Cellular and Molecular Methods in Neuroscience Research

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2-Minute Neuroscience: Neuroimaging

This is largely due to fundamental differences in size, structure, complexity and functional capacity between rodents and humans. Human brain shows also substantial genetic variability and sensitivity to environmental and life style factors. We have taken advantage of human induced pluripotent stem cell iPSC technology and generated iPSC lines from various neurological and psychiatric diseases.

Differentiation of these patient-specific iPSC lines into neurons, astrocytes and microglia allow us to analyze aberrant gene and protein expression as well function and metabolism in developing human brain well before the disease onset. The interplay between different types of glia and neurons can be analyzed in 3-dimentional cultures and cerebral organoids. Transplantation of these cells into the mouse CNS helps us further define the contribution of different human brain cells to the disease.

Our models can be exposed to various environmental risk factors and acute brain insults, such as stroke and trauma. As blood-brain barrier is frequently compromised or its dysfunction otherwise contributes to human brain disease, we have combined endothelial cells, pericytes and astrocytes for modelling this important brain structure. We have found that in addition to neurons, astrocytes show aberrant transcriptomic and protein expression profile and have strong phenotype in several neurological and psychiatric disease, which we have confirmed in humanized chimeric mice generated by early cell transplantation.

Importantly, we have observed that human brain diseases frequently share the same cellular dysfunction that takes place in different cell types in a disease-specific manner. Using the iPSC-based platform, we are screening small molecule libraries and developing novel biological and small molecules to facilitate drug discovery.

Functional imaging and electrophysiological characterization of diseased human brain cells in organoids and living animals is an important part of our future strategy for better understanding the human brain disease.

Principal investigators

Our research I s funded by Academy of Finland. Business Finland, European Union and several Finnish and foreign research foundations. Group Leader Mikko Airavaara, Ph. We are interested in mechanisms of neurodegeneration, neuroprotection and brain repair.

Key focus areas

Drug therapies for neurodegeneration and stroke are based on alleviating symptoms, and the major challenge we have is to find life quality improving treatments for age-related diseases. Our work is based on neuroinflammation, neurogenesis, neurotrophic factors, protein aggregates, endoplasmic reticulum homeostasis and neurotransmission. We have a passion for excellent level research and by internationally evaluated funding and with excellent level collaborators we can push the frontiers of science.

Our mission is to provide the highest quality science-based teaching and training.

Automatic Translation

Neuronal networks are tuned to optimally represent external and internal milieu through neuronal plasticity during critical periods of juvenile life. The Trophin lab is investigating the role of neurotrophic factors and their receptors in neuronal plasticity and drug responses in developing and adult brain. We have particularly focused on the role of the neurotrophin BDNF brain-derived neurotrophic factor and its receptor TrkB in neuronal plasticity and we have shown that antidepressant drugs and anesthetic agents activate BDNF signaling through TrkB. We have further found that antidepressants reactivate developmental-like plasticity in the visual cortex and fear extinction circuitry in the adult brain in rodents.

When drug-induced plasticity is combined with training or rehabilitation, maladaptive networks wired by an abnormal early life environment can be beneficially rewired in adulthood, which might explain why a combination of antidepressants with psychotherapy work better than either treatment alone. We are now focusing on the neuronal and molecular mechanisms underlying drug-induced TrkB signaling and investigating how adult plasticity could promote recovery in a variety of neuronal disorders.

Group Leader Henrike Hartung, D. Oxon Academy Research Fellow P. My newly formed research group investigates the causes and mechanisms of increased susceptibility to neuropsychiatric disorders by adverse early-life events. These early-life risk-factors include social stress by parental maltreatment, neglect or abuse but also birth-related complications. They have in common that they activate the stress axis of the body and trigger release of stress hormones during critical periods of brain development.

We aim to reveal how this postnatal surge in stress hormones affects the ongoing functional development of the serotonergic and dopaminergic system, whose malfunction has long been implicated in mental illness. Moreover, we study long-range interactions after early-life stress within networks regulating emotional behaviour and reactivity such as medial prefrontal cortex, hippocampus and amygdala. We posit that their altered maturation might underlie increased vulnerability to disease later on in life. Our research efforts have the goal to contribute further insights into the mechanisms that underlie predisposition to neuropsychiatric disorders.

Cellular & Molecular Neurobiology

Such knowledge is crucial for the development of new treatment strategies that aim at disease prevention. Our experimental approach includes in vivo electrophysiological recording techniques in combination with pharmacological manipulations and anatomical studies in rodent models. Currently, only symptomatic treatment options are available for AD. Although recent AD research has focused on how to reverse or delay the cerebral amyloid pathology, amyloid-based therapies have not translated well into humans.

The functionality of all cells depends critically on protein-protein interactions PPI , particularly on the formation of multi-protein complexes. The traditional methods for studying PPIs rely on steady-state analysis of protein complexes that have been extracted from their native cellular environment. This is a significant shortcoming for functional studies.


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We use Protein-fragment Complementation Assays PCA , a novel group of methods that allows studying dynamics of PPIs in live cells, to understand basic molecular mechanisms involved in pathophysiology of neurodegenerative diseases. Our technology platform allows various types of approaches, including mechanistic studies and screening of novel small-molecule modulators of PPIs. GABAA receptor is a target of many psychoactive drugs, such as benzodiazepines, and we are now working to understand what is the role of Tau in these drug responses.

These findings are connected to neuronal cholesterol metabolism, an important player in both AD pathophysiology and neuronal plasticity. The concept of brain as an immune-privileged organ has been permanently bypassed by recent discoveries, including the characterization of a system of lymphatic vessels present in the meninges.

These vessels, together with the anatomical structures and the molecular players regulating the movement of fluids within the Central Nervous System CNS , constitute the unique CNS lymphatic system. CNS lymphatic system is pivotal in the control of the homeostasis of the brain. In addition, we have recently contribute to demonstrate its key role in the neuro-immune interaction: however, understanding the basic of CNS-immune system communication and of regulation of the different immune responses in the brain remains an unmet priority.

Aim of Neuro-lymphatic Lab is to decipher the functionality of the CNS lymphatic system with a specific focus on its role in the neuro-immune interaction. This is important in order to determine the role of immunity particularly T-cells in the pathophysiology of specific neurological diseases, such as traumatic brain injury TBI. Using several approaches to manipulate the CNS lymphatic system which includes transgenic mouse models, virus mediated gene transfer and pharmacological intervention , we analyze the activation of T-cells, their infiltration in the CNS and their interaction with brain- and meningeal-resident cells.

Our strategy is focused on in vivo studies using animal models of TBI, migraine and neuronal hyperexcitability. In this frame, we study mechanisms of macromolecules accumulation and clearance from the brain parenchyma, promoting the activation of the neuro-immune response. A multimodal approach based on in vivo imaging and electrophysiology, behavioral phenotyping and flow cytometry, in combination with molecular and histological techniques, let us to follow up the development and progression of the pathological processes related to the immune response.

Our research goal is to understand the basic mechanisms of neuro-immune interaction, in order to develop novel therapeutic strategies. Group Leader J. Matias Palva group studies the systems-level neuronal mechanisms of emergent neuronal and behavioral dynamics. Spontaneous brain activity fluctuates in time scales spanning at least across five orders of magnitude.

These fluctuations have also been observed on all studied spatial scales and they are statistically governed by spatio-temporal power-laws. Such a scale-free organization at a macroscopic level is, however, contrasted by salient scale-specific neuronal activities - neuronal oscillations.

An Introduction to Cellular and Molecular Neuroscience | Protocol

Our research addresses the functional significance of scale-free and scale-specific brain dynamics in human sensory perception, cognitive performance, and motor output. We are also in the process of translating our data management, analysis, and visualization platform into a more easily shareable python package. Our three main research lines are 1.

We are also performing simulations of brain dynamics and utilize several lines of interventional approaches, from electric and magnetic brain stimulation to cognitive training. Identifying the roles of dysconnectivity and dysdynamics in mental disorders such as depression, anxiety, ADHD and schizophrenia, with the major depressive disorder being our main research focus. Developing neuroplasticity-recruiting cognitive training methods for targeted alterations of cortical connectivity and dynamics. Satu Palva group investigates the functional relevance of neuronal dynamics and large-scale neuronal interactions in human cognition.

In humans, attention, working memory, and consciousness are fundamental cognitive functions, which are serial, introspectively coherent, and have a limited capacity of a few objects.

Neuronal processing underlying these cognitive functions is, however, distributed across the brain and over time. The central goal of our group is to understand how local neuronal oscillations, their large-scale interactions and dynamics are related to fundamental cognitive functions. We aim to test this framework at the level of large-scale neuronal interactions. Our central hypothesis is that cross-frequency interactions among slow and fast oscillations allow the integration and coordination of neuronal processing across cortical hierarchy.

Basic knowledge of molecular and cellular biology and cellular physiology.

Who is involved in molecular and cellular neuroscience?

Basic knowledge of physics and chemistry. Students accepted to the Master's program in Biomedicine at the University of Bergen have full access to the course. Other Masters students at the University of Bergen or exchange students who fulfil the pre-requirements have access to the course after obtaining permission from the course supervisor.

Skip to main content. There is now strong experimental evidence that changes in dendritic spine morphology play an important role in the cognitive processes in brain. We have recently shown that dynamic microtubules enter dendritic spines, are temporal and spatial regulators of spine actin dynamics and cause transient morphological spine alterations.