Chaotic recurrent neural networks for brain modelling: A review.

Even in the absence of external stimuli, the brain is spontaneously active. Indeed, most cortical activity is internally generated by recurrence. Both theoretical and experimental studies suggest that chaotic dynamics characterize this spontaneous activity.

A neuro-inspired computational model of life-long learning and catastrophic interference, mimicking hippocampus novelty-based dopamine modulation and lateral inhibitory plasticity.

The human brain has a remarkable lifelong learning capability to acquire new experiences while retaining previously acquired information. Several hypotheses have been proposed to explain this capability, but the underlying mechanisms are still unclear. Here, we propose a neuro-inspired firing-rate computational model involving the hippocampus and surrounding areas, that encompasses two key mechanisms possibly underlying this capability.

A computational model of inner speech supporting flexible goal-directed behaviour in Autism.

Experimental and computational studies propose that inner speech boosts categorisation skills and executive functions, making human behaviour more focused and flexible. In addition, many clinical studies highlight a relationship between poor inner-speech and an executive impairment in autism spectrum condition (ASC), but contrasting findings are reported. Here we directly investigate the latter issue through a previously implemented and validated computational model of the Wisconsin Cards Sorting Tests.

A Biologically Inspired Neural Network Model to Gain Insight Into the Mechanisms of Post-Traumatic Stress Disorder and Eye Movement Desensitization and Reprocessing Therapy.

Eye movement desensitization and reprocessing (EMDR) therapy is a well-established therapeutic method to treat post-traumatic stress disorder (PTSD). However, how EMDR exerts its therapeutic action has been studied in many types of research but still needs to be completely understood. This is in part due to limited knowledge of the neurobiological mechanisms underlying EMDR, and in part to our incomplete understanding of PTSD.

Integrating unsupervised and reinforcement learning in human categorical perception: A computational model.

Categorical perception identifies a tuning of human perceptual systems that can occur during the execution of a categorisation task. Despite the fact that experimental studies and computational models suggest that this tuning is influenced by task-independent effects (e.g.

Neural Circuits Underlying Social Fear in Rodents: An Integrative Computational Model.

Social avoidance in rodents arises from a complex interplay between the prefrontal cortex and subcortical structures, such as the ventromedial hypothalamus and the dorsal periaqueductal gray matter. Experimental studies are revealing the contribution of these areas, but an integrative view and model of how they interact to produce adaptive behavior are still lacking. Here, we present a computational model of social avoidance, proposing a set of integrated hypotheses on the possible macro organization of the brain system underlying this phenomenon.

A Computational Model Integrating Multiple Phenomena on Cued Fear Conditioning, Extinction, and Reinstatement.

Conditioning, extinction, and reinstatement are fundamental learning processes of animal adaptation, also strongly involved in human pathologies such as post-traumatic stress disorder, anxiety, depression, and dependencies. Cued fear conditioning, extinction, restatement, and systematic manipulations of the underlying brain amygdala and medial prefrontal cortex, represent key experimental paradigms to study such processes. Numerous empirical studies have revealed several aspects and the neural systems and plasticity underlying them, but at the moment we lack a comprehensive view.

Enhancing Plasticity Mechanisms in the Mouse Motor Cortex by Anodal Transcranial Direct-Current Stimulation: The Contribution of Nitric Oxide Signaling.

Consistent body of evidence shows that transcranial direct-current stimulation (tDCS) over the primary motor cortex (M1) facilitates motor learning and promotes recovery after stroke. However, the knowledge of molecular mechanisms behind tDCS effects needs to be deepened for a more rational use of this technique in clinical settings. Here we characterized the effects of anodal tDCS of M1, focusing on its impact on glutamatergic synaptic transmission and plasticity.

Glutamate/GABA co-release selectively influences postsynaptic glutamate receptors in mouse cortical neurons.

Cultured rat cortical neurons co-expressing VGLUT1 and VGAT (mixed synapses) co-release Glu and GABA. Here, mixed synapses were studied in cultured mouse cortical neurons to verify whether in mice mixed synapses co-release Glu and GABA, and to gain insight into how they may influence excitation/inhibition balance. Results showed the existence of synapses and autapses that co-release Glu and GABA in cultured mouse cortical neurons, and the ability of both neurotransmitters to evoke postsynaptic responses mediated by ionotropic receptors.

GSK3β Modulates Timing-Dependent Long-Term Depression Through Direct Phosphorylation of Kv4.2 Channels.

Spike timing-dependent plasticity (STDP) is a form of activity-dependent remodeling of synaptic strength that underlies memory formation. Despite its key role in dictating learning rules in the brain circuits, the molecular mechanisms mediating STDP are still poorly understood. Here, we show that spike timing-dependent long-term depression (tLTD) and A-type K+ currents are modulated by pharmacological agents affecting the levels of active glycogen-synthase kinase 3 (GSK3) and by GSK3β knockdown in layer 2/3 of the mouse somatosensory cortex.

Brain insulin resistance impairs hippocampal synaptic plasticity and memory by increasing GluA1 palmitoylation through FoxO3a.

High-fat diet (HFD) and metabolic diseases cause detrimental effects on hippocampal synaptic plasticity, learning, and memory through molecular mechanisms still poorly understood. Here, we demonstrate that HFD increases palmitic acid deposition in the hippocampus and induces hippocampal insulin resistance leading to FoxO3a-mediated overexpression of the palmitoyltransferase zDHHC3. The excess of palmitic acid along with higher zDHHC3 levels causes hyper-palmitoylation of AMPA glutamate receptor subunit GluA1, hindering its activity-dependent trafficking to the plasma membrane.

Loss of Leptin-Induced Modulation of Hippocampal Synaptic Trasmission and Signal Transduction in High-Fat Diet-Fed Mice.

Hippocampal plasticity is triggered by a variety of stimuli including sensory inputs, neurotrophins and inflammation. Leptin, whose primary function is to regulate food intake and energy expenditure, has been recently shown to affect hippocampal neurogenesis and plasticity. Interestingly, mice fed a high-fat diet (HFD) exhibit impaired hippocampal function, but the underlying mechanisms are poorly understood.

Tis21 is required for adult neurogenesis in the subventricular zone and for olfactory behavior regulating cyclins, BMP4, Hes1/5 and Ids.

Bone morphogenic proteins (BMPs) and the Notch pathway regulate quiescence and self-renewal of stem cells of the subventricular zone (SVZ), an adult neurogenic niche. Here we analyze the role at the intersection of these pathways of Tis21 (Btg2/PC3), a gene regulating proliferation and differentiation of adult SVZ stem and progenitor cells. In Tis21-null SVZ and cultured neurospheres, we observed a strong decrease in the expression of BMP4 and its effectors Smad1/8, while the Notch anti-neural mediators Hes1/5 and the basic helix-loop-helix (bHLH) inhibitors Id1-3 increased.

Running rescues defective adult neurogenesis by shortening the length of the cell cycle of neural stem and progenitor cells.

Physical exercise increases the generation of new neurons in adult neurogenesis. However, only few studies have investigated the beneficial effects of physical exercise in paradigms of impaired neurogenesis. Here, we demonstrate that running fully reverses the deficient adult neurogenesis within the hippocampus and subventricular zone of the lateral ventricle, observed in mice lacking the antiproliferative gene Btg1.