Social media has become an essential tool in the distribution of scientific information amongst professionals in the field of neuroscience and the general population, with Twitter being the platform most commonly used by scientists. How can scientists (and more specifically neuroscientists) best use Twitter to communicate science (both their own and that of others). This workshop will bring together a panel of four specialists who use Twitter on a regular basis as a tool for science communication. They will share with the audience their tips and tricks on using Twitter from making a good profile and finding the relevant people to follow, to engaging on Twitter, finding content and the best ways to interact with a community.

This interactive Special Interest Event allows you as FENS Forum participant to meet with representatives from business, industry and public sectors, all with a neuroscience background. The speakers will share with you how their neuroscience background contributed to their career-paths.

Organised by The European Brain Council, in collaboration with FENS and the International Brain Research Organisation (IBRO) in the framework of the FENS Forum, this Special Interest Event will focus on the topic of Global Research Collaboration, highlighting the existing partnerships within research—specifically, brain research—in the European Union, the United States and China.

Supported by: EDAB / Max Cowan Special Lecture

Immunologists have long understood that the response of macrophages and other immune cells to different stimuli is tightly controlled by a coordinated epigenetic and metabolic reprogramming of the cell´s function. This “training” of the innate immune system is, however, little explored in brain microglia. The goal of the symposium is to engage the audience in a lively discussion about recently published and unpublished findings related to metabolic and epigenetic reprogramming of microglia. In the first part we will focus on physiological conditions, and describe the role of histone deacetylases on the microglial epigenetic landscape, survival and homeostasis during development (M. Prinz); and how the phagocytosis of apoptotic newborn cells triggers an integrated epigenetic, transcriptional and metabolic remodelling of the microglial mitochondrial network (A. Sierra). In the second part, we will move to a major pathology, Alzheimer´s disease, and discuss the key role of TREM2 and other innate immune receptors in maintaining microglial metabolic fitness (M. Colonna); and how microglial inflammatory imprinting leads to immune training and exacerbates cerebral β-amyloidosis (J. Neher). We have a balanced gender, geographical distribution, and scientific seniority of the speakers. The chairperson has previous experience in event organization (2015 Euroglia organizer, 2017 Euroglia program committee, 2020 EMBL Microglia meeting organizer).

Neuropsychiatric disorders exhibit sex differences in the age of onset, prevalence and symptomatology. The identification of the molecular pathways that contribute to the development and maintenance of neuronal dimorphic configurations will help us understand the link between sex and mental disorders. We will explore this topic from multiple angles and model organisms: The regulators that coordinate the development of sex differences in the brain in gene expression, circuit formation and behavior. Sex hormones, epigenetic and transcriptional mechanisms control the sexual differentiation of the brain in mammals, flies, and worms. C. elegans and Drosophila lack hormonal control of sexual traits, allowing us to explore the role of novel conserved genetic factors in the regulation of sex specific traits; The impact of sex determination in the configuration of neuronal networks to generate physiological and behavioral differences between the two sexes; Anatomical and functional delineation of neural circuits underlying sex-typical social behaviors and social interactions. We will overview the different structural and molecular designs that ensure that common sensory inputs elicit dimorphic behavioral outputs. We will bring together fundamental aspects in neuroscience that go beyond the neurobiology of sex in C. elegans, Drosophila and mouse nervous systems.

It is forty years since Norman G. Bowery started the journey for many of us, when he discovered and named the most abundant inhibitory G protein–coupled receptors in the mammalian brain, the GABA-B receptors. Although initially quite neglected, in the last few years their important role on a number of neural processes and conditions, including synaptic plasticity and desensitization, has been identified. Further, there has been substantial work indicating diversity of the GABA-B receptors in functional properties, cellular signaling and subcellular distribution affecting various neurotransmitter networks and brain regions. Most importantly, there has been extensive research on the role of GABA-B receptors in various neuropsychiatric disorders, including addiction, anxiety and major depressive disorder, at preclinical and/or clinical level. In this long journey, the role of GABA-B receptors as possible therapeutic targets for these disorders has also been investigated with promising findings. The journey (to Ithaca) continues and four of the leading scientists in the GABA-B receptor field, at junior and senior level, will be presenting their respective GABA-B receptor work that spreads from cellular/molecular to cognitive and behavioural processes, with a particular focus on depression, addiction and reward.

The brain uses up to 20% of the body’s energy budget, due largely to the inordinate amount of energy needed by neurons for electrical signalling. Classically, glucose was considered the neuron’s sole energy substrate. However, evidence accrued since the 1990s, has led to a paradigm shift in our understanding of neuronal energy metabolism; one in which astrocytes and myelinating glia can supply carbon fuels in the form of lactate, to neurons for energy and signalling purposes. In this symposium, pioneers in the field will highlight current understanding, investigative methods and implications for health and disease. The objectives are to: Provide a platform for junior and senior scientists of both genders, and from different geographical locations (including Glasgow!) to showcase state-of-the-art in our understanding of this field. Make the information accessible to a broad and multidisciplinary audience, through the skills of our experienced speakers. Approach the subject and its controversies from a range of different angles and based on diverse experimental approaches, from in vitro through in vivo studies, in vertebrate and invertebrate model organisms.

Sensory systems do not work in isolation but are influenced by each other. Multisensory interaction provides context to the sensory information, and acts as a platform for cross-modal plasticity when losing a sensory modality. Cross-modal and multisensory interactions are not only evident in multisensory cortical areas but are also present in the primary sensory cortices. Here, we will cover topics on how sensory experience in one domain leads to plasticity in cortical areas involved in processing the other senses, and how multisensory experience interacts to sculpt cortical circuits. Dr. Manuel Teichert will present data that a brief duration of auditory or whisker deprivation induces plasticity in the adult visual cortex (V1), such that there is recovery of ocular dominance plasticity and enhancement of visually guided behavior. Dr. Hey-Kyoung Lee follows by showing data that such enhancement of adult V1 plasticity is due to recovering thalamocortical plasticity in V1 by deafening. Dr. Patrick Kanold will discuss that visual deprivation changes the functional circuit of the primary auditory cortex (A1) to allow better feature selectivity and information processing. Dr. Tara Keck will talk about multisensory plasticity in the retrosplenial cortex (RSC), which normally responds to both auditory and visual stimuli. In RSC, deprivation of hearing or vision leads to homeostatic increases in responses to both modalities through amplification of the spontaneous network activity.