scholarly journals Hypothalamic Astrocytes as a Specialized and Responsive Cell Population in Obesity

2021 ◽  
Vol 22 (12) ◽  
pp. 6176
Author(s):  
Ismael González-García ◽  
Cristina García-Cáceres
Keyword(s):  
Functional Integral ◽  
Metabolic Disturbances ◽  
Brain Areas ◽  
The Core ◽  
Regulatory Aspects ◽  
Diet Induced Obesity ◽  
Obesity Research ◽  
Regulatory Circuits ◽  
The Brain ◽  
Responsive Cell

Astrocytes are a type of glial cell anatomically and functionally integrated into the neuronal regulatory circuits for the neuroendocrine control of metabolism. Being functional integral compounds of synapses, astrocytes are actively involved in the physiological regulatory aspects of metabolic control, but also in the pathological processes that link neuronal dysfunction and obesity. Between brain areas, the hypothalamus harbors specialized functional circuits that seem selectively vulnerable to metabolic damage, undergoing early cellular rearrangements which are thought to be at the core of the pathogenesis of diet-induced obesity. Such changes in the hypothalamic brain region consist of a rise in proinflammatory cytokines, the presence of a reactive phenotype in astrocytes and microglia, alterations in the cytoarchitecture and synaptology of hypothalamic circuits, and angiogenesis, a phenomenon that cannot be found elsewhere in the brain. Increasing evidence points to the direct involvement of hypothalamic astrocytes in such early metabolic disturbances, thus moving the study of these glial cells to the forefront of obesity research. Here we provide a comprehensive review of the most relevant findings of molecular and pathophysiological mechanisms by which hypothalamic astrocytes might be involved in the pathogenesis of obesity.

scholarly journals Imbalanced Dopaminergic Transmission Mediated by Serotonergic Neurons in L-DOPA-Induced Dyskinesia

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Sylvia Navailles ◽  
Philippe De Deurwaerdère
Keyword(s):  
Brain Regions ◽  
Term Treatment ◽  
Serotonergic Neurons ◽  
Brain Areas ◽  
Dopaminergic Transmission ◽  
The Core ◽  
Long Term Treatment ◽  
The Brain ◽  
Serotonergic Innervation

L-DOPA-induced dyskinesias (LIDs) are one of the main motor side effects of L-DOPA therapy in Parkinson's disease. The review will consider the biochemical evidence indicating that the serotonergic neurons are involved in the dopaminergic effects of L-DOPA in the brain. The consequences are an ectopic and aberrant release of dopamine that follows the serotonergic innervation of the brain. After mid- to long-term treatment with L-DOPA, the pattern of L-DOPA-induced dopamine release is modified. In several brain regions, its effect is dramatically reduced while, in the striatum, its effect is quite preserved. LIDs could appear when the dopaminergic effects of L-DOPA fall in brain areas such as the cortex, enhancing the subcortical impact of dopamine and promoting aberrant motor responses. The consideration of the serotonergic system in the core mechanism of action of L-DOPA opens an important reserve of possible strategies to limit LIDs.

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.

scholarly journals Microglia–Neuron Crosstalk in Obesity: Melodious Interaction or Kiss of Death?

2021 ◽  
Vol 22 (10) ◽  
pp. 5243
Author(s):  
Stéphane Léon ◽  
Agnès Nadjar ◽  
Carmelo Quarta
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Metabolic Disorders ◽  
Body Weight Gain ◽  
Metabolic Stress ◽  
Neuronal Circuits ◽  
Mechanistic Studies ◽  
The Core ◽  
Diet Induced Obesity ◽  
The Brain

Diet-induced obesity can originate from the dysregulated activity of hypothalamic neuronal circuits, which are critical for the regulation of body weight and food intake. The exact mechanisms underlying such neuronal defects are not yet fully understood, but a maladaptive cross-talk between neurons and surrounding microglial is likely to be a contributing factor. Functional and anatomical connections between microglia and hypothalamic neuronal cells are at the core of how the brain orchestrates changes in the body’s metabolic needs. However, such a melodious interaction may become maladaptive in response to prolonged diet-induced metabolic stress, thereby causing overfeeding, body weight gain, and systemic metabolic perturbations. From this perspective, we critically discuss emerging molecular and cellular underpinnings of microglia–neuron communication in the hypothalamic neuronal circuits implicated in energy balance regulation. We explore whether changes in this intercellular dialogue induced by metabolic stress may serve as a protective neuronal mechanism or contribute to disease establishment and progression. Our analysis provides a framework for future mechanistic studies that will facilitate progress into both the etiology and treatments of metabolic disorders.

The Core of What the Brain Does

PsycCRITIQUES ◽  
2017 ◽  
Vol 62 (44) ◽  
Author(s):  
David S. Kreiner
Keyword(s):  
The Core ◽  
The Brain

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 Limbic Expression of mRNA Coding for Chemoreceptors in Human Brain—Lessons from Brain Atlases

2021 ◽  
Vol 22 (13) ◽  
pp. 6858
Author(s):  
Fanny Gaudel ◽  
Gaëlle Guiraudie-Capraz ◽  
François Féron
Keyword(s):  
G Proteins ◽  
The Body ◽  
Trace Amines ◽  
Chemical Senses ◽  
Brain Areas ◽  
Genes Encoding ◽  
The Central Nervous System ◽  
Human Brains ◽  
The Brain ◽  
Brain Atlases

Animals strongly rely on chemical senses to uncover the outside world and adjust their behaviour. Chemical signals are perceived by facial sensitive chemosensors that can be clustered into three families, namely the gustatory (TASR), olfactory (OR, TAAR) and pheromonal (VNR, FPR) receptors. Over recent decades, chemoreceptors were identified in non-facial parts of the body, including the brain. In order to map chemoreceptors within the encephalon, we performed a study based on four brain atlases. The transcript expression of selected members of the three chemoreceptor families and their canonical partners was analysed in major areas of healthy and demented human brains. Genes encoding all studied chemoreceptors are transcribed in the central nervous system, particularly in the limbic system. RNA of their canonical transduction partners (G proteins, ion channels) are also observed in all studied brain areas, reinforcing the suggestion that cerebral chemoreceptors are functional. In addition, we noticed that: (i) bitterness-associated receptors display an enriched expression, (ii) the brain is equipped to sense trace amines and pheromonal cues and (iii) chemoreceptor RNA expression varies with age, but not dementia or brain trauma. Extensive studies are now required to further understand how the brain makes sense of endogenous chemicals.

scholarly journals The Skull’s Girder: A Brief Review of the Cranial Base

2021 ◽  
Vol 9 (1) ◽  
pp. 3
Author(s):  
Shankar Rengasamy Venugopalan ◽  
Eric Van Otterloo
Keyword(s):  
Birth Defects ◽  
Vertebral Column ◽  
Endochondral Ossification ◽  
Cranial Base ◽  
Facial Skeleton ◽  
The Core ◽  
Skull Vault ◽  
Congenital Birth Defects ◽  
Intimate Association ◽  
The Brain

The cranial base is a multifunctional bony platform within the core of the cranium, spanning rostral to caudal ends. This structure provides support for the brain and skull vault above, serves as a link between the head and the vertebral column below, and seamlessly integrates with the facial skeleton at its rostral end. Unique from the majority of the cranial skeleton, the cranial base develops from a cartilage intermediate—the chondrocranium—through the process of endochondral ossification. Owing to the intimate association of the cranial base with nearly all aspects of the head, congenital birth defects impacting these structures often coincide with anomalies of the cranial base. Despite this critical importance, studies investigating the genetic control of cranial base development and associated disorders lags in comparison to other craniofacial structures. Here, we highlight and review developmental and genetic aspects of the cranial base, including its transition from cartilage to bone, dual embryological origins, and vignettes of transcription factors controlling its formation.

scholarly journals Initiators of Classical and Lectin Complement Pathways Are Differently Engaged after Traumatic Brain Injury—Time-Dependent Changes in the Cortex, Striatum, Thalamus and Hippocampus in a Mouse Model

2020 ◽  
Vol 22 (1) ◽  
pp. 45
Author(s):  
Agata Ciechanowska ◽  
Katarzyna Ciapała ◽  
Katarzyna Pawlik ◽  
Marco Oggioni ◽  
Domenico Mercurio ◽  
...  
Keyword(s):  
Brain Injury ◽  
Microglial Cell ◽  
Lectin Pathway ◽  
Brain Areas ◽  
Mannose Binding ◽  
Primary Microglial Cell ◽  
Cellular Markers ◽  
The Brain ◽  
Binding Lectin ◽  
Complement Pathways

The complement system is involved in promoting secondary injury after traumatic brain injury (TBI), but the roles of the classical and lectin pathways leading to complement activation need to be clarified. To this end, we aimed to determine the ability of the brain to activate the synthesis of classical and lectin pathway initiators in response to TBI and to examine their expression in primary microglial cell cultures. We have modeled TBI in mice by controlled cortical impact (CCI), a clinically relevant experimental model. Using Real-time quantitative polymerase chain reaction (RT-qPCR) we analyzed the expression of initiators of classical the complement component 1q, 1r and 1s (C1q, C1r, and C1s) and lectin (mannose binding lectin A, mannose binding lectin C, collectin 11, ficolin A, and ficolin B) complement pathways and other cellular markers in four brain areas (cortex, striatum, thalamus and hippocampus) of mice exposed to CCI from 24 h and up to 5 weeks. In all murine ipsilateral brain structures assessed, we detected long-lasting, time- and area-dependent significant increases in the mRNA levels of all classical (C1q, C1s, C1r) and some lectin (collectin 11, ficolin A, ficolin B) initiator molecules after TBI. In parallel, we observed significantly enhanced expression of cellular markers for neutrophils (Cd177), T cells (Cd8), astrocytes (glial fibrillary acidic protein—GFAP), microglia/macrophages (allograft inflammatory factor 1—IBA-1), and microglia (transmembrane protein 119—TMEM119); moreover, we detected astrocytes (GFAP) and microglia/macrophages (IBA-1) protein level strong upregulation in all analyzed brain areas. Further, the results obtained in primary microglial cell cultures suggested that these cells may be largely responsible for the biosynthesis of classical pathway initiators. However, microglia are unlikely to be responsible for the production of the lectin pathway initiators. Immunofluorescence analysis confirmed that at the site of brain injury, the C1q is localized in microglia/macrophages and neurons but not in astroglial cells. In sum, the brain strongly reacts to TBI by activating the local synthesis of classical and lectin complement pathway activators. Thus, the brain responds to TBI with a strong, widespread and persistent upregulation of complement components, the targeting of which may provide protection in TBI.

scholarly journals What is special about L3 processing?

2013 ◽  
Vol 18 (2) ◽  
pp. 130-144 ◽  
Author(s):  
KEES DE BOT ◽  
CAROL JAENSCH
Keyword(s):  
Second Language ◽  
Language Processing ◽  
Language Use ◽  
Fundamental Question ◽  
Third Language ◽  
The Core ◽  
Dynamic Perspective ◽  
Core Issue ◽  
The Brain ◽  
Over Time

While research on third language (L3) and multilingualism has recently shown remarkable growth, the fundamental question of what makes trilingualism special compared to bilingualism, and indeed monolingualism, continues to be evaded. In this contribution we consider whether there is such a thing as a true monolingual, and if there is a difference between dialects, styles, registers and languages. While linguistic and psycholinguistic studies suggest differences in the processing of a third, compared to the first or second language, neurolinguistic research has shown that generally the same areas of the brain are activated during language use in proficient multilinguals. It is concluded that while from traditional linguistic and psycholinguistic perspectives there are grounds to differentiate monolingual, bilingual and multilingual processing, a more dynamic perspective on language processing in which development over time is the core issue, leads to a questioning of the notion of languages as separate entities in the brain.

Comparing the brain areas supporting nondeclarative categorization and recognition memory

2002 ◽  
Vol 14 (2) ◽  
pp. 245-257 ◽  
Author(s):  
Paul J Reber ◽  
Eric C Wong ◽  
Richard B Buxton
Keyword(s):  
Recognition Memory ◽  
Brain Areas ◽  
The Brain
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