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• Recent studies have revealed the physiological roles of glutamate receptor-like channels (GLRs) in Arabidopsis; however, the functions of GLRs in rice remain largely unknown. • Here, we show that knockout of OsGLR3.4 in rice leads to brassinosteroid (BR)-regulated growth defects and reduced BR sensitivity. Electrophoretic mobility shift assays and transient transactivation assays indicated that OsGLR3.4 is the downstream target of OsBZR1. Further, agonist profile assays showed that multiple amino acids can trigger transient Ca2+ influx in an OsGLR3.4-dependent manner, indicating that OsGLR3.4 is a Ca2+-permeable channel. Meanwhile, the study of internode cells demonstrated that OsGLR3.4-mediated Ca2+ flux is required for actin filament organization and vesicle trafficking. • Following root injury, the triggering of both slow wave potentials (SWPs) in leaves and the jasmonic acid (JA) response are impaired in osglr3.4 mutants, indicating that OsGLR3.4 is required for root-to-shoot systemic wound signaling in rice. Brassinosteroid treatment enhanced SWPs and OsJAZ8 expression in root-wounded plants, suggesting that BR signaling synergistically regulates the OsGLR3.4-mediated systemic wound response. • In summary, this article describes a mechanism of OsGLR3.4-mediated cell elongation and long-distance systemic wound signaling in plants and provides new insights into the contribution of GLRs to plant growth and responses to mechanical wounding.

Slow wave potentials (SWPs) are damage-induced electrical signals which, based on experiments in which organs are burned, have been linked to rapid increases in leaf or stem thickness. The possibility that pressure surges in injured xylem underlie these events has been evoked frequently. We sought evidence for insect feeding-induced positive pressure changes in the petioles of Arabidopsis thaliana. Instead, we found that petiole surfaces of leaves distal to insect-feeding sites subsided. We also found that insect damage induced longer-duration downward leaf movements in undamaged leaves. The transient petiole deformations were contemporary with and dependent on the SWP. We then investigated if mutants that affect the xylem, which has been implicated in SWP transmission, might modify SWP architecture. irregular xylem mutants strongly affected SWP velocity and kinetics and, in parallel, restructured insect damage-induced petiole deformations. Together, with force change measurements on the primary vein, the results suggest that extravascular water fluxes accompany the SWP. Moreover, petiole deformations in Arabidopsis mimic parts of the spectacular distal leaf collapse phase seen in wounded Mimosa pudica. We genetically link electrical signals to organ movement and deformation and suggest an evolutionary origin of the large leaf movements seen in wounded Mimosa.

Slow wave potentials (SWPs) are transitory depolarizations occurring in response to treatments that result in a pressure increase in the xylem conduits (Px). Here SWPs are induced by excision of the root under water in 40- to 50-cm-tall light-grown sunflower plants in order to determine the effective signal range to a naturally sized pressure signal. The induced slow wave depolarization appears to move up the stem while it is progressively decremented (i.e. the amplitude decreases with increasing distance from the point of excision) with a rate that appears to rise acropetally from 2.5 to 5.5% cm-1. The decline of the SWP signal, in both amplitude and range, could be experimentally increased (i) when root excision was carried out in air and (ii) when the transpiration of the sunflower shoot was minimized by a preceding removal or coating of the leaves. A further decline of the SW signal was expected to occur when leaves were included in the measured path. However, when the most distant apical electrode was attached to an upper leaf, it showed a considerably larger depolarization than a neighboring stem position. This apparent amplification of the SWP signal is not confined to the leaf blade but includes the petiole as well. The amplification disappeared (i) when the illumination level was lowered to room light, (ii) when the blade was excised either completely or along the remaining midvein and (iii) when the intact leaf blade was submersed in water. These treatments reduce the SWP at the petiole to a small fraction of the signal in the opposite control leaf and specify bright illumination and blade-mediated transpiration as prerequisites of a signal increase that is confined to young, expanding leaves.

The contingent negative variation, a slow cortical potential, occurs when humans are warned by a stimulus about an upcoming task. The cognitive processes that give rise to this EEG potential are not yet well understood. To explain these processes, we adopt a recently developed theoretical framework from the area of perceptual decision-making. This framework assumes that the basal ganglia control the tradeoff between fast and accurate decision-making in the cortex. It suggests that an increase in cortical excitability serves to lower response caution, which results in faster but more error prone responding. We propose that the CNV reflects this increased cortical excitability. To test this hypothesis, we conducted an EEG experiment in which participants performed the random dot motion task either under speed or under accuracy stress. Our results show that trial-by-trial fluctuations in participants' response speed as well as model-based estimates of response caution correlated with single-trial CNV amplitude under conditions of speed but not accuracy stress. We conclude that the CNV might reflect adjustments of response caution, which serves to enhance quick decision-making. •A neurophysiological model of decision-making is applied to EEG data.•Single-trial estimates of speed-accuracy tradeoff are correlated with EEG data.•Contingent negative variation reflects the setting of the speed-accuracy tradeoff.•Speed-accuracy tradeoff is set before the decision process.

A variation potential (VP) is an electrical signal unique to plants that occurs in response to wounding or flaming. The propagation mechanism itself, however, is known not to be electrical. Here we examine the hypothesis that VP transmission occurs via the transport of a chemical agent in the xylem. We assume the electrical signal is generated locally by the activation of an ion channel at the plasma membrane of cells adjacent to the xylem. We work on the assumption that the ion channels are triggered when the chemical concentration exceeds a threshold value. We use numerical computations to demonstrate the combined effect of advection and diffusion on chemical transport in a tube flow, and propose shear-enhanced Taylor-Aris dispersion as a candidate mechanism to explain VP rates observed in experiments.

This work demonstrates the use of optical coherence tomography (OCT) for studying a plant’s long-range signaling in real time, in vivo , and non-invasively. This feat is achieved using OCT as a novel technique to visualize minute cellular displacements and deformations within the plant’s leaves. The use of bespoke registration algorithms enables tracking displacements with a precision greater than 0.1 μm. This measurement precision is one order of magnitude better than the typical ~1-μm optical resolution of OCT images. In the present work, OCT is used to analyze the time evolution of deformations incurred by wounding. The use of OCT enabled to 1) visualize, in real time, the propagation and evolution of the morphological changes associated with slow wave potentials (onset, peak, and recovery); 2) compute propagation speeds (~0.07 cm s −1 ); and 3) distinguish the type of deformation incurred (transient bending of the leaf due to changes in turgor cell pressure). This proof-of-concept study thus exemplifies the potential of OCT as a convenient and complementary tool to study the plant’s response mechanisms in vivo and in real time.

We investigated how two different reading tasks, namely reading to memorize [Read & Memorize (RM)] and reading to decide whether a text was relevant to a given topic [Read & Decide (RD)], modulated both eye movements (EM) and brain activity. To this end, we set up an ecological paradigm using the eye fixation-related potentials (EFRP) technique, in which participants freely moved their eyes to process short paragraphs, while their electroencephalography (EEG) activity was recorded in synchronization with their EM. A general linear model was used to estimate at best EFRP, taking account of the overlap between adjacent potentials, and more precisely with the potential elicited at text onset, as well as saccadic potentials. Our results showed that EM patterns were top-down modulated by different task demands. More interestingly, in both tasks, we observed slow-wave potentials that gradually increased across the first eye fixations. These slow waves were larger in the RD task than in the RM task, specifically over the left hemisphere. These results suggest that the decision-making process during reading in the RD task engendered a greater memory load in working memory than that generated in a classic reading task. The significance of these findings is discussed in the light of recent theories and models of working memory processing.

Slow wave potentials (SWPs) are transient depolarizations which propagate substantial distances from their point of origin. They were induced in the epidermal cells of pea epicotyls by injurious methods such as root excision and heat treatment, as well as by externally applied, defined steps in xylem pressure (Px) in the absence of wounding. The common principle of induction was a rapid increase in Px. Such a stimulus appeared under natural conditions after (i) bending of the epicotyl, (ii) wounding of the epidermis, (iii) rewatering of dehydrated roots, and (iv) embolism. The induced depolarization was not associated with a change in cell input resistance. This result and the ineffectiveness of ion channel blockers point to H+-pumps rather than ion channels as the ionic basis of the SWP. Stimuli such as excision, heat treatment and pressure steps, which generate SWPs, caused a transient increase in the fluorescence intensity of epicotyls loaded with the pH-indicator DM-NERF, a 2′, 7′-dimethyl derivative of rhodol, but not of those loaded with the pH indicator 2′,7′-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCECF). Matching kinetics of depolarization and pH response identify a transient inactivation of proton pumps in the plasma membrane as the causal mechanism of the SWP. Feeding pump inhibitors to the cut surface of excised epicotyls failed to chemically simulate a SWP; cyanide, azide and 2,4-dinitrophenol caused sustained, local depolarizations which did not propagate. Of all tested substances, only sodium cholate caused a transient and propagating depolarization whose arrival in the growing region of the epicotyl coincided with a transient growth rate reduction.

Excision of the epicotyl base of pea (Pisum sativum L.) seedlings in air results in a fast drop in the growth rate and rapid transient membrane depolarization of the surface cells near the cut. Subsequent immersion of the cut end into solution leads to a rapid, transient rise in the epicotyl growth rate and an acropetally propagating depolarization with an amplitude of about 35 mV and a speed of approx. 1 mm·s-1. The same result can be achieved directly by excision of the pea epicotyl under water. Shape, amplitude and velocity of the depolarization characterize it as a \"slow-wave potential\". These results indicate that the propagating depolarization is caused by a surge in water uptake. Neither a second surge in water uptake (measured as a rapid increase in growth rate when the cut end was placed in air and then back into solution) nor another cut can produce the depolarization a second time. Cyanide suppresses the electrical signal at the treated position without inhibiting its transmission through this area and its development in untreated parts of the epicotyl. The large depolarization and repolarization which occur in the epidermal and subepidermal cells are not associated with changes in cell input resistance. Both results indicate that it is a transient shut-down of the plasma-membrane proton pump rather than large ion fluxes which is causing the depolarization. We conclude that the slow wave potential is spread in the stem via a hydraulic surge occurring upon relief of the negative xylem pressure after the hydraulic resistance of the root has been removed by excision.