Salter, E. | bioRxiv Science

bioRxiv2021

Quantifying the Invasive Secondary Metabolome

Invasive plants drive ecosystem degradation through developing aggressive phenotypes that can outcompete native flora. Several hypotheses explain this, like the Evolution of Increased Competitive Ability hypothesis and the Novel Weapons Hypothesis, but none have been proven conclusively. Changes in plant metabolites are critical to these hypotheses, but complete invasive secondary metabolomes have not been quantified. Here, statistical and unsupervised machine-learning approaches were used to analyse chemotype-to-phenotype relationships in invasive and non-invasive populations in species Ageratum conyzoides, Lantana camara, Melaleuca quinquenervia and Psidium cattleainum and on a family level analysing Asteraceae, Myrtaceae and Verbenaceae. Invasive metabolomes evolved according to the EICA and NWH, involving optimisation of aggressive strategies present in native populations and local adaptation. O_FIG O_LINKSMALLFIG WIDTH=135 HEIGHT=200 SRC="FIGDIR/small/471125v1_ufig1.gif" ALT="Figure 1"> View larger version (24K): org.highwire.dtl.DTLVardef@1bd2d02org.highwire.dtl.DTLVardef@d5e660org.highwire.dtl.DTLVardef@107d008org.highwire.dtl.DTLVardef@1eaf62a_HPS_FORMAT_FIGEXP M_FIG C_FIG

plant biology↗

bioRxiv2019

Stress-induced neuronal hypertrophy decreases the intrinsic excitability in stress habituation

A rapid activation of the hypothalamic-pituitary-adrenal (HPA) axis is a hallmark stress response to an imminent threat, but its chronic activation can be detrimental. Thus, the long-term survival of animals requires experience-dependent fine-tuning of the stress response. However, the cellular mechanisms underlying the ability to decrease the stress responsiveness of the HPA axis remain largely unsolved. Using a stress habituation model in male mice and slice patch-clamp electrophysiology, we studied hypothalamic corticotropin-releasing hormone neurons that form the apex of the HPA axis. We found that the intrinsic excitability of these neurons substantially decreased after daily repeated restraint stress in a time course that coincided with their loss of stress responsiveness in vivo. This plasticity of intrinsic excitability co-developed with an expansion of surface membrane area, resulting in an increase in input conductance with minimal changes in conductance density. Moreover, multi-photon and electron microcopy data found that repeated stress augmented ruffling of the plasma membrane, suggesting an ultrastructural plasticity that efficiently accommodates membrane area expansion with proportionally less expansion of gross cell volume. Overall, we report a novel structure-function relationship for intrinsic excitability plasticity that correlates with habituation of the neuroendocrine stress response.\n\nSignificance statementThe long-term survival of animals requires experience-dependent fine-tuning of stress response. Using a mouse model of repeated stress that develops habituation of the hypothalamic-pituitary-adrenal (HPA) axis, our study demonstrates a robust decrease in the intrinsic excitability of the output neuroendocrine neurons of the HPA axis. Mechanistically, we show that repeated stress increases the cell size of these neurons (i.e. surface membrane area). This cell-size change increases input conductance, and hence decreases excitability. Our findings challenge a conventional view that plasticity of intrinsic excitability relies on changes on membrane excitability resulting from up- and down-regulation of various voltage-gated ion channels. Our study reports a novel structure-function relationship for intrinsic excitability plasticity that correlates with habituation of the neuroendocrine stress response.

neuroscience↗