcium-related proteins, delineated byCALB1(calbindin), and high levels ofCACNA1C(Cav1.2),GRIN2B(NMDA receptor GluN2B), andKCNN3(SK3 potassium channel), concentrated in dendritic spines near the calcium-storing smooth endoplasmic reticulum. L-type calcium channels influenced neuronal firing needed for working memory, where either blockade or increased drive by β1-adrenoceptors, reduced neuronal firing by a mean (SD) 37.3% (5.5%) or 40% (6.3%), respectively, the latter via SK potassium channel opening. An L-type calcium channel blocker or β1-adrenoceptor antagonist protected working memory from stress. Conclusions and RelevanceThe layer III pyramidal cells in the dorsolateral prefrontal cortex especially vulnerable in cognitive disorders differentially express calbindin and a constellation of calcium-related proteins including L-type calcium channels Cav1.2 (CACNA1C), GluN2B-NMDA receptors (GRIN2B), and SK3 potassium channels (KCNN3), which influence memory-related neuronal firing. The finding that either inadequate or excessive L-type calcium channel activation reduced neuronal firing explains why either loss- or gain-of-function variants inCACNA1Cwere associated with increased risk of cognitive disorders. The selective expression of calbindin in these pyramidal cells highlights the importance of regulatory mechanisms in neurons with high calcium signaling, consistent with Alzheimer tau pathology emerging when calbindin is lost with age and/or inflammation. 

Abstract. Isoprene emissions are a key component in biosphere–atmosphere interactions, and the most significant global source is the Amazonrainforest. However, intra- and interannual variations in biological and environmental factors that regulate isoprene emission from Amazonia arenot well understood and, thereby, are poorly represented in models. Here, with datasets covering several years of measurements at the Amazon Tall TowerObservatory (ATTO) in central Amazonia, Brazil, we (1) quantified canopy profiles of isoprene mixing ratios across seasons of normal and anomalousyears and related them to the main drivers of isoprene emission – solar radiation, temperature, and leaf phenology; (2) evaluated the effect ofleaf age on the magnitude of the isoprene emission factor (Es) from different tree species and scaled up to canopy with intra- andinterannual leaf age distribution derived by a phenocam; and (3) adapted the leaf age algorithm from the Model of Emissions of Gasesand Aerosols from Nature (MEGAN) with observed changes in Esacross leaf ages. Our results showed that the variability in isoprene mixing ratios was higher between seasons (max during the dry-to-wettransition seasons) than between years, with values from the extreme 2015 El Niño year not significantly higher than in normal years. Inaddition, model runs considering in situ observations of canopy Es and the modification on the leaf age algorithm with leaf-levelobservations of Es presented considerable improvements in the simulated isoprene flux. This shows that MEGAN estimates of isopreneemission can be improved when biological processes are mechanistically incorporated into the model. 

Abstract Numerous studies have shown reduced performance in plants that are surrounded by neighbours of the same species^1,2, a phenomenon known as conspecific negative density dependence (CNDD)³. A long-held ecological hypothesis posits that CNDD is more pronounced in tropical than in temperate forests^4,5, which increases community stabilization, species coexistence and the diversity of local tree species^6,7. Previous analyses supporting such a latitudinal gradient in CNDD^8,9have suffered from methodological limitations related to the use of static data^10–12. Here we present a comprehensive assessment of latitudinal CNDD patterns using dynamic mortality data to estimate species-site-specific CNDD across 23 sites. Averaged across species, we found that stabilizing CNDD was present at all except one site, but that average stabilizing CNDD was not stronger toward the tropics. However, in tropical tree communities, rare and intermediate abundant species experienced stronger stabilizing CNDD than did common species. This pattern was absent in temperate forests, which suggests that CNDD influences species abundances more strongly in tropical forests than it does in temperate ones¹³. We also found that interspecific variation in CNDD, which might attenuate its stabilizing effect on species diversity^14,15, was high but not significantly different across latitudes. Although the consequences of these patterns for latitudinal diversity gradients are difficult to evaluate, we speculate that a more effective regulation of population abundances could translate into greater stabilization of tropical tree communities and thus contribute to the high local diversity of tropical forests. 

Abstract It is largely unknown how South America’s Andean forests affect the global carbon cycle, and thus regulate climate change. Here, we measure aboveground carbon dynamics over the past two decades in 119 monitoring plots spanning a range of >3000 m elevation across the subtropical and tropical Andes. Our results show that Andean forests act as strong sinks for aboveground carbon (0.67 ± 0.08 Mg C ha −1 y −1 ) and have a high potential to serve as future carbon refuges. Aboveground carbon dynamics of Andean forests are driven by abiotic and biotic factors, such as climate and size-dependent mortality of trees. The increasing aboveground carbon stocks offset the estimated C emissions due to deforestation between 2003 and 2014, resulting in a net total uptake of 0.027 Pg C y −1 . Reducing deforestation will increase Andean aboveground carbon stocks, facilitate upward species migrations, and allow for recovery of biomass losses due to climate change. 

Recent evidence suggests that the ecological footprints of pre-Columbian Indigenous peoples in Amazonia persist in modern forests. Ecological impacts resulting from European colonization c. 1550 CE and the Amazonian Rubber Boom c. 1850 to 1920 CE are largely unexplored but could be important additive influences on forest structure and tree species composition. Using environmental niche models, we show the highest probabilities of pre-Columbian and colonial occupation sites, and hence human-induced ecological influences, occurred in forests along rivers. In many areas, the predicted pre-Columbian and colonial distributions overlap spatially with the potential for superimposed ecological influences. Environmental gradients are known to structure Amazonian vegetation composition, but they are also strong predictors of past human influence, both spatially and temporally. Our comparisons of model outputs with relative abundances of Amazonian tree species suggest that pre-Columbian and colonial-period ecological legacies are associated with modern forest composition.