scholarly journals Astrocytes in the Ventromedial Hypothalamus Involve Chronic Stress-Induced Anxiety and Bone Loss in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Yunhui Liu ◽  
Jie Shao ◽  
Dashuang Gao ◽  
Lu Zhang ◽  
Fan Yang
Keyword(s):  
Bone Loss ◽  
Chronic Stress ◽  
Neural Circuits ◽  
Cell Function ◽  
Ventromedial Hypothalamus ◽  
Brain Regions ◽  
Receptor Blocker ◽  
Steroidogenic Factor 1 ◽  
Regulation Of Metabolism ◽  
Nmda Receptor Blocker

Chronic stress is one of the main risk factors of bone loss. While the neurons and neural circuits of the ventromedial hypothalamus (VMH) mediate bone loss induced by chronic stress, the detailed intrinsic mechanisms within the VMH nucleus still need to be explored. Astrocytes in brain regions play important roles in the regulation of metabolism and anxiety-like behavior through interactions with surrounding neurons. However, whether astrocytes in the VMH affect neuronal activity and therefore regulate chronic stress-induced anxiety and bone loss remain elusive. In this study, we found that VMH astrocytes were activated during chronic stress-induced anxiety and bone loss. Pharmacogenetic activation of the Gi and Gq pathways in VMH astrocytes reduced and increased the levels of anxiety and bone loss, respectively. Furthermore, activation of VMH astrocytes by optogenetics induced depolarization in neighboring steroidogenic factor-1 (SF-1) neurons, which was diminished by administration of N-methyl-D-aspartic acid (NMDA) receptor blocker but not by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor blocker. These results suggest that there may be a functional “glial-neuron microcircuit” in VMH nuclei that mediates anxiety and bone loss induced by chronic stress. This study not only advances our understanding of glial cell function but also provides a potential intervention target for chronic stress-induced anxiety and bone loss therapy.

scholarly journals A GABAergic neural circuit in the ventromedial hypothalamus mediates chronic stress–induced bone loss

2020 ◽  
Vol 130 (12) ◽  
pp. 6539-6554
Author(s):  
Fan Yang ◽  
Yunhui Liu ◽  
Shanping Chen ◽  
Zhongquan Dai ◽  
Dazhi Yang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Chronic Stress ◽  
Neural Circuit ◽  
Ventromedial Hypothalamus

scholarly journals On the Role of Bilateral Brain Hypofunction and Abnormal Lateralization of Cortical Information Flow as Neural Underpinnings of Conventional Metaphor Processing Impairment in Schizophrenia: An fMRI and EEG Study

2021 ◽  
Author(s):  
Przemysław Adamczyk ◽  
Martin Jáni ◽  
Tomasz S. Ligeza ◽  
Olga Płonka ◽  
Piotr Błądziński ◽  
...  
Keyword(s):  
Information Flow ◽  
Language Processing ◽  
Time Course ◽  
Figurative Language ◽  
Neural Circuits ◽  
Effective Connectivity ◽  
Brain Regions ◽  
Blood Oxygenation ◽  
Control Group ◽  
Metaphor Processing

AbstractFigurative language processing (e.g. metaphors) is commonly impaired in schizophrenia. In the present study, we investigated the neural activity and propagation of information within neural circuits related to the figurative speech, as a neural substrate of impaired conventional metaphor processing in schizophrenia. The study included 30 schizophrenia outpatients and 30 healthy controls, all of whom were assessed with a functional Magnetic Resonance Imaging (fMRI) and electroencephalography (EEG) punchline-based metaphor comprehension task including literal (neutral), figurative (metaphorical) and nonsense (absurd) endings. The blood oxygenation level-dependent signal was recorded with 3T MRI scanner and direction and strength of cortical information flow in the time course of task processing was estimated with a 64-channel EEG input for directed transfer function. The presented results revealed that the behavioral manifestation of impaired figurative language in schizophrenia is related to the hypofunction in the bilateral fronto-temporo-parietal brain regions (fMRI) and various differences in effective connectivity in the fronto-temporo-parietal circuit (EEG). Schizophrenia outpatients showed an abnormal pattern of connectivity during metaphor processing which was related to bilateral (but more pronounced at the left hemisphere) hypoactivation of the brain. Moreover, we found reversed lateralization patterns, i.e. a rightward-shifted pattern during metaphor processing in schizophrenia compared to the control group. In conclusion, the presented findings revealed that the impairment of the conventional metaphor processing in schizophrenia is related to the bilateral brain hypofunction, which supports the evidence on reversed lateralization of the language neural network and the existence of compensatory recruitment of alternative neural circuits in schizophrenia.

Effects of Adult Neurogenesis on Synaptic Plasticity in the Rat Dentate Gyrus

2001 ◽  
Vol 85 (6) ◽  
pp. 2423-2431 ◽  
Author(s):  
J. S. Snyder ◽  
N. Kee ◽  
J. M. Wojtowicz
Keyword(s):  
Synaptic Plasticity ◽  
Dentate Gyrus ◽  
Adult Neurogenesis ◽  
Long Term Potentiation ◽  
Receptor Blocker ◽  
Granule Neurons ◽  
Term Potentiation ◽  
Cell Recording ◽  
Similar Preparation ◽  
Nmda Receptor Blocker

Ongoing neurogenesis in the adult hippocampal dentate gyrus (DG) generates a substantial population of young neurons. This phenomenon is present in all species examined thus far, including humans. Although the regulation of adult neurogenesis by various physiologically relevant factors such as learning and stress has been documented, the functional contributions of the newly born neurons to hippocampal functions are not known. We investigated possible contributions of the newly born granule neurons to synaptic plasticity in the hippocampal DG. In the standard hippocampal slice preparation perfused with artificial cerebrospinal fluid (ACSF), a small (10%) long-term potentiation (LTP) of the evoked field potentials is seen after tetanic stimulation of the afferent medial perforant pathway (MPP). The induction of this ACSF-LTP is resistant to a N-methyl-d-aspartate (NMDA) receptor blocker,d,l-2-amino-5-phosphonovaleric acid (APV), but is completely prevented by ifenprodil, a blocker of NR2B subtype of NMDA receptors. In contrast, slices perfused with picrotoxin (PICRO), a GABA-receptor blocker, revealed a larger (40–50%), APV-sensitive but ifenprodil-insensitive LTP. The ACSF-LTP required lower frequency of stimulation and fewer stimuli for its induction than the PICRO-LTP. All these characteristics of ACSF-LTP are in agreement with the properties of the putative individual new granule neurons examined previously with the use of the whole cell recording technique in a similar preparation. A causal relationship between neurogenesis and ACSF-LTP was confirmed in experiments using low dose of gamma radiation applied to the brain 3 wk prior to the electrophysiological experiments. In these experiments, the new cell proliferation was drastically reduced and ACSF-LTP was selectively blocked. We conclude that the young, adult-generated granule neurons play a significant role in synaptic plasticity in the DG. Since DG is the major source of the afferent inputs into the hippocampus, the production and the plasticity of new neurons may have an important role in the hippocampal functions such as learning and memory.

Setting the Scene

2021 ◽  
pp. 1-8
Author(s):  
John Zerilli
Keyword(s):  
Neural Circuits ◽  
Brain Regions ◽  
Basic Assumptions ◽  
The Subject ◽  
Basic Argument ◽  
The Mind ◽  
Relationship Of ◽  
The Relationship

The modularity of mind has been understood in various ways, amended as evidence from neuroscience has forced the theory to shed various structural assumptions. Neuroplasticity has, for better or worse, challenged many of the orthodox conceptions of the mind that originally led cognitive scientists to postulate mental modules. Similarly, rapidly accumulating neuroscientific evidence of the reuse or redeployment of neural circuits, revealing the integrated and interactive structure of brain regions, has upset basic assumptions about the relationship of function to structure upon which modularity—not to say neuroscience itself—originally depended. These movements, developments, and cross-currents are the subject of this book. This chapter outlines the basic argument of the book and its motivation.

scholarly journals Choosing to view morbid information involves reward circuitry

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Suzanne Oosterwijk ◽  
Lukas Snoek ◽  
Jurriaan Tekoppele ◽  
Lara H. Engelbert ◽  
H. Steven Scholte
Keyword(s):  
Neural Circuits ◽  
Inferior Frontal Gyrus ◽  
Brain Regions ◽  
Anterior Cingulate ◽  
Viewing Condition ◽  
Verbal Cues ◽  
Negative Image ◽  
Reward Circuitry ◽  
Starting Point ◽  
Passive Viewing

Abstract People often seek out stories, videos or images that detail death, violence or harm. Considering the ubiquity of this behavior, it is surprising that we know very little about the neural circuits involved in choosing negative information. Using fMRI, the present study shows that choosing intensely negative stimuli engages similar brain regions as those that support extrinsic incentives and “regular” curiosity. Participants made choices to view negative and positive images, based on negative (e.g., a soldier kicks a civilian against his head) and positive (e.g., children throw flower petals at a wedding) verbal cues. We hypothesized that the conflicting, but relatively informative act of choosing to view a negative image, resulted in stronger activation of reward circuitry as opposed to the relatively uncomplicated act of choosing to view a positive stimulus. Indeed, as preregistered, we found that choosing negative cues was associated with activation of the striatum, inferior frontal gyrus, anterior insula, and anterior cingulate cortex, both when contrasting against a passive viewing condition, and when contrasting against positive cues. These findings nuance models of decision-making, valuation and curiosity, and are an important starting point when considering the value of seeking out negative content.

scholarly journals Mitochondrial gene signature in the prefrontal cortex for differential susceptibility to chronic stress

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Meltem Weger ◽  
Daniel Alpern ◽  
Antoine Cherix ◽  
Sriparna Ghosal ◽  
Jocelyn Grosse ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mitochondrial Dna ◽  
Prefrontal Cortex ◽  
Mitochondrial Dysfunction ◽  
Chronic Stress ◽  
Mitochondrial Gene ◽  
Brain Regions ◽  
Mitochondrial Gene Expression ◽  
Data Set ◽  
A Genome

Abstract Mitochondrial dysfunction was highlighted as a crucial vulnerability factor for the development of depression. However, systemic studies assessing stress-induced changes in mitochondria-associated genes in brain regions relevant to depression symptomatology remain scarce. Here, we performed a genome-wide transcriptomic study to examine mitochondrial gene expression in the prefrontal cortex (PFC) and nucleus accumbens (NAc) of mice exposed to multimodal chronic restraint stress. We identified mitochondria-associated gene pathways as most prominently affected in the PFC and with lesser significance in the NAc. A more detailed mitochondrial gene expression analysis revealed that in particular mitochondrial DNA-encoded subunits of the oxidative phosphorylation complexes were altered in the PFC. The comparison of our data with a reanalyzed transcriptome data set of chronic variable stress mice and major depression disorder subjects showed that the changes in mitochondrial DNA-encoded genes are a feature generalizing to other chronic stress-protocols as well and might have translational relevance. Finally, we provide evidence for changes in mitochondrial outputs in the PFC following chronic stress that are indicative of mitochondrial dysfunction. Collectively, our work reinforces the idea that changes in mitochondrial gene expression are key players in the prefrontal adaptations observed in individuals with high behavioral susceptibility and resilience to chronic stress.

scholarly journals Altered neural activity in brain cough suppression networks in cigarette smokers

2019 ◽  
Vol 54 (3) ◽  
pp. 1900362 ◽  
Author(s):  
Ayaka Ando ◽  
Stuart B. Mazzone ◽  
Michael J. Farrell
Keyword(s):  
Prefrontal Cortex ◽  
Neural Circuits ◽  
Brain Regions ◽  
Smoking Behaviour ◽  
Brain Network ◽  
Functional Brain Imaging ◽  
Cigarette Smokers ◽  
Dorsolateral Prefrontal ◽  
Cortical Regions ◽  
Airway Irritation

Cough is important for airway defence, and studies in healthy animals and humans have revealed multiple brain networks intimately involved in the perception of airway irritation, cough induction and cough suppression. Changes in cough sensitivity and/or the ability to suppress cough accompany pulmonary pathologies, suggesting a level of plasticity is possible in these central neural circuits. However, little is known about how persistent inputs from the lung might modify the brain processes regulating cough.In the present study, we used human functional brain imaging to investigate the central neural responses that accompany an altered cough sensitivity in cigarette smokers.In nonsmokers, inhalation of the airway irritant capsaicin induced a transient urge-to-cough associated with the activation of a distributed brain network that included sensory, prefrontal and motor cortical regions. Cigarette smokers demonstrated significantly higher thresholds for capsaicin-induced urge-to-cough, consistent with a reduced sensitivity to airway irritation. Intriguingly, this was accompanied by increased activation in brain regions known to be involved in both cough sensory processing (primary sensorimotor cortex) and cough suppression (dorsolateral prefrontal cortex and the midbrain nucleus cuneiformis). Activations in the prefrontal cortex were highest among participants with the least severe smoking behaviour, whereas those in the midbrain correlated with more severe smoking behaviour.These outcomes suggest that smoking-induced sensitisation of central cough neural circuits is offset by concurrently enhanced central suppression. Furthermore, central suppression mechanisms may evolve with the severity of smoke exposure, changing from initial prefrontal inhibition to more primitive midbrain processes as exposure increases.

scholarly journals Laboratory markers predict bone loss in Crohn's disease: relationship to blood mononuclear cell function and nutritional status

2004 ◽  
Vol 19 (10) ◽  
pp. 1063-1071 ◽  
Author(s):  
T. M. Trebble ◽  
S. A. Wootton ◽  
M. A. Stroud ◽  
M. A. Mullee ◽  
P. C. Calder ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Bone Loss ◽  
Nutritional Status ◽  
Mononuclear Cell ◽  
Cell Function ◽  
Laboratory Markers

scholarly journals Connectional architecture of a mouse hypothalamic circuit node controlling social behavior

2019 ◽  
Vol 116 (15) ◽  
pp. 7503-7512 ◽  
Author(s):  
Liching Lo ◽  
Shenqin Yao ◽  
Dong-Wook Kim ◽  
Ali Cetin ◽  
Julie Harris ◽  
...  
Keyword(s):  
Ventromedial Hypothalamus ◽  
Brain Regions ◽  
Feed Forward ◽  
Motor Processing ◽  
Central Processing ◽  
Indirect Feedback ◽  
High Level ◽  
High Degree ◽  
The Brain

Type 1 estrogen receptor-expressing neurons in the ventrolateral subdivision of the ventromedial hypothalamus (VMHvlEsr1) play a causal role in the control of social behaviors, including aggression. Here we use six different viral-genetic tracing methods to systematically map the connectional architecture of VMHvlEsr1 neurons. These data reveal a high level of input convergence and output divergence (“fan-in/fan-out”) from and to over 30 distinct brain regions, with a high degree (∼90%) of bidirectionality, including both direct as well as indirect feedback. Unbiased collateralization mapping experiments indicate that VMHvlEsr1 neurons project to multiple targets. However, we identify two anatomically distinct subpopulations with anterior vs. posterior biases in their collateralization targets. Nevertheless, these two subpopulations receive indistinguishable inputs. These studies suggest an overall system architecture in which an anatomically feed-forward sensory-to-motor processing stream is integrated with a dense, highly recurrent central processing circuit. This architecture differs from the “brain-inspired,” hierarchical feed-forward circuits used in certain types of artificial intelligence networks.

scholarly journals Glial pathology in neuropsychiatric disorders: a brief review

2019 ◽  
Vol 30 (4) ◽  
Author(s):  
Shilpa Borehalli Mayegowda ◽  
Christofer Thomas
Keyword(s):  
Nervous System ◽  
Prefrontal Cortex ◽  
Glial Cells ◽  
Cell Function ◽  
Neuropsychiatric Disorders ◽  
Brain Regions ◽  
Neuronal Function ◽  
Glial Function ◽  
Clinical Conditions ◽  
Stress Models

Abstract Neurons have been considered the major functional entities of the nervous system that are responsible for most of the functions even though glial cells largely outnumber them. However, recent reports have proved that glial cells do not function just like glue in the nervous system but also substantially affect neuronal function and activities, and are significantly involved in the underlying pathobiology of various psychiatric disorders. Dysfunctional astrocytes and degeneration of glial cells are postulated to be critical factors contributing to the aggravation of depressive-like symptoms in humans, which was proved using animal models. Alteration in glial cell function predominantly targets three main brain regions – the prefrontal cortex, limbic areas including the hippocampus, and the amygdala, which have been extensively studied by various researchers across the globe. These studies have postulated that failure in adopting to the changing neurophysiology due to stress will lead to regressive plasticity in the hippocampus and prefrontal cortex, but to progressive plasticity in the amygdala. In this present review, an effort has been made to understand the different alterations in chronic stress models in correlation with clinical conditions, providing evidence on the defective maintenance of glial function and its potential role in the precipitation of neuropsychiatric disorders.

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