Welcome to the IBRO 2023 Interactive Programme

The aim of this symposium proposal is to bring together major advances on how neuroglia interactions shape brain (dys)function in health, ageing and disease. Specifically, we will introduce and discuss state-of-the-art information on the following aspects: 1-age-dependent structural defects of myelin leading to neuronal and glia adaptations that make the brain vulnerable to the manifestation of neurodegenerative diseases (Constanze Depp, Max-Plank-Institute, Göttingen); 2- the contribution of complement and microglia-mediated synapse pruning to synapse loss in Alzheimer´s disease (Soyon Hong, University College, London; 3- how neuronal activity regulates oligodendroglia lineage progression as well as myelin remodeling and plasticity (Erin Gibson, Stanford, Palo Alto); 4- and the mechanisms of demyelination and remyelination involving neurotransmitter signaling in glial cells (Carlos Matute, Achucarro, Bilbao).

Aging and neurodegeneration are associated with declines in energy production in the brain as well as parallel changes in redox status with a pro-oxidant shift associated with mitochondrial defects. Mitochondria regulate distinct cytosolic signaling pathways and have vital roles, including production of ATP; generation of second messengers implicated in the modulation of redox-sensitive signaling and transcriptional pathways; regulation of NAD+/NADH homeostasis. Conversely, mitochondria are targets and recipients of cytosolic redox-sensitive signaling and nuclear transcriptional pathways. The symposium aims to tackle the intricate signaling network that has evolved around mitochondrial metabolism, generation of ROS, and cellular responses. The four speakers (1 junior) will discuss different aspects of redox signaling involved in energy homeostasis and how dysfunction of this complex network, that occurs with aging and neurodegeneration, contributes to cognitive decline and dementia onset. The talks will span from genes to proteins to intracellular signaling, to better understand the close association between redox-signaling and metabolic pathways at the basis of cognition. Considering that the mitochondrial energy-redox axis is compromised in brain aging and neurodegeneration, elucidating the signaling events originating from mitochondria and converging on mitochondria from different disease models might unravel the molecular targets for novel, promising therapeutic strategies.

Neuromodulators play a critical role in cognition via slow, diffuse control of neural activity. Recent technological advancements, however, catalyzed a new view that neuromodulatory systems flexibly control specific circuit components supporting complex cognitive operations. This symposium will highlight these exciting developments by featuring a gender-balanced, international panel of outstanding researchers. Dr. Johansen is a Team Leader at Riken Center for Brain Science in Japan. He will show how the locus coeruleus noradrenaline system regulates different aspects of emotional processing through a modular input/output organization. Dr. Warden will discuss new perspectives on dopamine signals and their role in tracking progress toward spatial and non-spatial goals. Dr. Takehara will present her works on how acetylcholine modulates prefrontal neuronal ensembles to encode uncertain threats. Dr. Ramaswamy will provide theoretical frameworks to bridge empirical findings on neuromodulators with the development of artificial neural networks. With diverse expertise and background, these speakers will provide the audience with a holistic understanding of the new perspectives on neuromodulation underlying high-level cognition.

When encountering potentially dangerous situations the brain needs to respond with appropriate defensive behaviors. What are the neuronal processes that help decide when we need to react to a threat and how to react? The symposia will cover these questions showing emerging work from outstanding laboratories in the field. The different speakers' expertise will give a broad but complementary perspective to the symposium by approaching the topic from different angles: Dr. Likhtik will demonstrate how the communication between brain regions shapes fear states. Dr. Paz will present neuronal codes relevant for aversive learning. Dr. Mederos will reveal a novel cortical-subcortical inhibitory pathway critical for habituating to threats during fear behaviors. Dr. Martin-Fernandez will demonstrate simultaneous neuronal representations of defensive states and specific threats. Together, bringing different views on neuronal processing of aversive information. Covering the interactions between neuronal populations from different brain regions but also the mechanisms that neurons use to encode and represent emotionally relevant information.

Despite immense progress, knowledge of the cellular and molecular events underlying human brain development and of how abnormalities in this process lead to neurological disease remains rather superficial. The lack of experimental models holds back the study of a process that largely occurs during in utero development, which has hindered progress in mechanistic understanding. The recent advances in stem cell-derived models of human organogenesis are at the center of experimental models to tackle this problem. Our symposium emphasizes these issues by highlighting the work of pioneers in the field of mammalian cortical development. Both co-organizers are group leaders with long-standing interest in Developmental Neurobiology with an emphasis on oligodendrogenesis, myelination and their implications in pathologies.This symposium is dedicated to the recent advances in the field of neurodevelopment with emphasis on the cerebral cortex. Flora Vaccarino (USA) will focus on multiple in vivo and in vitro models to understand the genetics of brain pathologies, Silvia Velasco (Australia) on the use of 3D organoids, Valentina Fossati (USA) will emphasize the generation of human tools to study glial cells and glia-neuron interactions, and María Cecilia Angulo (France) will discuss the hot issue of myelination of neocortical interneurons and how it influences inhibitory circuits.

The developing brain generates patterned spontaneous activity before the sensory systems are naturally exposed to external stimuli. This patterned spontaneous activity has been implicated in several developmental processes and there is growing evidence that abnormal spontaneous activity patterns may underlie sensory and cognitive deficits associated with neurodevelopmental disorders. Recent technological advances have led to more detailed descriptions of the properties of the earliest forms of spontaneous activity and the mechanisms by which this activity drive the cellular and molecular processes, such as those that influence neural identity, circuit organization and plasticity, that prepare the brain for processing sensory inputs. This session will focus on current advances in the mechanisms by which spontaneous activity sculpts the development of sensory circuits using a variety of animal models and in vivo approaches. In drosophila -a relatively new model in the field- it has been recently demonstrated that a population of neurons expressing the Trpγ channel are required for the patterning and propagation of spontaneous activity throughout the nervous system. Furthermore, speakers will describe advances in the analysis of circuit formation and refinement, with emphasis on the role of GABAergic neuronal populations in setting the temporal properties in different sensory systems. Moreover, methodological advances in in vivo recording in pre and neonatal preparations have led to a description of the earliest forms of spontaneous retinal activity and its role in the functional segregation of distinct sensory pathways.

The main aim of the symposium is to draw attention on the profound influence that the nervous system exerts on the immune system. In particular, we aim to highlight recent discoveries about the inhibitory function of peripheral autonomic nerves on inflammatory responses at the whole body and organ level. Prof Martelli will show recent data on how and where sympathetic splanchnic nerves endogenously inhibit inflammation and produce a status of immunosuppression during the course of a systemic infection. Dr Brognara will contribute to highlight the recent discoveries on the neural reflex control of inflammation, by showing how the physiological activation of the cardiac baroreflex can modulate the cytokine response in endotoxemic rats. Prof de Jonge will focus on the last findings about the autonomic neural control of intestinal diseases. He will demonstrate the key role of autonomic nerves in specific animal models of inflammatory bowel disease but also in human irritable bowel syndrome and intestinal failure after surgery. Finally, Prof Wong will focus on how the nervous system profoundly alters immunity, inducing a life-threatening immunodeficiency, after a stroke. In particular, she will focus on the specific post-stroke effects on the gut barrier, mediated by autonomic nerves.

A new era on comparative neurobiology has arrived, with the advent of omics methods and the establishment of a multitude of animal models away from the traditional mammals. We will explore the origins of the mammalian and human brains, by introducing current ideas on brain diversity and evolution. This symposium aims to present classic and novel concepts and bring them to the discussion of the IBRO’s audience. Comparative neurobiology is a global discipline whose endeavors require multidisciplinary research and a strong focus on comparison between species and brain features. As such, we are committed to present such a variety of tools, concepts and species. The symposium talks comprise an evolutionary journey through the brain of multiple species. From the brain of lampreys and sharks, to the brain and circuits of amphibians, reptiles and birds. The four speakers work each on disparate animal models.

Sex hormones affect brain function and behavior throughout lifespan by changing the connections between neurons (the synapses). Similarly, both natural and industrial chemicals can interact with hormone receptors, and hence interfere with synaptic function and cognition. However, the molecular mechanisms underlying estrogen actions and the impact of estrogen-like molecules in the brain are not yet fully understood. This symposium is aimed at shedding light into these issues by addressing different aspects of the neuroendocrinology of synapses and cognition both in health and disease. Prof. Deepak Srivastava will present recent work related to human induced pluripotent stem cells (including patient-derived cells) showing that estradiol modulates synapses during brain development. Prof. Elena Choleris will present some of her latest work on hormone regulation of social behavior and cognition. Dr. Guoqi Zhu will show us his most recent data on the therapeutic uses of natural products targeting estrogen receptors against different brain disorder whereas XX will talk about the mechanisms of synaptic dysfunction caused by pesticides and their relevance for neurodevelopmental disorders.

Neurodegenerative disorders are the complex and the challenging and by 2050, become huge burden all over the world. Emerging studies reveal that neurodegenerative disorders, including Alzheimer’s, Parkinson, and Amyotrophic Lateral Sclerosis (ALS) etc are commonly linked to DNA damage accumulation and repair deficiency. The reasons why people get these diseases are still not clear. The current symposia explain these concepts. The session will include a debate regarding the following emerging research areas highly relevant to the neurochemistry mission, namely, 1) Emerging role of Genome Damage and Repair Defects in Aging Neurons and CNC (CNS) cells affected in neurodegenerative diseases, 2) Novel neurochemical pathways involved in genome damage and DNA repair pathways, and 3) Role of DNA Damage Response (DDR) factors in CNS cell survival versus death after chronic damage and its potential as therapeutic target.

Our 24/7 lifestyle demands exposure to artificial light at night, people working at night and travelling across time zones. The exposure to this environment has been associated with an increased risk to develop metabolic disorders such as obesity. This is because our circadian (24-h) timing system, which normally anticipates recurring changes in the environment (e.g. day-night transition) and optimizes our physiology, has troubles to adapt to such a lifestyle. To find solutions and alleviate the burden caused by metabolic disorders, it is imperative to understand the physiology of the circadian system and those clock-dependent mechanisms that drive appetite and regulate weight. This symposium brings together researchers that have contributed with breakthrough discoveries. The pioneer work of Rae Silver has led to the identification and characterization of the suprachiasmatic nucleus (SCN) as the master circadian clock in the mammalian brain. The original work of Marco Brancaccio has identified that a cross-talk neuronal-glia is essential to ensure the time-keeping function of the SCN. Furthermore, the elegant and comprehensive work of Henrik Oster and Olga Barca-Mayo, have shown how the clock regulates appetite and weight gain, uncovering novel neuronal and glial mechanisms that build the fundamental knowledge necessary for the design of therapeutic strategies.

Despite Sphingosine 1-Phosphate (S1P) emerges as an important molecular target for neurodegenerative diseases, little is known about its role in the central nervous system (CNS). The evolving understanding of S1P’s biological role in glial cells opens up new vistas for understanding nervous system function, thus, it is the time to show the cutting-edge research focusing on S1P signalling in glial cell function. Dr Chun is a world leader and pioneer in S1P signaling and therapeutic development. His talk will focus on a novel glial cell driven mechanisms by which S1P regulates CNS function, providing new insights into potential therapeutic treatments for CNS diseases. Dr. van Echten-Deckert will discuss the emerging roles that S1P plays in microglia, adding new evidence into how S1P regulates CNS neuroinflammation. Dr Don will present how endogenous S1P signalling in oligodendrocytes contributes to myelination and remyelination after injury. Dr Monk will present their new finding concerning how S1P signalling regulates astrocyte function using the Zebrafish model organism. This symposium will be chaired by Dr Junhua Xiao, an established neuroscientist focusing on glial cell biology. This symposium will showcase the latest and high-impact discoveries on S1P signalling in glial cell function by internationally leading experts.