Abstracts – SPEAKERS

2. Dr David Belin – There is more to drug addiction than the drug: psychological and neural mechanisms of incentive habits

There is increasing evidence that Substance Use Disorders stem from loss of control over maladaptive drug seeking habits. The psychological and neural basis of the maladaptive nature of these drug seeking habits remains unknown. The incentive habit hypothesis of addiction suggests that incentive habits, which are instrumental habits that develop under the motivational influence of the conditioned reinforcing properties of drug-paired cues, contribute to the persistence of drug seeking in the face of negative consequences and the high tendency to relapse that jointly characterise Substance Use Disorders. In longitudinal studies in rats, we used a combination of refined self-administration procedures, causal manipulations of the corticostriatal circuits, such as functional disconnections or pathway specific manipulations of the brain in rats seeking drugs, in vivo extracellular electrophysiological recordings and molecular biology to identify the neural and psychological basis of these incentive habits. We further demonstrated that incentive habits result in the aberrant engagement of excessive drug seeking behaviour despite past or future negative consequences, or following abstinence. During this talk I will present this novel psychobiological model of addiction and discuss its neural and cellular substrates. I will particularly focus on the notion that once incentive habits have developed, as a result of prolonged exposure to drug seeking under conditioned reinforcement, there is a shift in the goal of this persistent drug seeking from the drug to the response itself.

3. Prof. Laura Andreae – Activity and noise: wiring the brain

The role of neuronal activity in the development of neurons and circuits remains controversial. Historically, activity has been seen to be critical for the sculpting of connectivity patterns after the period of synapse formation, often pruning unused synapses and helping to maintain or grow active ones. We now have evidence that a specific type of activity, spontaneous transmitter release, in the past often regarded as simply 'noise’, plays a role in synapse formation and the development of dendritic morphology at early stages in the developmental period. Using both in vitro and in vivo approaches in mice to manipulate spontaneous transmitter release and the postsynaptic receptors that detect it, we show that these effects are connection specific in the developing hippocampal circuit. Many of the key synaptic proteins involved are known to be mutated in severe neurodevelopmental disorders, indicating how important these early roles may be in healthy brain development.

4. Prof. Lisa Marshall – Investigations on sleep-associated brain rhythms using exogenous stimuli and optogentics

Decades have past since arguments against brain rhythms as epiphenomenon emerged. One apparently straightforward way of investigating the causality of brain rhythms was not only to perturb, but to simulate them. Here, data of studies using electric, acoustic and optogenetic manipulations to modulate brain rhythms and learning and/or memory consolidation in humans and rodents will be presented. Furthermore, interindividual features contribute essentially to the efficiency of applied stimulation. Investigating interactions between cognitive ability and electrophysiological activity may help predict susceptibility to exogenous stimulation.

5. Dr Christian Machens –  Coordinated Spike Coding in EI networks

Models of neural networks can be largely divided into two camps. On one end, mechanistic models such as balanced spiking networks resemble activity regimes observed in data, but are often limited to simple computations. On the other end, functional models like trained deep networks can perform a multitude of computations, but are far removed from experimental physiology. Here, I will introduce a new framework for excitatory-inhibitory spiking networks which retains key properties of both mechanistic and functional models. The key insight is to cast the problem of spiking dynamics in the low-dimensional space of population modes rather than in the original neural space. Neural thresholds then become convex boundaries in the population space, and population dynamics is either attracted (I population) or repelled (E population) by these boundaries. The combination of E and I populations results in balanced, inhibition-stabilized networks which are capable of universal function approximation. I will illustrate these insights with simple, geometric toy models, and I will argue that they force us to reconsider the very basics of how we think about neural networks.

6. Dr Dirk Schubert – From neurodevelopmental disorder gene to mechanism: generating & phenotyping human neuronal networks in the dish

The possibility to produce human induced pluripotent stem cells (hIPSCs) and to let them differentiate into human neuronal-glial in vitro networks has opened doors for investigating the gene to function relation in neurological disorders with high translational power. In this presentation we will briefly discuss challenges involved in identifying risk genes for neurodevelopmental disorders and how selected genes can be tested for their impact on neuronal structural/functional connectivity in a human genetic background in-vitro. To this end we will discuss the steps involved in generating hIPSC derived neuronal in vitro models and how they can be assessed for gene or disorder specific molecular, structural and functional phenotyping, eventually aiming for identifying fundamental disease mechanisms. As an example, we will use a recent study on a rare monogenic de novo mutation associated with schizophrenia.

7. Dr Daniel McNamee – The neural microdynamics of cognition

The entorhinal cortex and hippocampus form a recurrent circuit involved in many cognitive processes including memory, planning, navigation, and imagination. Neural recordings in these regions reveal multiplicitous constructions of latent spaces which subserve these computations. Disparate experiments demonstrate a surprising level of complexity and disorder in the intricate spatiotemporal dynamics of sequential hippocampal reactivations within such latent spaces and provide evidence of a modulatory role for entorhinal cortex. In this talk, I’ll discuss a theoretical cognitive framework and proposed circuit mechanism to integrate and normatively characterize this neural microdynamical complexity and sketch current work on aligning these ideas with those emerging in the generative artificial intelligence literature.