Ginsenoside Rb1 attenuates lipopolysaccharide-induced neural damage in the brain of mice via regulating the dysfunction of microglia and astrocytes

This study attempted to ascertain whether the ischemic damage to neurons and monoamine overload in brain that occur during rat heatstroke can be attenuated by heat shock protein (HSP) 72 induction. Effects of heatstroke on mean arterial pressure (MAP), cerebral blood flow (CBF), brain dopamine (DA) and serotonin (5-HT) release, and neural damage score were assayed in rats 0, 16, or 48 h after heat shock (42°C for 15 min) or chemical stress (5 mg/kg sodium arsenite ip). Brain HSP 72 in rats after heat shock or chemical stress was detected by Western blot, and brain monoamine was determined by a microdialysis probe combined with high-performance liquid chromatography. Heatstroke was induced by exposing the animal to a high ambient temperature (43°C); the moment at which MAP and CBF decreased from their peak values was taken as the time of heatstroke onset. Prior heat shock or chemical stress conferred significant protection against heatstroke-induced hyperthermia, arterial hypotension, cerebral ischemia, cerebral DA and 5-HT overload, and neural damage and correlated with expression of HSP 72 in brain at 16 h. However, at 48 h, when HSP 72 expression returned to basal values, the above responses that occurred during the onset of heatstroke were indistinguishable between the two groups (0 h vs. 48 h). These results lead to the hypothesis that the brain can be preconditioned by thermal or chemical injury, that this preconditioning will induce HSP 72, and that HSP 72 induction will correlate quite well with anatomic, histochemical, and hemodynamic protection in rat heatstroke.

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Optimal compensation for neuron loss

eLife ◽

10.7554/elife.12454 ◽

2016 ◽

Vol 5 ◽

Cited By ~ 13

Author(s):

David GT Barrett ◽

Sophie Denève ◽

Christian K Machens

Keyword(s):

Visual Cortex ◽

Neural Circuits ◽

Behavioral Effect ◽

Brain Lesions ◽

Compensatory Mechanism ◽

Compensatory Mechanisms ◽

Neuron Loss ◽

Tuning Curves ◽

Neural Damage ◽

The Brain

The brain has an impressive ability to withstand neural damage. Diseases that kill neurons can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to produce any behavioral effect. How does the brain compensate for such damage, and what are the limits of this compensation? We propose that neural circuits instantly compensate for neuron loss, thereby preserving their function as much as possible. We show that this compensation can explain changes in tuning curves induced by neuron silencing across a variety of systems, including the primary visual cortex. We find that compensatory mechanisms can be implemented through the dynamics of networks with a tight balance of excitation and inhibition, without requiring synaptic plasticity. The limits of this compensatory mechanism are reached when excitation and inhibition become unbalanced, thereby demarcating a recovery boundary, where signal representation fails and where diseases may become symptomatic.

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Particulate Air Pollution and Risk of Neuropsychiatric Outcomes. What We Breathe, Swallow, and Put on Our Skin Matters

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph182111568 ◽

2021 ◽

Vol 18 (21) ◽

pp. 11568

Author(s):

Lilian Calderón-Garcidueñas ◽

Elijah W. Stommel ◽

Ravi Philip Rajkumar ◽

Partha S. Mukherjee ◽

Alberto Ayala

Keyword(s):

Air Pollution ◽

Neurovascular Unit ◽

Ambient Air ◽

Anthropogenic Sources ◽

Neural Damage ◽

Parkinson’S Diseases ◽

Particle Pollution ◽

Psychiatric Outcomes ◽

The Impact ◽

The Brain

We appraise newly accumulated evidence of the impact of particle pollution on the brain, the portals of entry, the neural damage mechanisms, and ultimately the neurological and psychiatric outcomes statistically associated with exposures. PM pollution comes from natural and anthropogenic sources such as fossil fuel combustion, engineered nanoparticles (NP ≤ 100 nm), wildfires, and wood burning. We are all constantly exposed during normal daily activities to some level of particle pollution of various sizes—PM2.5 (≤2.5 µm), ultrafine PM (UFP ≤ 100 nm), or NPs. Inhalation, ingestion, and dermal absorption are key portals of entry. Selected literature provides context for the US Environmental Protection Agency (US EPA) ambient air quality standards, the conclusions of an Independent Particulate Matter Review Panel, the importance of internal combustion emissions, and evidence suggesting UFPs/NPs cross biological barriers and reach the brain. NPs produce oxidative stress and neuroinflammation, neurovascular unit, mitochondrial, endoplasmic reticulum and DNA damage, protein aggregation and misfolding, and other effects. Exposure to ambient PM2.5 concentrations at or below current US standards can increase the risk for TIAs, ischemic and hemorrhagic stroke, cognitive deficits, dementia, and Alzheimer’s and Parkinson’s diseases. Residing in a highly polluted megacity is associated with Alzheimer neuropathology hallmarks in 99.5% of residents between 11 months and ≤40 y. PD risk and aggravation are linked to air pollution and exposure to diesel exhaust increases ALS risk. Overall, the literature supports that particle pollution contributes to targeted neurological and psychiatric outcomes and highlights the complexity of the pathophysiologic mechanisms and the marked differences in pollution profiles inducing neural damage. Factors such as emission source intensity, genetics, nutrition, comorbidities, and others also play a role. PM2.5 is a threat for neurological and psychiatric diseases. Thus, future research should address specifically the potential role of UFPs/NPs in inducing neural damage.

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Optimal compensation for neuron death

10.1101/029512 ◽

2015 ◽

Cited By ~ 2

Author(s):

David Barrett ◽

Sophie Deneve ◽

Christian Machens

Keyword(s):

Synaptic Plasticity ◽

Visual Cortex ◽

Primary Visual Cortex ◽

Neural Circuits ◽

Brain Lesions ◽

Compensatory Mechanism ◽

Neuron Death ◽

Tuning Curves ◽

Neural Damage ◽

The Brain

The brain has an impressive ability to withstand neural damage. Diseases that kill neurons can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to produce any effect. How does the brain compensate for such damage, and what are the limits of this compensation? We propose that neural circuits optimally compensate for neuron death, thereby preserving their function as much as possible. We show that this compensation can explain changes in tuning curves induced by neuron silencing across a variety of systems, including the primary visual cortex. We find that optimal compensation can be implemented through the dynamics of networks with a tight balance of excitation and inhibition, without requiring synaptic plasticity. The limits of this compensatory mechanism are reached when excitation and inhibition become unbalanced, thereby demarcating a recovery boundary, where signal representation fails and where diseases may become symptomatic.

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Advances in the Pathophysiology of Episode-Related Cognitive Impairment in Bipolar Disorder

European Psychiatry ◽

10.1016/s0924-9338(09)70247-0 ◽

2009 ◽

Vol 24 (S1) ◽

pp. 1-1

Author(s):

F. Kapczinski ◽

B.N. Frey ◽

M. Kauer-Sant'Anna ◽

A.C. Andreazza ◽

S. Brissos ◽

...

Keyword(s):

Bipolar Disorder ◽

Cognitive Impairment ◽

Brain Cell ◽

Cognitive Disability ◽

Neural Damage ◽

Biological Domain ◽

New Research ◽

New Treatments ◽

The Brain ◽

Degree Of Severity

There have been a number of recent findings that elucidate the ways repeated episodes relate to cognitive impairment and poor functioning in Bipolar Disorder. While available treatments are undoubtedly helpful, many patients are still lacking improvement and adequate prophylaxis even when adherence to treatment is accomplished. New research point to neural glial cells resilience and connectivity as major contributors to the pathophysiology of the disorder. In this context, growth factors such as the brain-derived neurotrophic factor (BDNF) have been pointed out as potential targets for the development of new treatments. In the psychological domain, better assessment of the cognitive decline associated with the disorder is a major issue. Once cognitive disability is present, interventions with the potential to recover functioning have been put forward. In the biological domain, strategies aiming at reducing neural damage and with the potential to regenerate connectivity among brain cell are promising avenues for the development of new treatments. Another important development would be the incorporation of biological markers as a means to help staging the degree of severity of the disorder and guide the pharmacological treatment. These topics and their relationship to the clinical context will be discussed in this session.

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