scholarly journals Regulation of Central Nervous System Myelination in Higher Brain Functions

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Mara Nickel ◽  
Chen Gu
Keyword(s):  
Prefrontal Cortex ◽  
Neural Plasticity ◽  
Lipid Membranes ◽  
Neural Circuit ◽  
Brain Regions ◽  
Research Field ◽  
Brain Functions ◽  
Experimental Systems ◽  
And Function ◽  
Higher Brain Functions

The hippocampus and the prefrontal cortex are interconnected brain regions, playing central roles in higher brain functions, including learning and memory, planning complex cognitive behavior, and moderating social behavior. The axons in these regions continue to be myelinated into adulthood in humans, which coincides with maturation of personality and decision-making. Myelin consists of dense layers of lipid membranes wrapping around the axons to provide electrical insulation and trophic support and can profoundly affect neural circuit computation. Recent studies have revealed that long-lasting changes of myelination can be induced in these brain regions by experience, such as social isolation, stress, and alcohol abuse, as well as by neurological and psychiatric abnormalities. However, the mechanism and function of these changes remain poorly understood. Myelin regulation represents a new form of neural plasticity. Some progress has been made to provide new mechanistic insights into activity-independent and activity-dependent regulations of myelination in different experimental systems. More extensive investigations are needed in this important but underexplored research field, in order to shed light on how higher brain functions and myelination interplay in the hippocampus and prefrontal cortex.

Recalling Safety: Cooperative Functions of the Ventromedial Prefrontal Cortex and the Hippocampus in Extinction

CNS Spectrums ◽  
2007 ◽  
Vol 12 (3) ◽  
pp. 200-206 ◽  
Author(s):  
Kevin A. Corcoran ◽  
Gregory J. Quirk
Keyword(s):  
Prefrontal Cortex ◽  
Neural Plasticity ◽  
Neural Circuit ◽  
Contextual Information ◽  
Conditioned Fear ◽  
Brain Regions ◽  
Ventromedial Prefrontal Cortex ◽  
Fear Learning ◽  
Extinction Learning ◽  
Fear And Anxiety

ABSTRACTAnxiety disorders are commonly treated with exposure-based therapies that rely on extinction of conditioned fear. Persistent fear and anxiety following exposure therapy could reflect a deficit in the recall of extinction learning. Animal models of fear learning have elucidated a neural circuit for extinction learning and recall that includes the amygdala, ventromedial prefrontal cortex (vmPFC), and hippocampus. Whereas the amygdala is important for extinction learning, the vmPFC is a site of neural plasticity that allows for the inhibition of fear during extinction recall. We suggest that the vmPFC receives convergent information from other brain regions, such as contextual information from the hippocampus, to determine the circumstances under which extinction or fear will be recalled. Imaging studies of human fear conditioning and extinction lend credence to this extinction network. Understanding the neural circuitry underlying extinction recall will lead to more effective therapies for disorders of fear and anxiety.

scholarly journals The Participation of Hormones in the Processes of Cognitive and Socio-Emotional Aging

2020 ◽  
Vol 6 (8) ◽  
pp. 97-129
Author(s):  
S. Bulgakova ◽  
N. Romanchuk
Keyword(s):  
Sex Hormones ◽  
Neural Plasticity ◽  
Emotion Dysregulation ◽  
Emotional Functioning ◽  
Progesterone Receptors ◽  
Endocrine System ◽  
Neurite Growth ◽  
Brain Regions ◽  
Adult Brain ◽  
Brain Functions

Aging is associated with generally accepted changes in brain functions, including cognitive ones. In addition, age makes its own adjustments to the work of the endocrine system. In turn, a change in the hormonal background during the aging process imprints the work of brain cells, cognitive functions, and socio-emotional functioning. Investigated, the relationship between sex hormones, cortisol, oxytocin and cognitive and socio-emotional functioning. Sex hormones are involved in neurite growth, synaptogenesis, dendritic branching, myelination, and other important mechanisms of neural plasticity. Physiological and pathological conceptualized theories suggest how sex hormones potentially cause neuroplasticity changes through four neurochemical neurotransmitter systems: serotonin, dopamine, GABA and glutamate. Many brain regions express high density estrogen and progesterone receptors such as the amygdala, hypothalamus, and hippocampus. The hippocampus is of particular importance in the context of mediating structural plasticity in the adult brain, differences in behavior, neurochemical patterns and structure of the hippocampus with a changing hormonal environment have been investigated. There is a significant association between emotion dysregulation and symptoms of depression, anxiety, eating pathology, and substance abuse. Higher levels of emotion regulation are associated with a high level of social competence.

scholarly journals Rapid and Reversible Development of Axonal Varicosities: A New Form of Neural Plasticity

2021 ◽  
Vol 14 ◽  
Author(s):  
Chen Gu
Keyword(s):  
Neural Plasticity ◽  
Brain Injuries ◽  
Brain Regions ◽  
Research Field ◽  
Pathological Feature ◽  
Axonal Pathology ◽  
Parkinson’S Diseases ◽  
New Form

Axonal varicosities are enlarged, heterogeneous structures along axonal shafts, profoundly affecting axonal conduction and synaptic transmission. They represent a key pathological feature believed to develop via slow accumulation of axonal damage that occurs during irreversible degeneration, for example in mild traumatic brain injury (mTBI), Alzheimer's and Parkinson's diseases, and multiple sclerosis. Here this review first discusses recent in vitro results showing that axonal varicosities can be rapidly and reversibly induced by mechanical stress in cultured primary neurons from the central nervous system (CNS). This notion is further supported by in vivo studies revealing the induction of axonal varicosities across various brain regions in different mTBI mouse models, as a prominent feature of axonal pathology. Limited progress in understanding intrinsic and extrinsic regulatory mechanisms of axonal varicosity induction and development is further highlighted. Rapid and reversible formation of axonal varicosities likely plays a key role in CNS neuron mechanosensation and is a new form of neural plasticity. Future investigation in this emerging research field may reveal how to reverse axonal injury, contributing to the development of new strategies for treating brain injuries and related neurodegenerative diseases.

scholarly journals Epigenetic signaling in psychiatric disorders: stress and depression

2014 ◽  
Vol 16 (3) ◽  
pp. 281-295 ◽  
Keyword(s):  
Environmental Factors ◽  
Psychiatric Disorders ◽  
Neural Circuit ◽  
Brain Regions ◽  
Transcriptional Dysregulation ◽  
Epigenetic Machinery ◽  
Multifactorial Disorders ◽  
As Stress ◽  
And Function ◽  
Circuit Function

Psychiatric disorders are complex multifactorial disorders involving chronic alterations in neural circuit structure and function. While genetic factors play a role in the etiology of disorders such as depression, addiction, and schizophrenia, relatively high rates of discordance among identical twins clearly point to the importance of additional factors. Environmental factors, such as stress, play a major role in the psychiatric disorders by inducing stable changes in gene expression, neural circuit function, and ultimately behavior. Insults at the developmental stage and in adulthood appear to induce distinct maladaptations. Increasing evidence indicates that these sustained abnormalities are maintained by epigenetic modifications in specific brain regions. Indeed, transcriptional dysregulation and associated aberrant epigenetic regulation is a unifying theme in psychiatric disorders. Aspects of depression can be modeled in animals by inducing disease-like states through environmental manipulations, and these studies can provide a more general understanding of epigenetic mechanisms in psychiatric disorders. Understanding how environmental factors recruit the epigenetic machinery in animal models is providing new insights into disease mechanisms in humans.

scholarly journals Characterization of an eutherian gene cluster generated after transposon domestication identifies Bex3 as relevant for advanced neurological functions

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Enrique Navas-Pérez ◽  
Cristina Vicente-García ◽  
Serena Mirra ◽  
Demian Burguera ◽  
Noèlia Fernàndez-Castillo ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Gene Cluster ◽  
Neurological Disorders ◽  
Evolutionary Process ◽  
Brain Functions ◽  
Molecular Domestication ◽  
Multigenic Family ◽  
Neurological Features ◽  
And Function ◽  
Higher Brain Functions

Abstract Background One of the most unusual sources of phylogenetically restricted genes is the molecular domestication of transposable elements into a host genome as functional genes. Although these kinds of events are sometimes at the core of key macroevolutionary changes, their origin and organismal function are generally poorly understood. Results Here, we identify several previously unreported transposable element domestication events in the human and mouse genomes. Among them, we find a remarkable molecular domestication that gave rise to a multigenic family in placental mammals, the Bex/Tceal gene cluster. These genes, which act as hub proteins within diverse signaling pathways, have been associated with neurological features of human patients carrying genomic microdeletions in chromosome X. The Bex/Tceal genes display neural-enriched patterns and are differentially expressed in human neurological disorders, such as autism and schizophrenia. Two different murine alleles of the cluster member Bex3 display morphological and physiopathological brain modifications, such as reduced interneuron number and hippocampal electrophysiological imbalance, alterations that translate into distinct behavioral phenotypes. Conclusions We provide an in-depth understanding of the emergence of a gene cluster that originated by transposon domestication and gene duplication at the origin of placental mammals, an evolutionary process that transformed a non-functional transposon sequence into novel components of the eutherian genome. These genes were integrated into existing signaling pathways involved in the development, maintenance, and function of the CNS in eutherians. At least one of its members, Bex3, is relevant for higher brain functions in placental mammals and may be involved in human neurological disorders.

scholarly journals Cytosolic PSD-95 Interactor Alters Functional Organization of Neural Circuits and AMPA Receptor Signaling Independent of PSD-95 Binding

2020 ◽  
pp. 1-72
Author(s):  
Ana R. Rodriguez ◽  
Erin D. Anderson ◽  
Kate M. O’Neill ◽  
Przemyslaw P. McEwan ◽  
Nicholas F. Vigilante ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Microelectrode Array ◽  
Neural Circuits ◽  
Neural Circuit ◽  
Functional Organization ◽  
Protein Localization ◽  
Postsynaptic Density ◽  
Brain Regions ◽  
Receptor Signaling ◽  
And Function

Cytosolic PSD-95 interactor (cypin) regulates many aspects of neuronal development and function, ranging from dendritogenesis to synaptic protein localization. While it is known that removal of postsynaptic density protein-95 (PSD-95) from the postsynaptic density decreases synaptic NMDA receptors and that cypin overexpression protects neurons from NMDA-induced toxicity, little is known about cypin’s role in AMPA receptor clustering and function. Experimental work shows that cypin overexpression decreases PSD-95 levels in synaptosomes and the PSD, decreases PSD-95 clusters/μm2, and increases mEPSC frequency. Analysis of microelectrode array (MEA) data demonstrates that cypin or cypinΔPDZ overexpression increases sensitivity to CNQX and AMPA receptor mediated decreases in spike waveform properties. Network-level analysis of MEA data reveals that cypinΔPDZ overexpression causes networks to be resilient to CNQX-induced changes in local efficiency. Incorporating these findings into a computational model of a neural circuit demonstrates a role for AMPA receptors in cypin-promoted changes to networks and shows that cypin increases firing rate while changing network functional organization, suggesting cypin overexpression facilitates information relay but modifies how information is encoded among brain regions. Our data show that cypin promotes changes to AMPA receptor signaling independent of PSD-95 binding, shaping neural circuits and output to regions beyond the hippocampus.

scholarly journals Clear optically matched panoramic access channel technique (COMPACT) for large-volume deep brain imaging

2020 ◽  
Author(s):  
Bowen Wei ◽  
Chenmao Wang ◽  
Zongyue Cheng ◽  
Wenbiao Gan ◽  
Meng Cui
Keyword(s):  
Large Volume ◽  
Neural Circuit ◽  
Tissue Imaging ◽  
Neuronal Structure ◽  
Brain Functions ◽  
Cellular Resolution ◽  
Access Channel ◽  
Resolution Imaging ◽  
And Function ◽  
Deep Brain

To understand neural circuit mechanisms underlying behavior, it is crucial to observe the dynamics of neuronal structure and function in different parts of the brain. Current imaging technologies allow cellular resolution imaging of neurons within ~1 millimeter below the cortical surface. Even for mice, the majority of brain tissue remains inaccessible. Although miniature optical imaging probes allow the access of deep brain regions, the cellular-resolution imaging is restricted to a small tissue volume. To drastically increase the tissue access volume and enable a high-throughput neurophotonic interface, we developed a clear optically matched panoramic access channel technique (COMPACT). With comparable probe dimension, COMPACT enables a two to three orders of magnitude greater tissue access volume for structural and function imaging. Leveraging the large-volume imaging capability of COMPACT, we demonstrated multiregional calcium imaging of deep brain functions associated with sleep for the first time. The compatibility of COMPACT for longitudinal large-volume in vivo imaging will be highly valuable to a variety of deep tissue imaging applications.

scholarly journals Neuron-glia Integrity: Functional Assessment, Molecular Underpinnings, and Implication for Higher Brain Functions

2020 ◽  
Author(s):  
Haiyan Zeng ◽  
Xiaolei Zhang ◽  
Wenqiang Wang ◽  
Zhiwei Shen ◽  
Zhuozhi Dai ◽  
...  
Keyword(s):  
Maternal Separation ◽  
Brain Regions ◽  
Behavioral Performance ◽  
Gaba Level ◽  
Early Weaning ◽  
Protein Levels ◽  
Brain Functions ◽  
Functional Assessments ◽  
The Central Nervous System ◽  
Higher Brain Functions

AbstractWe developed a theory of neuron-glia integrity to underline the fact that neurons and glia cells work together in the central nervous system. Here we substantiated this theory and exemplified the implication of intact neuron-glia integrity for higher brain functions. An animal model of maternal separation with early weaning (MSEW) was applied to neonatal rats to mimic early life neglect and abuse in humans. Behavioral performance of rats was evaluated at adulthood, followed by functional assessments of neuron-glia integrity in living rats, and the demonstration of molecular underpinnings of impaired neuron-glia integrity in MSEW rats. MSEW rats showed higher levels of anxiety and explorative activity, higher glutamate level, but lower GABA level in PFC and hippocampus. MSEW procedure down-regulated protein levels of GLT-1 and ATP-α, but up-regulated GAD65 and GS, while had no effects on GLAST and PAG. Moreover, it reduced the fractional anisotropy values in various brain regions, in addition to increasing NAA levels. Concurrently, MSEW led to hypomyelination in PFC as evidenced by relevant cellular and molecular changes.

scholarly journals CaMKII holoenzyme mechanisms that govern the LTP versus LTD decision

2021 ◽  
Vol 7 (16) ◽  
pp. eabe2300
Author(s):  
Sarah G. Cook ◽  
Olivia R. Buonarati ◽  
Steven J. Coultrap ◽  
K. Ulrich Bayer
Keyword(s):  
Stimulus Frequency ◽  
Long Term Potentiation ◽  
Inhibitory Synapses ◽  
Brain Functions ◽  
Term Potentiation ◽  
Autonomous Activity ◽  
And Function ◽  
Higher Brain Functions ◽  
Feed Forward Inhibition

Higher brain functions are thought to require synaptic frequency decoding that can lead to long-term potentiation (LTP) or depression (LTD). We show that the LTP versus LTD decision is determined by complex cross-regulation of T286 and T305/306 autophosphorylation within the 12meric CaMKII holoenzyme, which enabled molecular computation of stimulus frequency, amplitude, and duration. Both LTP and LTD require T286 phosphorylation, but T305/306 phosphorylation selectively promoted LTD. In response to excitatory LTP versus LTD stimuli, the differential T305/306 phosphorylation directed CaMKII movement to either excitatory or inhibitory synapses, thereby coordinating plasticity at both synapse types. Fast T305/306 phosphorylation required prior T286 phosphorylation and then curbed CaMKII activity by two mechanisms: (i) a cis-subunit reaction reduced both Ca2+ stimulation and autonomous activity and (ii) a trans-subunit reaction enabled complete activity shutdown and feed-forward inhibition of further T286 phosphorylation. These are fundamental additions to the long-studied CaMKII regulation and function in neuronal plasticity.

scholarly journals The role of astrocyte‐mediated plasticity in neural circuit development and function

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Nelson A. Perez-Catalan ◽  
Chris Q. Doe ◽  
Sarah D. Ackerman
Keyword(s):  
Nervous System ◽  
Neural Plasticity ◽  
Neural Circuit ◽  
System Development ◽  
Critical Role ◽  
Nervous System Development ◽  
Functional Changes ◽  
Sensory Evoked ◽  
And Function

AbstractNeuronal networks are capable of undergoing rapid structural and functional changes called plasticity, which are essential for shaping circuit function during nervous system development. These changes range from short-term modifications on the order of milliseconds, to long-term rearrangement of neural architecture that could last for the lifetime of the organism. Neural plasticity is most prominent during development, yet also plays a critical role during memory formation, behavior, and disease. Therefore, it is essential to define and characterize the mechanisms underlying the onset, duration, and form of plasticity. Astrocytes, the most numerous glial cell type in the human nervous system, are integral elements of synapses and are components of a glial network that can coordinate neural activity at a circuit-wide level. Moreover, their arrival to the CNS during late embryogenesis correlates to the onset of sensory-evoked activity, making them an interesting target for circuit plasticity studies. Technological advancements in the last decade have uncovered astrocytes as prominent regulators of circuit assembly and function. Here, we provide a brief historical perspective on our understanding of astrocytes in the nervous system, and review the latest advances on the role of astroglia in regulating circuit plasticity and function during nervous system development and homeostasis.

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