scholarly journals Astrocytic Regulation of Neural Circuits Underlying Behaviors

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 296
Author(s):  
Sun-Nyoung Hwang ◽  
Jae Seung Lee ◽  
Kain Seo ◽  
Hyosang Lee

Astrocytes, characterized by a satellite-like morphology, are the most abundant type of glia in the central nervous system. Their main functions have been thought to be limited to providing homeostatic support for neurons, but recent studies have revealed that astrocytes actually actively interact with local neural circuits and play a crucial role in information processing and generating physiological and behavioral responses. Here, we review the emerging roles of astrocytes in many brain regions, particularly by focusing on intracellular changes in astrocytes and their interactions with neurons at the molecular and neural circuit levels.

2011 ◽  
Vol 7 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Hiroaki Wake ◽  
Andrew J. Moorhouse ◽  
Junichi Nabekura

Microglia cells are the immune cells of the central nervous system and consequently play important roles in brain infections and inflammation. Recent in vivo imaging studies have revealed that in the resting healthy brain, microglia are highly dynamic, moving constantly to actively survey the brain parenchyma. These active microglia can rapidly respond to pathological insults, becoming activated to induce a range of effects that may contribute to both pathogenesis, or to confer neuronal protection. However, interactions between microglia and neurons are being recognized as important in shaping neural circuit activity under more normal, physiological conditions. During development and neurogenesis, microglia interactions with neurons help to shape the final patterns of neural circuits important for behavior and with implications for diseases. In the mature brain, microglia can respond to changes in sensory activity and can influence neuronal activity acutely and over the long term. Microglia seem to be particularly involved in monitoring the integrity of synaptic function. In this review, we discuss some of these new insights into the involvement of microglia in neural circuits.


1992 ◽  
Vol 70 (11) ◽  
pp. 1515-1518 ◽  
Author(s):  
B. Skrajny ◽  
R. S. Hannah ◽  
S. H. Roth

The central nervous system is one of the primary target organs for hydrogen sulphide (H2S) toxicity; however, there are limited data on the neurotoxic effects of low-dose chronic exposure on the developing nervous system. Levels of serotonin and norepinephrine in the developing rat cerebellum and frontal cortex were determined following chronic exposure to 20 and 75 ppm H2S during perinatal development. Both monoamines were altered in rats exposed to 75 ppm H2S compared with controls; serotonin levels were significantly increased at days 14 and 21 postnatal in both brain regions, and norepinephrine levels were significantly increased at days 7, 14, and 21 postnatal in cerebellum and at day 21 in the frontal cortex. Exposure to 20 ppm H2S significantly increased the levels of serotonin in the frontal cortex at day 21, whereas levels of norepinephrine were significantly reduced in the frontal cortex at days 14 and 21, and at day 14 in the cerebellum.Key words: hydrogen sulphide, monoamines, serotonin, norepinephrine, neurotoxicity.


Author(s):  
Mitsuo Tonoike

Though olfaction is one of the necessary senses and indispensable for the maintenance of the life of the animal, the mechanism of olfaction had not yet been understood well compared with other sensory systems such as vision and audition. However, recently, the most basic principle of “signal transduction on the reception and transmission for the odor” has been clarified. Therefore, the important next problem is how the information of odors about is processed in the Central Nervous System (CNS) and how odor is perceived in the human brain. In this chapter, the basic olfactory systems in animal and human are described and examples such as “olfactory acuity, threshold, adaptation, and olfactory disorders” are discussed. The mechanism of olfactory information processing is described under the results obtained by using a few new non-invasive measuring methods. In addition, from a few recent studies, it is shown that olfactory neurophysiological information is passing through some deep central regions of the brain before finally being processed in the orbito-frontal areas.


2019 ◽  
Vol 22 (6) ◽  
pp. 566-570
Author(s):  
Ahmed Gilani ◽  
Laura A Adang ◽  
Adeline Vanderver ◽  
Abigail Collins ◽  
BK Kleinschmidt-DeMasters

Aicardi–Goutières syndrome (AGS) is a rare syndrome characterized by calcification, diffuse demyelination, and variable degree of brain atrophy. The syndrome is genetically heterogeneous with mutations in 7 genes, including TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, ADAR1, and IFIH1 (interferon-induced helicase c domain-containing protein 1) associated with the syndrome, so far. These mutations lead to the overproduction of α-interferon within the central nervous system. Mutations in IFIH1 have been recently described in a subset of AGS, with only 1 previous report of neuropathological findings. We report neuropathological findings in a second case of AGS with a known mutation in IFIH1 gene. The patient is a 16-year-old adolescent boy with early-onset symptoms that progressed to profound loss of cognitive and motor functions. The patient experienced sudden cardiopulmonary arrest at the age of 16 years. At autopsy, the cause of death was determined to be pulmonary thromboembolism. Neuropathological examination revealed microcephaly (brain weight: 916 g) with relatively mild brain atrophy on gross examination. Microscopic examination revealed multifocal calcifications limited to small to medium central nervous system arteries (no evidence of calcification in other organs), involving bilateral cerebral cortex, basal ganglia, thalamus, and cerebellum. Ultrastructural examination showed Calcospherules limited to the vessel walls and the perivasulcar area without evidence of neuronal ferrugination or tubuloreticular bodies. The extent of calcifications was variable across different brain regions, resembling findings in previously reported cases and correlated with the extent of IFIH1 protein expression (data derived from Allen Brain Institute). AGS is a rare cause of brain calcifications that can closely mimic congenital and neonatal infections such as Rubella and similar infections.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Pablo Valle-Leija

The olfactory system provides a great opportunity to explore the mechanisms that underlie the formation and function of neural circuits because of the simplicity of its structure. Olfactory sensory neurons (OSNs) located in the peripheral olfactory epithelium (OE) take part in the initial formation and function of glomeruli in the olfactory bulb (OB) inside the central nervous system. Glomeruli are key in the process of transduction of olfactory information, as they constitute a map in the OB that sorts the different types of odorant inputs. This odorant categorization allows proper olfactory perception, and it is achieved through the anatomical organization and function of the different glomerular circuits. Once formed, glomeruli keep the capacity to undergo diverse plasticity processes, which is unique among the different neural circuits of the central nervous system. In this context, through the expression and function of the odorant receptors (ORs), OSNs perform two of the most important roles in the olfactory system: transducing odorant information to the nervous system and initiating the development of the glomerular map to organize olfactory information. This review addresses essential information that has emerged in recent years about the molecular basis of these processes.


2020 ◽  
Vol 21 (7) ◽  
pp. 2273
Author(s):  
Eunyoung Jung ◽  
Seong-Ho Koh ◽  
Myeongjong Yoo ◽  
Yoon Kyung Choi

Regeneration of adult neural circuits after an injury is limited in the central nervous system (CNS). Heme oxygenase (HO) is an enzyme that produces HO metabolites, such as carbon monoxide (CO), biliverdin and iron by heme degradation. CO may act as a biological signal transduction effector in CNS regeneration by stimulating neuronal intrinsic and extrinsic mechanisms as well as mitochondrial biogenesis. CO may give directions by which the injured neurovascular system switches into regeneration mode by stimulating endogenous neural stem cells and endothelial cells to produce neurons and vessels capable of replacing injured neurons and vessels in the CNS. The present review discusses the regenerative potential of CO in acute and chronic neuroinflammatory diseases of the CNS, such as stroke, traumatic brain injury, multiple sclerosis and Alzheimer’s disease and the role of signaling pathways and neurotrophic factors. CO-mediated facilitation of cellular communications may boost regeneration, consequently forming functional adult neural circuits in CNS injury.


Author(s):  
Bruna Bueno de Campos ◽  
Alessandro dos Santos Farias ◽  
Rani Cocenza ◽  
Fernando Pradella

It has been demonstrated the cytotoxic activity of TCD4+ encaphalitogenic lymphocytes and it's crucial role in the development of Experimental Autoimmune Encephalomyelitis (EAE). Furthermore, our laboratory has seen a switch from Th17 profile to Th1-like during the evolution of EAE. Thus, these lymphocytes decreased IL-17A production while begin to produce IFNγ when infiltrate the central nervous system. Therefore, our goal was to verify the mechanisms that governs the convertion of Th17 cells into IFNγ-producing cells.


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