11 research outputs found
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Integration of Inkjet Printed Graphene as a Hole Transport Layer in Organic Solar Cells
Peer reviewed: TrueAcknowledgements: Thanks to Assoz. Univ. Markus Clark Scharber for fruitful discussions and helpful advice.This work demonstrates the green production of a graphene ink for inkjet printing and its use as a hole transport layer (HTL) in an organic solar cell. Graphene as an HTL improves the selective hole extraction at the anode and prevents charge recombination at the electronic interface and metal diffusion into the photoactive layer. Graphite was exfoliated in water, concentrated by iterative centrifugation, and characterized by Raman. The concentrated graphene ink was incorporated into inverted organic solar cells by inkjet printing on the active polymer in an ambient atmosphere. Argon plasma was used to enhance wetting of the polymer with the graphene ink during printing. The argon plasma treatment of the active polymer P3HT:PCBM was investigated by XPS, AFM and contact angle measurements. Efficiency and lifetime studies undertaken show that the device with graphene as HTL is fully functional and has good potential for an inkjet printable and flexible alternative to PEDOT:PSS
Changes in neural network homeostasis trigger neuropsychiatric symptoms
The mechanisms that regulate the strength of synaptic transmission and intrinsic neuronal excitability are well characterized; however, the mechanisms that promote disease-causing neural network dysfunction are poorly defined. We generated mice with targeted neuron type-specific expression of a gain-of-function variant of the neurotransmitter receptor for glycine (GlyR) that is found in hippocampectomies from patients with temporal lobe epilepsy. In this mouse model, targeted expression of gain-of-function GlyR in terminals of glutamatergic cells or in parvalbumin-positive interneurons persistently altered neural network excitability. The increased network excitability associated with gain-of-function GlyR expression in glutamatergic neurons resulted in recurrent epileptiform discharge, which provoked cognitive dysfunction and memory deficits without affecting bidirectional synaptic plasticity. In contrast, decreased network excitability due to gain-of-function GlyR expression in parvalbumin-positive interneurons resulted in an anxiety phenotype, but did not affect cognitive performance or discriminative associative memory. Our animal model unveils neuron type-specific effects on cognition, formation of discriminative associative memory, and emotional behavior in vivo. Furthermore, our data identify a presynaptic disease-causing molecular mechanism that impairs homeostatic regulation of neural network excitability and triggers neuropsychiatric symptoms