Environmental enrichment and the striatum: the influence of environment on inhibitory circuitry within the striatum of environmentally enriched animals and behavioural consequences

The nervous system is integral to the healthy and whole functioning of an organism, mediating interactions with and responses to an organism’s surroundings. Environmental enrichment (EE) provides stimuli above that usually experienced within the laboratory environment, and has been shown to greatly impact the nervous system. The maturation of inhibitory circuitry controls the level of neuroplasticity and functional maturity present within neural systems. This thesis investigates the effect of EE upon the development of inhibitory circuitry within the striatum. The striatum is the entry nucleus to the basal ganglia, and as such mediates various cognitive and sensorimotor behaviours. This thesis investigates the effect of EE upon striatally-mediated behaviours of both juvenile and adult animals. This thesis demonstrates that exposure to an enriched environment accelerates maturation of inhibitory circuitry within the striatum and increases the number of active inhibitory interneurons within the adult striatum; improves problem solving and goal-orientated learning; and influences animal behaviours within automated testing apparatus. This work sheds light on the mechanisms by which EE impacts an important nucleus within the brain, and has implications for potential treatments of neurological disorders. Determining the optimum environment for healthy brain development may also aid in early education and intervention programs targeted at young children

Environmental enrichment and the striatum: the influence of environment on inhibitory circuitry within the striatum of environmentally enriched animals and behavioural consequences

The nervous system is integral to the healthy and whole functioning of an organism, mediating interactions with and responses to an organism’s surroundings. Environmental enrichment (EE) provides stimuli above that usually experienced within the laboratory environment, and has been shown to greatly impact the nervous system. The maturation of inhibitory circuitry controls the level of neuroplasticity and functional maturity present within neural systems. This thesis investigates the effect of EE upon the development of inhibitory circuitry within the striatum. The striatum is the entry nucleus to the basal ganglia, and as such mediates various cognitive and sensorimotor behaviours. This thesis investigates the effect of EE upon striatally-mediated behaviours of both juvenile and adult animals. This thesis demonstrates that exposure to an enriched environment accelerates maturation of inhibitory circuitry within the striatum and increases the number of active inhibitory interneurons within the adult striatum; improves problem solving and goal-orientated learning; and influences animal behaviours within automated testing apparatus. This work sheds light on the mechanisms by which EE impacts an important nucleus within the brain, and has implications for potential treatments of neurological disorders. Determining the optimum environment for healthy brain development may also aid in early education and intervention programs targeted at young children

Animal Experimentation: Working Towards a Paradigm Change

Animal experimentation has been one of the most controversial areas of animal use, mainly due to the intentional harms inflicted upon animals for the sake of hoped-for benefits in humans. Despite this rationale for continued animal experimentation, shortcomings of this practice have become increasingly more apparent and well-documented. However, these limitations are not yet widely known or appreciated, and there is a danger that they may simply be ignored. The 51 experts who have contributed to Animal Experimentation: Working Towards a Paradigm Change critically review current animal use in science, present new and innovative non-animal approaches to address urgent scientific questions, and offer a roadmap towards an animal-free world of science.https://www.wellbeingintlstudiesrepository.org/ebooks/1018/thumbnail.jp

Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia.

Parvalbumin inhibitory interneurons (PVIs) are crucial for maintaining proper excitatory/inhibitory balance and high-frequency neuronal synchronization. Their activity supports critical developmental trajectories, sensory and cognitive processing, and social behavior. Despite heterogeneity in the etiology across schizophrenia and autism spectrum disorder, PVI circuits are altered in these psychiatric disorders. Identifying mechanism(s) underlying PVI deficits is essential to establish treatments targeting in particular cognition. On the basis of published and new data, we propose oxidative stress as a common pathological mechanism leading to PVI impairment in schizophrenia and some forms of autism. A series of animal models carrying genetic and/or environmental risks relevant to diverse etiological aspects of these disorders show PVI deficits to be all accompanied by oxidative stress in the anterior cingulate cortex. Specifically, oxidative stress is negatively correlated with the integrity of PVIs and the extracellular perineuronal net enwrapping these interneurons. Oxidative stress may result from dysregulation of systems typically affected in schizophrenia, including glutamatergic, dopaminergic, immune and antioxidant signaling. As convergent end point, redox dysregulation has successfully been targeted to protect PVIs with antioxidants/redox regulators across several animal models. This opens up new perspectives for the use of antioxidant treatments to be applied to at-risk individuals, in close temporal proximity to environmental impacts known to induce oxidative stress

Transitioning to Quality Education

Transitioning to Quality Education focuses on the fourth UN Sustainable Development Goal. According to SDG 4, every learner should acquire the knowledge and skills needed to promote sustainable development (UN 2015, 17). Thus, the aim of sustainability education is to foster learners to be creative and responsible global citizens, who critically reflect on the ideas of sustainable development and the values that underlie them, and take responsible actions for sustainable development (UNESCO 2017). Sustainability is strongly connected to attitudes and values, therefore, applications of sustainability are complicated. Quality education requires teachers to have competences, knowledge, and skills to be able to plan and carry out meaningful education and teaching in sustainability. The aim of Transitioning to Quality Education is to provide versatile experiences and new knowledge on the cognitive, affective, and social issues that are important for promoting sustainable development in formal and non-formal education. Transitioning to Quality Education is part of MDPI's new Open Access book series Transitioning to Sustainability. With this series, MDPI pursues environmentally and socially relevant research which contributes to efforts toward a sustainable world. Transitioning to Sustainability aims to add to the conversation about regional and global sustainable development according to the 17 SDGs. Set to be published in 2020/2021, the book series is intended to reach beyond disciplinary, even academic boundaries

Proceedings of the 18th Irish Conference on Artificial Intelligence and Cognitive Science

These proceedings contain the papers that were accepted for publication at AICS-2007, the 18th Annual Conference on Artificial Intelligence and Cognitive Science, which was held in the Technological University Dublin; Dublin, Ireland; on the 29th to the 31st August 2007. AICS is the annual conference of the Artificial Intelligence Association of Ireland (AIAI)

Trajectory Data Mining in Mouse Models of Stroke

Contains fulltext : 273912.pdf (Publisher’s version ) (Open Access)Radboud University, 04 oktober 2022Promotor : Kiliaan, A.J. Co-promotor : Wiesmann, M.167 p

The Importance Of Neuronal Plasticity In The Prognosis Of Cases Of Cerebral Ischemia: A Systematic Review

Background: Neuronal plasticity is the capacity that the neurons have to make new connections and enable new ways of transmitting information. Under this context, new methodologies are being addressed in order to measure how important this neuronal capacity is in the process of full recovery of learning in subjects who suffered damage from cerebral ischemia.Methods: A systematic review was performed on the online databases: Medical Literature Analysis and Retrieval System Online (MEDLINE) and Scopus, between 1998 and 2014. The MeSH (Medical Subject Headings) descriptors used in this review were: "neuronal plasticity", "brain ischemia" and "learning". We found 164 articles that, when screened, resulted in 46 articles that met the criteria of evidence and were included in this review.Results: There are several ways available in the literature to increase neuronal plasticity to keep the learning process after bad conformations resulting from cerebral ischemia. We highlighted the most elucidated: those promoted by SMe1EC2 antioxidant, which brings therapeutic benefits when neuronal plasticity is impaired; and Atorvastatin, a statin which facilitates recovery of spatial learning. It is further observed that the body has a number of intrinsic devicessuch as the endogenous compensatory mechanisms that contribute to the development of neuronal plasticity when there is brain damage caused by ischemia.Conclusion: The improvement of neuronal plasticity appears in several studies mapped as a new and still little explored possibility of treatment of damages caused by brain processes of oxygen deprivation. Multiple devices, endogenous and exogenous, that promote an increase in neuronal plasticity, are being elucidated in an attempt to promote the full recovery of the learning process, decreased by brain damage from ischemic processes. Thus, it is pointed the necessity of scientific studies that allows to define and maximize the potentials of the neuronal plasticity

Activation of the pro-resolving receptor Fpr2 attenuates inflammatory microglial activation

Poster number: P-T099 Theme: Neurodegenerative disorders & ageing Activation of the pro-resolving receptor Fpr2 reverses inflammatory microglial activation Authors: Edward S Wickstead - Life Science & Technology University of Westminster/Queen Mary University of London Inflammation is a major contributor to many neurodegenerative disease (Heneka et al. 2015). Microglia, as the resident immune cells of the brain and spinal cord, provide the first line of immunological defence, but can become deleterious when chronically activated, triggering extensive neuronal damage (Cunningham, 2013). Dampening or even reversing this activation may provide neuronal protection against chronic inflammatory damage. The aim of this study was to determine whether lipopolysaccharide (LPS)-induced inflammation could be abrogated through activation of the receptor Fpr2, known to play an important role in peripheral inflammatory resolution. Immortalised murine microglia (BV2 cell line) were stimulated with LPS (50ng/ml) for 1 hour prior to the treatment with one of two Fpr2 ligands, either Cpd43 or Quin-C1 (both 100nM), and production of nitric oxide (NO), tumour necrosis factor alpha (TNFα) and interleukin-10 (IL-10) were monitored after 24h and 48h. Treatment with either Fpr2 ligand significantly suppressed LPS-induced production of NO or TNFα after both 24h and 48h exposure, moreover Fpr2 ligand treatment significantly enhanced production of IL-10 48h post-LPS treatment. As we have previously shown Fpr2 to be coupled to a number of intracellular signaling pathways (Cooray et al. 2013), we investigated potential signaling responses. Western blot analysis revealed no activation of ERK1/2, but identified a rapid and potent activation of p38 MAP kinase in BV2 microglia following stimulation with Fpr2 ligands. Together, these data indicate the possibility of exploiting immunomodulatory strategies for the treatment of neurological diseases, and highlight in particular the important potential of resolution mechanisms as novel therapeutic targets in neuroinflammation. References Cooray SN et al. (2013). Proc Natl Acad Sci U S A 110: 18232-7. Cunningham C (2013). Glia 61: 71-90. Heneka MT et al. (2015). Lancet Neurol 14: 388-40