scholarly journals Untangling the two-way signalling route from synapses to the nucleus, and from the nucleus back to the synapses

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130150 ◽  
Author(s):  
Mio Nonaka ◽  
Hajime Fujii ◽  
Ryang Kim ◽  
Takashi Kawashima ◽  
Hiroyuki Okuno ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Synaptic Weight ◽  
External Environment ◽  
Synaptic Activity ◽  
Early Gene ◽  
Cellular Mechanisms ◽  
Brain Areas ◽  
Neuronal Soma ◽  
The Brain ◽  
Over Time

During learning and memory, it has been suggested that the coordinated electrical activity of hippocampal neurons translates information about the external environment into internal neuronal representations, which then are stored initially within the hippocampus and subsequently into other areas of the brain. A widely held hypothesis posits that synaptic plasticity is a key feature that critically modulates the triggering and the maintenance of such representations, some of which are thought to persist over time as traces or tags. However, the molecular and cell biological basis for these traces and tags has remained elusive. Here, we review recent findings that help clarify some of the molecular and cellular mechanisms critical for these events, by untangling a two-way signalling crosstalk route between the synapses and the neuronal soma. In particular, a detailed interrogation of the soma-to-synapse delivery of immediate early gene product Arc/Arg3.1, whose induction is triggered by heightened synaptic activity in many brain areas, teases apart an unsuspected ‘inverse’ synaptic tagging mechanism that likely contributes to maintaining the contrast of synaptic weight between strengthened and weak synapses within an active ensemble.

scholarly journals Social instigation and repeated aggressive confrontations in male Swiss mice: analysis of plasma corticosterone, CRF and BDNF levels in limbic brain areas

2017 ◽  
Vol 39 (2) ◽  
pp. 98-105 ◽  
Author(s):  
Paula Madeira Fortes ◽  
Lucas Albrechet-Souza ◽  
Mailton Vasconcelos ◽  
Bruna Maria Ascoli ◽  
Ana Paula Menegolla ◽  
...  
Keyword(s):  
Aggressive Behavior ◽  
Physiological Responses ◽  
Plasma Corticosterone ◽  
Corticotropin Releasing Factor ◽  
Brain Areas ◽  
Social Stressors ◽  
Swiss Mice ◽  
The Brain ◽  
Over Time ◽  
Resident Intruder

Abstract Introduction: Agonistic behaviors help to ensure survival, provide advantage in competition, and communicate social status. The resident-intruder paradigm, an animal model based on male intraspecific confrontations, can be an ethologically relevant tool to investigate the neurobiology of aggressive behavior. Objectives: To examine behavioral and neurobiological mechanisms of aggressive behavior in male Swiss mice exposed to repeated confrontations in the resident intruder paradigm. Methods: Behavioral analysis was performed in association with measurements of plasma corticosterone of mice repeatedly exposed to a potential rival nearby, but inaccessible (social instigation), or to 10 sessions of social instigation followed by direct aggressive encounters. Moreover, corticotropin-releasing factor (CRF) and brain-derived neurotrophic factor (BNDF) were measured in the brain of these animals. Control mice were exposed to neither social instigation nor aggressive confrontations. Results: Mice exposed to aggressive confrontations exhibited a similar pattern of species-typical aggressive and non-aggressive behaviors on the first and the last session. Moreover, in contrast to social instigation only, repeated aggressive confrontations promoted an increase in plasma corticosterone. After 10 aggressive confrontation sessions, mice presented a non-significant trend toward reducing hippocampal levels of CRF, which inversely correlated with plasma corticosterone levels. Conversely, repeated sessions of social instigation or aggressive confrontation did not alter BDNF concentrations at the prefrontal cortex and hippocampus. Conclusion: Exposure to repeated episodes of aggressive encounters did not promote habituation over time. Additionally, CRF seems to be involved in physiological responses to social stressors.

scholarly journals Identification and analysis of vocal communication pathways in birds through inducible gene expression

2004 ◽  
Vol 76 (2) ◽  
pp. 243-246 ◽  
Author(s):  
Claudio V. Mello
Keyword(s):  
Gene Expression ◽  
Auditory Processing ◽  
Vocal Communication ◽  
Vocal Learning ◽  
Early Gene ◽  
Brain Areas ◽  
Control Brain ◽  
Activity Dependent ◽  
The Brain ◽  
Inducible Gene

The immediate-early gene zenk is an activity-dependent gene highly induced in auditory processing or vocal motor control brain areas when birds engage in hearing or producing song, respectively. Studies of the expression of zenk in songbirds and other avian groups will be reviewed here briefly, with a focus on how this analysis has generated new insights on the brain pathways and mechanisms involved in perceptual and motor aspects of vocal communication and vocal learning.

scholarly journals Mechanisms of secretion and spreading of pathological tau protein

2019 ◽  
Vol 77 (9) ◽  
pp. 1721-1744 ◽  
Author(s):  
Cecilia A. Brunello ◽  
Maria Merezhko ◽  
Riikka-Liisa Uronen ◽  
Henri J. Huttunen
Keyword(s):  
Tau Protein ◽  
Molecular Mechanisms ◽  
Recent Literature ◽  
General Mechanism ◽  
Cell Transfer ◽  
Tau Pathology ◽  
Cellular Mechanisms ◽  
Brain Areas ◽  
Cell To Cell Transfer ◽  
The Brain

Abstract Accumulation of misfolded and aggregated forms of tau protein in the brain is a neuropathological hallmark of tauopathies, such as Alzheimer’s disease and frontotemporal lobar degeneration. Tau aggregates have the ability to transfer from one cell to another and to induce templated misfolding and aggregation of healthy tau molecules in previously healthy cells, thereby propagating tau pathology across different brain areas in a prion-like manner. The molecular mechanisms involved in cell-to-cell transfer of tau aggregates are diverse, not mutually exclusive and only partially understood. Intracellular accumulation of misfolded tau induces several mechanisms that aim to reduce the cellular burden of aggregated proteins and also promote secretion of tau aggregates. However, tau may also be released from cells physiologically unrelated to protein aggregation. Tau secretion involves multiple vesicular and non-vesicle-mediated pathways, including secretion directly through the plasma membrane. Consequently, extracellular tau can be found in various forms, both as a free protein and in vesicles, such as exosomes and ectosomes. Once in the extracellular space, tau aggregates can be internalized by neighboring cells, both neurons and glial cells, via endocytic, pinocytic and phagocytic mechanisms. Importantly, accumulating evidence suggests that prion-like propagation of misfolding protein pathology could provide a general mechanism for disease progression in tauopathies and other related neurodegenerative diseases. Here, we review the recent literature on cellular mechanisms involved in cell-to-cell transfer of tau, with a particular focus in tau secretion.

Dorsal Hippocampal–Dependent Episodic Memory Inhibits Eating

2016 ◽  
Vol 25 (6) ◽  
pp. 461-466 ◽  
Author(s):  
Marise B. Parent
Keyword(s):  
Episodic Memory ◽  
Cognitive Processes ◽  
Hippocampal Neurons ◽  
Hippocampal Function ◽  
Brain Areas ◽  
Diet Induced Obesity ◽  
Dorsal Hippocampal ◽  
Meal Timing ◽  
Personal Experiences ◽  
The Brain

Research regarding how the brain regulates eating behavior has focused largely on homeostatic (i.e., need-based) and hedonic (i.e., pleasure-based) controls. By contrast, there is a large gap in our understanding of how brain areas involved in cognitive processes, such as memory, impact energy intake. Moreover, compared to meal size and satiety, little is known about how the brain controls meal timing and frequency. My research team and I hypothesize that dorsal hippocampal neurons, which are critical for episodic memory of personal experiences, form a memory of a meal, inhibit meal initiation during the period following that meal, and limit the amount ingested at the next meal. I review evidence supporting this hypothesis and raise the possibility that impaired dorsal hippocampal function contributes to diet-induced obesity.

Mitochondrial function and inflammation pathways in the neuroprogression of mental disorders

2019 ◽  
pp. 35-62
Author(s):  
Ana C. Andreazza ◽  
Rajas P. Kale ◽  
Angela Duong ◽  
Fabio Molina ◽  
Susannah J. Tye
Keyword(s):  
Mental Illness ◽  
Mental Disorders ◽  
Mitochondrial Function ◽  
Cellular Mechanisms ◽  
Cellular Debris ◽  
Efficient Communication ◽  
Increase Risk ◽  
And Function ◽  
The Brain ◽  
Over Time

Stress, mitochondrial dysfunction, and inflammation are key pathophysiological processes contributing to neuroprogression in mental illness. These factors independently and collectively impact critical cellular mechanisms essential for healthy brain development and function. As these damaging processes continue, cellular debris (damaged DNA and proteins) accumulates, and neuronal integrity is impaired. In addition to this, the myelin sheath that encapsulates neurones to enable smooth and efficient communication throughout the brain is impaired. This chapter outlines how these factors are impacted by stress, inflammation, and mitochondrial function and how they work independently, and together, to increase risk for the development of mental illness, as well as to promote neuroprogression of the illness over time. We discuss how targeting these pathophysiological processes through interdependent factors such as the NLRP3 inflammasome, which sits at the intersection of these mechanistic pathways, may unlock opportunities to limit neuroprogression in the future.

scholarly journals Neuronal activity regulates extracellular tau in vivo

2014 ◽  
Vol 211 (3) ◽  
pp. 387-393 ◽  
Author(s):  
Kaoru Yamada ◽  
Jerrah K. Holth ◽  
Fan Liao ◽  
Floy R. Stewart ◽  
Thomas E. Mahan ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Extracellular Space ◽  
Glutamate Release ◽  
Elimination Rate ◽  
In Vivo Microdialysis ◽  
Synaptic Activity ◽  
Tau Pathology ◽  
Cellular Mechanisms ◽  
The Brain

Tau is primarily a cytoplasmic protein that stabilizes microtubules. However, it is also found in the extracellular space of the brain at appreciable concentrations. Although its presence there may be relevant to the intercellular spread of tau pathology, the cellular mechanisms regulating tau release into the extracellular space are not well understood. To test this in the context of neuronal networks in vivo, we used in vivo microdialysis. Increasing neuronal activity rapidly increased the steady-state levels of extracellular tau in vivo. Importantly, presynaptic glutamate release is sufficient to drive tau release. Although tau release occurred within hours in response to neuronal activity, the elimination rate of tau from the extracellular compartment and the brain is slow (half-life of ∼11 d). The in vivo results provide one mechanism underlying neuronal tau release and may link trans-synaptic spread of tau pathology with synaptic activity itself.

scholarly journals It's about Space, It's about Time, Neuroeconomics and the Brain Sublime

2011 ◽  
Vol 25 (4) ◽  
pp. 31-56 ◽  
Author(s):  
Marieke van Rooij ◽  
Guy Van Orden
Keyword(s):  
Decision Making ◽  
Brain Dynamics ◽  
Alternative View ◽  
Brain Areas ◽  
Change Over Time ◽  
Economic Decision ◽  
Economic Decision Making ◽  
Contemporary Status ◽  
The Brain ◽  
Over Time

Neuroeconomics has investigated which regions of the brain are associated with the factors contributing to economic decision making, emphasizing the position in space of brain areas associated with the factors of decision making—cognitive or emotive, rational or irrational. An alternative view of the brain has given priority to time over space, investigating the temporal patterns of brain dynamics to determine the nature of the brain's intrinsic dynamics, how its various activities change over time. These two ways of approaching the brain are contrasted in this essay to gauge the contemporary status of neuroeconomics.

Hippocampus is more vulnerable to neural damages induced by repeated sevoflurane exposure in the second trimester than other brain areas

2020 ◽  
Vol 52 (8) ◽  
pp. 864-874
Author(s):  
Bing Chen ◽  
Yanjun Liu ◽  
Yirong Cai ◽  
Dan Tang ◽  
Saihong Xu ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Brain Regions ◽  
Sensitive Period ◽  
Second Trimester ◽  
Brain Areas ◽  
Axon Development ◽  
The Central Nervous System ◽  
New Perspective ◽  
Anesthetic Exposure ◽  
The Brain

Abstract During the rapidly developing and sensitive period of the central nervous system (CNS), a harmful stimulus may have serious consequences. The effect of anesthetic exposure on the development of the offspring’s CNS during pregnancy is still unclear and has been widely concerned. In the present study, we compared the susceptibility of the hippocampus with those of other brain regions in offsprings when the mother mice were exposed to repeated sevoflurane. We found that other than affecting motor sensation, emotion, or social behavior of offspring mice, repeated sevoflurane exposure induced significant memory deficiency. Compared with other brain regions, the hippocampus, which is the key component of the brain serving for learning and memory, was more vulnerable to repeated sevoflurane exposure. We also found that repeated sevoflurane exposure to mother mice could inhibit the axon development of hippocampal neurons. We also predicted that N6-methyladenosine modification of mRNA might play an essential role in the vulnerability of the hippocampus to sevoflurane, while the underlying cellular mechanism needs to be explored in the future. Our study may provide a new perspective for studying the mechanism of hippocampus-specific injury induced by sevoflurane exposure.

Aetiologies and anatomy of confabulation

2017 ◽  
Author(s):  
Armin Schnider
Keyword(s):  
Brain Damage ◽  
Limbic Encephalitis ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Brain Areas ◽  
Anatomical Basis ◽  
Korsakoff Syndrome ◽  
Hypoxic Brain ◽  
Degenerative Dementia ◽  
The Brain

What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.

scholarly journals Safety of Catheter Embolization of Pulmonary Arteriovenous Malformations—Evaluation of Possible Cerebrovascular Embolism after Catheter Embolization of Pulmonary Arteriovenous Malformations in Patients with Hereditary Hemorrhagic Telangiectasia/Osler Disease by Pre- and Post-Interventional DWI

2021 ◽  
Vol 10 (4) ◽  
pp. 887
Author(s):  
Guenther Schneider ◽  
Alexander Massmann ◽  
Peter Fries ◽  
Felix Frenzel ◽  
Arno Buecker ◽  
...  
Keyword(s):  
Arteriovenous Malformations ◽  
Pulmonary Arteriovenous Malformations ◽  
B Values ◽  
Safe Method ◽  
Embolization Therapy ◽  
Catheter Embolization ◽  
Contrast Enhanced ◽  
Previously Treated ◽  
The Brain ◽  
Over Time

Background. This paper aimed to prospectively evaluate the safety of embolization therapy of pulmonary arteriovenous malformations (PAVMs) for the detection of cerebral infarctions by pre- and post-interventional MRI. Method One hundred and five patients (male/female = 44/61; mean age 48.6+/−15.8; range 5–86) with pre-diagnosed PAVMs on contrast-enhanced MRA underwent embolization therapy. The number of PAVMs treated in each patient ranged from 1–8 PAVMs. Depending on the size and localization of the feeding arteries, either Nester-Coils or Amplatzer vascular plugs were used for embolization therapy. cMRI was performed immediately before, and at the 4 h and 3-month post-embolization therapy. Detection of peri-interventional cerebral emboli was performed via T2w and DWI sequences using three different b-values, with calculation of ADC maps. Results Embolization did not show any post-/peri-interventional, newly developed ischemic lesions in the brain. Only one patient who underwent re-embolization and was previously treated with tungsten coils that corroded over time showed newly developed, small, diffuse emboli in the post-interventional DWI sequence. This patient already had several episodes of brain emboli before re-treatment due to the corroded coils, and during treatment, when passing the corroded coils, experienced additional small, clinically inconspicuous brain emboli. However, this complication was anticipated but accepted, since the vessel had to be occluded distally. Conclusion Catheter-based embolization of PAVMs is a safe method for treatment and does not result in clinically inconspicuous cerebral ischemia, which was not demonstrated previously.

Sign in / Sign up

Export Citation Format

Share Document