Future brain-machine interfaces, prosthetics, and intelligent soft robotics will require integrating artificial neuromorphic devices with biological systems. Due to their poor biocompatibility, circuit complexity, low energy efficiency, and operating principles fundamentally different from the ion signal modulation of biology, traditional Silicon-based neuromorphic implementations have limited bio-integration potential. Here, we report the first organic electrochemical neurons (OECNs) with ion-modulated spiking, based on all-printed complementary organic electrochemical transistors. We demonstrate facile bio-integration of OECNs with Venus Flytrap (Dionaea muscipula) to induce lobe closure upon input stimuli. The OECNs can also be integrated with all-printed organic electrochemical synapses (OECSs), exhibiting short-term plasticity with paired-pulse facilitation and long-term plasticity with retention >1000 s, facilitating Hebbian learning. These soft and flexible OECNs operate below 0.6 V and respond to multiple stimuli, defining a new vista for localized artificial neuronal systems possible to integrate with bio-signaling systems of plants, invertebrates, and vertebrates.

Excitotoxicity is a phenomenon that describes the toxic actions of excitatory neurotransmitters, primarily glutamate, where the exacerbated or prolonged activation of glutamate receptors starts a cascade of neurotoxicity that ultimately leads to the loss of neuronal function and cell death. In this process, the shift between normal physiological function and excitotoxicity is largely controlled by astrocytes since they can control the levels of glutamate on the synaptic cleft. This control is achieved through glutamate clearance from the synaptic cleft and its underlying recycling through the glutamate-glutamine cycle. The molecular mechanism that triggers excitotoxicity involves alterations in glutamate and calcium metabolism, dysfunction of glutamate transporters, and malfunction of glutamate receptors, particularly N-methyl-D-aspartic acid receptors (NMDAR). On the other hand, excitotoxicity can be regarded as a consequence of other cellular phenomena, such as mitochondrial dysfunction, physical neuronal damage, and oxidative stress. Regardless, it is known that the excessive activation of NMDAR results in the sustained influx of calcium into neurons and leads to several deleterious consequences, including mitochondrial dysfunction, reactive oxygen species (ROS) overproduction, impairment of calcium buffering, the release of pro-apoptotic factors, among others, that inevitably contribute to neuronal loss. A large body of evidence implicates NMDAR-mediated excitotoxicity as a central mechanism in the pathogenesis of many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), and epilepsy. In this review article, we explore different causes and consequences of excitotoxicity, discuss the involvement of NMDAR-mediated

Life in our planet is highly dependent on plants as they are the primary source of food, regulators of the atmosphere, and providers of a variety of materials. In this work, we review the progress on bioelectronic devices for plants and biohybrid systems based on plants, therefore discussing advancements that view plants either from a biological or a technological perspective, respectively. We give an overview on wearable and implantable bioelectronic devices for monitoring and modulating plant physiology that can be used as tools in basic plant science or find application in agriculture. Furthermore, we discuss plant-wearable devices for monitoring a plant’s microenvironment that will enable optimization of growth conditions. The review then covers plant biohybrid systems where plants are an integral part of devices or are converted to devices upon functionalization with smart materials, including self-organized electronics, plant nanobionics, and energy applications. The review focuses on advancements based on organic electronic and carbon-based materials and discusses opportunities, challenges, as well as future steps.

Excitotoxicity is a common phenomenon in several neurological diseases, associated with an impaired clearance of synaptically released glutamate, which leads to an overactivation of postsynaptic glutamate receptors. This will, in turn, start an intracellular cascade of neurotoxic events, which include exacerbated production of reactive oxygen species and ammonia toxicity. We report the assembly of microreactors equipped with platinum nanoparticles as artificial enzymes and polymer terminating layers including poly(dopamine). The biological response to these microreactors is assessed in human neuroblastoma cell culture. The microreactors' function to deplete hydrogen peroxide (HO) and ammonia is confirmed. While the proliferation of the cells depends on the number of microreactors present, no inherent toxicity is found. Furthermore, the microreactors are able to ameliorate the effects of excitotoxicity in cell culture by scavenging HO and ammonia, thus having the potential to provide a therapeutic approach for several neurological diseases in which excitotoxicity is observed.