Abstract

Biomimetic Biohybrid Synapses

Claudia Lubrano, Post doc, Juelich Forshcungszentrum

Synaptic plasticity is at the base of learning and memory capabilities of the human brain and lately recent studies reported a strong correlation between synaptic dysfunction and neurodegenerative diseases. Unfortunately, the complexity of the brain and the nervous system prevents the investigation of mechanisms underlying cognitive impairment, and for this reason the possibility to inhibit neurodegeneration at the early stage of disease is still far from being concrete. In this scenario, in vitro platforms have attracted significant interest as they could provide simplified biomimetic models of neuronal systems and allow for the investigation of synaptic dysfunctions in neurodegeneration. In this context, organic electrochemical transistors (OECTs) have recently emerged as neuromorphic devices that exhibit synaptic plasticity and adaptive behavior as biological neuronal cells. Furthermore, the recent implementation of supported lipid bilayers (SLBs) on conductive polymers and OECTs lead to the development of a new class of bionsensors able to mimic cells native environment. Here, we present a biomimetic in vitro platform which displays a neuronal membrane outer architecture and is able to recapitulate the same functionalities of neurons (i.e., neurotransmitter-mediated synaptic plasticity). In detail, we engineered a biohybrid platform where dopamine directly secreted from cells is able to modulate the conductance of an OECT on the short and long-time scale mimicking synaptic potentiation of biological systems. Furthermore, we investigated the role of an artificial biomembrane on the neuromorphic functionalities of the OECT exploiting the SLB ionic barrier behavior to enhance the plasticity behavior of the device. We expect that such biomembrane-based organic neuromorphic transistor could represent a first step towards the implementation of fully biomimetic in vitro systems, which resemble composition and functionalities of neuronal networks and as such, could contribute to unwind the complex mechanisms underlying neurodegeneration and synaptic plasticity loss.