Methylmercury distribution, metabolism, and neurotoxicity in the mouse brain

1983 ◽  
Vol 61 (12) ◽  
pp. 1487-1493 ◽  
Author(s):  
Laurie J. S. Vandewater ◽  
William J. Racz ◽  
Albert R. Norris ◽  
Erwin Buncel
Keyword(s):  
Cerebral Cortex ◽  
Brain Stem ◽  
Brain Damage ◽  
Structural Damage ◽  
Total Mercury ◽  
Inorganic Mercury ◽  
Positive Correlation ◽  
Structural Brain Damage ◽  
The Brain ◽  
Structural Brain

Methylmercury distribution, biotransformation, and neurotoxicity in the brain of male Swiss albino mice were investigated. Mice were orally dosed with [203Hg]methylmercury chloride (10 mg/kg) for 1 to 9 days. Methylmercury was evenly distributed among the posterior cerebral cortex, subcortex, brain stem, and cerebellum. The anterior cerebral cortex had a significantly higher methylmercury concentration than the rest of the brain. The distribution of methylmercury's inorganic mercury metabolite was found to be uneven in the brain. The pattern of distribution was cerebellum > brain stem > subcortex > cerebral cortex. The order of the severity of histological damage was cerebral cortex > cerebellum > subcortex > brain stem. There was no correlation between methylmercury distribution in the brain and structural brain damage. However, there was a relationship between the distribution of methylmercury's inorganic mercury metabolite and structural damage in the anterior cerebral cortex (positive correlation) and the anterior subcortex (negative correlation). There was also a positive correlation between the fraction of methylmercury's metabolite of the total mercury present and structural brain damage in the anterior cerebral cortex. This study suggests that biotransformation may have a role in mediating methylmercury neurotoxicity.

scholarly journals Injury protection strategies for H63D syndrome patients suffering from cataplexy

2021 ◽  
Author(s):  
Jacob S Adams ◽  
David Seideman ◽  
Riku Honda ◽  
Lucas Smith ◽  
Carolina Diamandis
Keyword(s):  
Brain Damage ◽  
Surrogate Marker ◽  
Significant Incidence ◽  
Protection Strategies ◽  
Structural Brain Damage ◽  
Injury Protection ◽  
Structural Brain

Abstract Patients suffering from H63D syndrome have a significant incidence of narcolepsy with cataplexy as a symptom. Previous studies have shown that the presence of narcolepsy with cataplexy in the context of H63D syndrome is a surrogate marker for structural brain damage. Now, the aim was to clarify which measures best protect affected patients with cataplexy from injury.

Concepts, Conferences, and Controversies

2019 ◽  
pp. 12-31
Author(s):  
Alan J. McComas
Keyword(s):  
Cerebral Cortex ◽  
Brain Stem ◽  
Brain Science ◽  
History Of Research ◽  
History Of ◽  
The Brain

This chapter outlines the history of research meetings dealing with consciousness, beginning with that hosted by Herbert Jasper in the Laurentian mountains of Quebec in 1953. It starts, however, with a brief discussion on ancient scientific approaches to medicine, which was jump-started by the Greek physician, Hippocrates. Afterward, the chapter skips forward two millennia to major figures who made breakthroughs in the field of brain science. It also touches on a central debate that reached its climax a little later, as to which part of the brain was responsible for consciousness. The chapter considers whether it was the cerebral cortex, as had been the prevailing assumption, or if it was the brain stem.

Cognitive impairment and structural brain damage in multiple system atrophy-parkinsonian variant

2019 ◽  
Vol 267 (1) ◽  
pp. 87-94 ◽  
Author(s):  
Francesca Caso ◽  
Elisa Canu ◽  
Milica Jecmenica Lukic ◽  
Igor N. Petrovic ◽  
Andrea Fontana ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Multiple System Atrophy ◽  
Brain Damage ◽  
Structural Brain Damage ◽  
Structural Brain

Prevention of CA2+-Overload and Structural Brain Damage after Transient Cerebral Ischemia

Cephalalgia ◽  
1985 ◽  
Vol 5 (3_suppl) ◽  
pp. 42-43
Author(s):  
Jos Van Reempts ◽  
Marcel Borgers ◽  
Marc Haseldonckx ◽  
Bruno Van Deuren
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Transient Cerebral Ischemia ◽  
Structural Brain Damage ◽  
Structural Brain

scholarly journals Branching Thalamic Afferents Link Action and Perception

2003 ◽  
Vol 90 (2) ◽  
pp. 539-548 ◽  
Author(s):  
R. W. Guillery
Keyword(s):  
Cerebral Cortex ◽  
Brain Stem ◽  
Visual Pathways ◽  
Perceptual Processing ◽  
Axonal Branching ◽  
Action And Perception ◽  
The Brain ◽  
Anatomical Evidence

Recent observations of single axons and review of older literature show that axons afferent to the thalamus commonly branch, sending one branch to the thalamus and another to a motor or premotor center of the brain stem. That is, the messages that the thalamus relays to the cerebral cortex can be regarded as copies of motor instructions. This pattern of axonal branching is reviewed, particularly for the somatosensory and the visual pathways. The extent to which this anatomical evidence relates to views that link action to perception is explored. Most pathways going through the thalamus to the cortex are already involved in motor mechanisms. These motor links occur before and during activity in the parallel and hierarchical corticocortical circuitry that currently forms the focus of many studies of perceptual processing.

Spontaneous Rem Behaviors in a Microcephalic Infant

1972 ◽  
Vol 34 (3) ◽  
pp. 827-833 ◽  
Author(s):  
Robert J. Harmon ◽  
Robert N. Emde
Keyword(s):  
Cerebral Cortex ◽  
Brain Stem ◽  
Limbic System ◽  
Comparison Group ◽  
Post Mortem ◽  
Tentative Conclusion ◽  
Previous Evidence ◽  
Human Newborn ◽  
The Brain ◽  
Cerebral Structures

A microcephalic human newborn exhibited a repertoire of spontaneous REM behaviors, including REM smiling, at rates characteristic of a normal newborn comparison group. Cyclical alternations between behavioral REM and non-REM states were also documented. A detailed post-mortem examination supported an inference that this infant had severely impaired functioning of cerebral cortex and limbic system during its brief postuterine life. The findings support a tentative conclusion that the observed spontaneous REM behaviors are mediated through the brain stem and that cerebral structures, including the limbic system, are not necessary for this mediation. The findings are also consistent with previous evidence that the seat of organization of REM and non-REM sleep is in the brain stem.

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