scholarly journals Astrocytes, Noradrenaline, α1-Adrenoreceptors, and Neuromodulation: Evidence and Unanswered Questions

2021 ◽  
Vol 15 ◽  
Author(s):  
Jérôme Wahis ◽  
Matthew G. Holt
Keyword(s):  
Critical Appraisal ◽  
Brain Regions ◽  
Synaptic Activity ◽  
Physiological Effects ◽  
Astrocyte Heterogeneity ◽  
Main Effect ◽  
The Central Nervous System ◽  
Noradrenergic Modulation ◽  
The Brain ◽  
Experimental Strategies

Noradrenaline is a major neuromodulator in the central nervous system (CNS). It is released from varicosities on neuronal efferents, which originate principally from the main noradrenergic nuclei of the brain – the locus coeruleus – and spread throughout the parenchyma. Noradrenaline is released in response to various stimuli and has complex physiological effects, in large part due to the wide diversity of noradrenergic receptors expressed in the brain, which trigger diverse signaling pathways. In general, however, its main effect on CNS function appears to be to increase arousal state. Although the effects of noradrenaline have been researched extensively, the majority of studies have assumed that noradrenaline exerts its effects by acting directly on neurons. However, neurons are not the only cells in the CNS expressing noradrenaline receptors. Astrocytes are responsive to a range of neuromodulators – including noradrenaline. In fact, noradrenaline evokes robust calcium transients in astrocytes across brain regions, through activation of α1-adrenoreceptors. Crucially, astrocytes ensheath neurons at synapses and are known to modulate synaptic activity. Hence, astrocytes are in a key position to relay, or amplify, the effects of noradrenaline on neurons, most notably by modulating inhibitory transmission. Based on a critical appraisal of the current literature, we use this review to argue that a better understanding of astrocyte-mediated noradrenaline signaling is therefore essential, if we are ever to fully understand CNS function. We discuss the emerging concept of astrocyte heterogeneity and speculate on how this might impact the noradrenergic modulation of neuronal circuits. Finally, we outline possible experimental strategies to clearly delineate the role(s) of astrocytes in noradrenergic signaling, and neuromodulation in general, highlighting the urgent need for more specific and flexible experimental tools.

Neurotrophins and Proneurotrophins: Focus on Synaptic Activity and Plasticity in the Brain

2017 ◽  
Vol 23 (6) ◽  
pp. 587-604 ◽  
Author(s):  
Julien Gibon ◽  
Philip A. Barker
Keyword(s):  
Long Term Potentiation ◽  
Synaptic Activity ◽  
Cellular Processes ◽  
Term Potentiation ◽  
Neurotrophin 3 ◽  
New Findings ◽  
The Central Nervous System ◽  
The Brain

Neurotrophins have been intensively studied and have multiple roles in the brain. Neurotrophins are first synthetized as proneurotrophins and then cleaved intracellularly and extracellularly. Increasing evidences demonstrate that proneurotrophins and mature neurotrophins exerts opposing role in the central nervous system. In the present review, we explore the role of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4) and their respective proform in cellular processes related to learning and memory. We focused on their roles in synaptic activity and plasticity in the brain with an emphasis on long-term potentiation, long-term depression, and basal synaptic transmission in the hippocampus and the temporal lobe area. We also discuss new findings on the role of the Val66Met polymorphism on the BDNF propeptide on synaptic activity.

scholarly journals Supportive or information-processing functions of the mature protoplasmic astrocyte in the mammalian CNS? A critical appraisal

2007 ◽  
Vol 3 (3) ◽  
pp. 181-189 ◽  
Author(s):  
Harold K. Kimelberg
Keyword(s):  
Information Processing ◽  
Blood Vessel ◽  
Critical Appraisal ◽  
Vessel Diameter ◽  
Synaptic Activity ◽  
Metabolic Substrates ◽  
Processing Properties ◽  
New Evidence ◽  
The Brain ◽  
Domain Concept

AbstractIt has been proposed that astrocytes should no longer be viewed purely as support cells for neurons, such as providing a constant environment and metabolic substrates, but that they should also be viewed as being involved in affecting synaptic activity in an active way and, therefore, an integral part of the information-processing properties of the brain. This essay discusses the possible differences between a support and an instructive role, and concludes that any distinction has to be blurred. In view of this, and a brief overview of the nature of the data, the new evidence seems insufficient to conclude that the physiological roles of mature astrocytes go beyond a general support role. I propose a model of mature protoplasmic astrocyte function that is drawn from the most recent data on their structure, the domain concept and their syncytial characteristics, of an independent rather than integrative functioning of the ends of each process where the activities that affect synaptic activity and blood vessel diameter will be concentrated.

scholarly journals Effects of tiletamine-xylazine-tramadol combination and its specific antagonist on AMPK in the brain of rats

2019 ◽  
Vol 63 (2) ◽  
pp. 285-292
Author(s):  
Ning Ma ◽  
Xin Li ◽  
Hong-bin Wang ◽  
Li Gao ◽  
Jian-hua Xiao
Keyword(s):  
Mrna Expression ◽  
Opposite Effect ◽  
Brain Regions ◽  
Control Group ◽  
Sprague Dawley ◽  
Sd Rats ◽  
The Central Nervous System ◽  
Specific Antagonist ◽  
Sedation And Analgesia ◽  
The Brain

AbstractIntroduction:Tiletamine-xylazine-tramadol (XFM) has few side effects and can provide good sedation and analgesia. Adenosine 5’-monophosphate-activated protein kinase (AMPK) can attenuate trigeminal neuralgia. The study aimed to investigate the effects of XFM and its specific antagonist on AMPK in different regions of the brain.Material and Methods:A model of XFM in the rat was established. A total of 72 Sprague Dawley (SD) rats were randomly divided into three equally sized groups: XFM anaesthesia (M group), antagonist (W group), and XFM with antagonist interactive groups (MW group). Eighteen SD rats were in the control group and were injected intraperitoneally with saline (C group). The rats were sacrificed and the cerebral cortex, cerebellum, hippocampus, thalamus, and brain stem were immediately separated, in order to detect AMPKα mRNA expression by quantitative PCR.Results:XFM was able to increase the mRNA expression of AMPKα1 and AMPKα2 in all brain regions, and the antagonist caused the opposite effect, although the effects of XFM could not be completely reversed in some areas.Conclusion:XFM can influence the expression of AMPK in the central nervous system of the rat, which can provide a reference for the future development of anaesthetics for animals.

The somatic error hypothesis of anxiety

2018 ◽  
Author(s):  
Sahib S. Khalsa ◽  
Justin S. Feinstein
Keyword(s):  
Central Nervous System ◽  
Physiological State ◽  
Brain Regions ◽  
Novel Therapies ◽  
Body State ◽  
Long Term Changes ◽  
The Central Nervous System ◽  
And Behavior ◽  
The Brain

A regulatory battle for control ensues in the central nervous system following a mismatch between the current physiological state of an organism as mapped in viscerosensory brain regions and the predicted body state as computed in visceromotor control regions. The discrepancy between the predicted and current body state (i.e. the “somatic error”) signals a need for corrective action, motivating changes in both cognition and behavior. This chapter argues that anxiety disorders are fundamentally driven by somatic errors that fail to be adaptively regulated, leaving the organism in a state of dissonance where the predicted body state is perpetually out of line with the current body state. Repeated failures to quell somatic error can result in long-term changes to interoceptive circuitry within the brain. This chapter explores the neuropsychiatric sequelae that can emerge following chronic allostatic dysregulation of somatic errors and discusses novel therapies that might help to correct this dysregulation.

Increased µ-opioid receptors in sheep brain after transport

1995 ◽  
Vol 1995 ◽  
pp. 204-204
Author(s):  
E.A. Azaga ◽  
R.G. Rodway
Keyword(s):  
Opioid Receptors ◽  
Opioid Peptide ◽  
Brain Regions ◽  
Long Distance ◽  
Long Distance Transport ◽  
The Central Nervous System ◽  
Sheep Brain ◽  
Transport Stress ◽  
Distance Transport ◽  
The Brain

The long distance transport of sheep before slaughter is at present a very important topic in animal welfare. However, Modulation of opioid receptors can be influenced by chronic treatment with opioid agonists and antagonists (Blanchard, and Chang, 1988). Similarly, opioid receptors can be up or down-regulated by stressful stimuli such as restraint, electric footshock or social isolation and housing (Zeman et al., 1988 and Zanella et al., 1991). The present study was carried out to assess the effects of transport stress on the properties of one class of opioid peptide receptor in the brain of sheep after transport stress. Opioid peptides such as β-endorphin are released by the central nervous system during application of stresses such as transport. They are believed to exert analgesic properties and their effectiveness depends partly on the concentration (Bmax) and affinity (Kd) of their receptors. µ-Opioid receptors are found in various brain regions and are selective for endorphins and similar peptides.

Exposure to 835 MHz radiofrequency electromagnetic field induces autophagy in hippocampus but not in brain stem of mice

2017 ◽  
Vol 34 (1) ◽  
pp. 23-35 ◽  
Author(s):  
Ju Hwan Kim ◽  
Da-Hyeon Yu ◽  
Hyo-Jeong Kim ◽  
Yang Hoon Huh ◽  
Seong-Wan Cho ◽  
...  
Keyword(s):  
Brain Stem ◽  
Mobile Phones ◽  
Hippocampal Neurons ◽  
Brain Regions ◽  
Pcr Analysis ◽  
Limited Information ◽  
The Central Nervous System ◽  
Neuronal Functions ◽  
Adaptation Processes ◽  
The Brain

The exploding popularity of mobile phones and their close proximity to the brain when in use has raised public concern regarding possible adverse effects from exposure to radiofrequency electromagnetic fields (RF-EMF) on the central nervous system. Numerous studies have suggested that RF-EMF emitted by mobile phones can influence neuronal functions in the brain. Currently, there is still very limited information on what biological mechanisms influence neuronal cells of the brain. In the present study, we explored whether autophagy is triggered in the hippocampus or brain stem after RF-EMF exposure. C57BL/6 mice were exposed to 835 MHz RF-EMF with specific absorption rates (SAR) of 4.0 W/kg for 12 weeks; afterward, the hippocampus and brain stem of mice were dissected and analyzed. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis demonstrated that several autophagic genes, which play key roles in autophagy regulation, were significantly upregulated only in the hippocampus and not in the brain stem. Expression levels of LC3B-II protein and p62, crucial autophagic regulatory proteins, were significantly changed only in the hippocampus. In parallel, transmission electron microscopy (TEM) revealed an increase in the number of autophagosomes and autolysosomes in the hippocampal neurons of RF-EMF-exposed mice. The present study revealed that autophagy was induced in the hippocampus, not in the brain stem, in 835 MHz RF-EMF with an SAR of 4.0 W/kg for 12 weeks. These results could suggest that among the various adaptation processes to the RF-EMF exposure environment, autophagic degradation is one possible mechanism in specific brain regions.

scholarly journals Nanomedicine in Clinical Photodynamic Therapy for the Treatment of Brain Tumors

Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 96
Author(s):  
Hyung Shik Kim ◽  
Dong Yun Lee
Keyword(s):  
Photodynamic Therapy ◽  
Brain Tumors ◽  
Surgical Resection ◽  
Extent Of Resection ◽  
Brain Regions ◽  
Current Treatment ◽  
Point Of View ◽  
The Central Nervous System ◽  
One Year ◽  
The Brain

The current treatment for malignant brain tumors includes surgical resection, radiotherapy, and chemotherapy. Nevertheless, the survival rate for patients with glioblastoma multiforme (GBM) with a high grade of malignancy is less than one year. From a clinical point of view, effective treatment of GBM is limited by several challenges. First, the anatomical complexity of the brain influences the extent of resection because a fine balance must be struck between maximal removal of malignant tissue and minimal surgical risk. Second, the central nervous system has a distinct microenvironment that is protected by the blood–brain barrier, restricting systemically delivered drugs from accessing the brain. Additionally, GBM is characterized by high intra-tumor and inter-tumor heterogeneity at cellular and histological levels. This peculiarity of GBM-constituent tissues induces different responses to therapeutic agents, leading to failure of targeted therapies. Unlike surgical resection and radiotherapy, photodynamic therapy (PDT) can treat micro-invasive areas while protecting sensitive brain regions. PDT involves photoactivation of photosensitizers (PSs) that are selectively incorporated into tumor cells. Photo-irradiation activates the PS by transfer of energy, resulting in production of reactive oxygen species to induce cell death. Clinical outcomes of PDT-treated GBM can be advanced in terms of nanomedicine. This review discusses clinical PDT applications of nanomedicine for the treatment of GBM.

Learning styles and the human brain: what does the evidence tell us?

2019 ◽  
Author(s):  
Francisco J. Álvarez-Montero
Keyword(s):  
Learning Styles ◽  
Human Brain ◽  
Instructional Strategy ◽  
Multimodal Interaction ◽  
Reliability And Validity ◽  
Brain Regions ◽  
Learning Preferences ◽  
Synaptic Activity ◽  
Physical Infrastructure ◽  
The Brain

Learning Styles (LS) are a very popular idea in Education and Psychology. However, most studies indicate that matching the instructional strategy to the students’ LS does not improve learning, and that their inventories do not have acceptable levels of reliability and validity. The research presented here compares the theoretical hypotheses of LS, with what is currently known about the architecture of the human brain, and the way it processes information to make sense of the environment and learn. Thus, providing new evidence on the subject that has not been previously discussed. The analysis shows that the brain is composed of a set of anatomically distributed networks, where there is a permanent cross-modal or multimodal interaction, between different types of specialized neuron modules and brain regions. Something which is not compatible with the notions of unimodality and fractional or partial modality, proposed by LS advocates. Furthermore, evidence on white matter plasticity and synaptic activity, point out that part of the physical infrastructure required to master a new ability, needs to be created on demand, contradicting the hypothesis that LS are innate learning preferences. Finally, although it can be said that there is some level of resemblance between LS and the brain, such an association cannot be easily made.

Partial saturation and regional variation in the blood-to-brain transport of leptin in normal weight mice

2000 ◽  
Vol 278 (6) ◽  
pp. E1158-E1165 ◽  
Author(s):  
William A. Banks ◽  
Cecilia M. Clever ◽  
Catherine L. Farrell
Keyword(s):  
Arcuate Nucleus ◽  
Maximum Velocity ◽  
Brain Perfusion ◽  
Serum Levels ◽  
Brain Regions ◽  
Normal Weight ◽  
Normal Serum ◽  
Optimal Function ◽  
The Central Nervous System ◽  
The Brain

Impaired blood-brain barrier transport of leptin into the arcuate nucleus has been suggested to underlie obesity in humans and outbred aging mice. Here, we used a brain perfusion method in mice to measure transport rates and kinetic parameters for leptin at vascular concentrations between 0.15 and 130 ng/ml. Transport into whole brain was partially saturated at all concentrations, not only those seen in obesity. Leptin entered all regions of the brain, not only the hypothalamus, with entry and saturation rates differing among the brain regions. The value of the Michaelis-Menten constant of the transporter approximates normal serum levels and the maximum velocity value varies significantly among brain regions. These results suggest an important role for low serum levels signaling starvation status to the brain and show that the levels of leptin seen in obesity greatly saturate the transporter. Differences in regional uptake and saturation provide a mechanism by which leptin can control events mediated at the arcuate nucleus and other regions of the central nervous system with different regional thresholds for optimal function.

Relative contributions of a CVO and the microvascular bed to delivery of blood-borne IL-1α to the brain

1998 ◽  
Vol 275 (2) ◽  
pp. E207-E212 ◽  
Author(s):  
Lawrence M. Maness ◽  
Abba J. Kastin ◽  
William A. Banks
Keyword(s):  
Brain Regions ◽  
Intravenous Injections ◽  
The Central Nervous System ◽  
Major Route ◽  
Grain Distribution ◽  
Interleukin 1Α ◽  
High Degree ◽  
The Brain ◽  
Silver Grains

Diffusion from brain regions lacking a blood-brain barrier (BBB) and saturable transport across capillaries are possible pathways for the entry of blood-borne interleukin-1α into the central nervous system (CNS). To assess the involvement of these putative routes, mice received intravenous injections of radioiodinated interleukin-1α, and their brains were subjected to emulsion autoradiography. The resulting patterns of silver grain distribution showed that diffusion of interleukin-1α from the choroid plexus and the subfornical organ was greatly restricted. These restrictive properties were quantified by the determination of D1/2 values, the distances needed for the concentration of silver grains to decrease by one-half. Within several brain regions, a subset of the microvasculature indicated transport of interleukin-1α across the BBB. Individual microvessels showed different patterns of transport ranging from robust to absent. The high degree of containment of blood-borne interleukin-1α within the regions lacking a BBB indicates that these sites cannot account for total delivery of the cytokine into the brain and suggests instead that the microvascular network may serve as the major route of entry into the CNS.

Sign in / Sign up

Export Citation Format

Share Document