Neurotoxicity, Blood-Brain Barrier Breakdown, Demyelination and Remyelination Associated With NMDA-Induced Lesions of the Rat Lateral Hypothalamus

Brace, Helen; Latimer, Mary P.; Winn, Philip

doi:10.1016/s0361-9230(97)00064-6

Cited by 39 publications

(27 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The hypertrophy of stellate and basket cells of the molecular layer, and that of the granular layer observed in the DS group may also be due to excessive excitation of these cells. This is in line with a report that the excitotoxins acting at different sites within the central nervous system could strip myelin from fibers and destroying neurons 19 . Lutsey et al 20 reported that consuming just a can of diet soda increases one's risk of developing metabolic syndrome.…”

Section: Discussionsupporting

confidence: 92%

A comparative study of the effect of diet and soda carbonated drinks on the histology of the cerebellum of adult female albino Wistar rats

Eluwa

Inyangmme²,

Akpantah³

et al. 2013

Afr H. Sci.

View full text Add to dashboard Cite

Background: Carbonated drinks are widely consumed because of their taste and their ability to refresh and quench thirst. These carbonated drinks also exist in the form of diet drinks, for example Diet Coke® , Pepsi®, extra. Objectives: A comparative effect of the diet and regular soda carbonated drinks on the histology of the cerebellum of female albino Wistar rats was investigated. Methods: Fifteen adult female Wistar rats weighing between 180-200g were divided into 3 groups; designated as groups A, B and C, and each group consisted of five rats. Group A was the Control group and received distilled water, while groups B and C were the experimental groups. Group B was administered 50 ml of regular soda (RS), and group C was administered 50 ml of diet soda (DS) each per day for 21 days, and the rats were sacrificed on Day 22, and their cerebellums excised and preserved. Results: Histological result of the sections of the cerebellum showed shrunken and degenerated Purkinje cells with hypertrophied dendrites, especially in the DS group, which was less in the RS group compared to the control group. Conclusions: These results suggest that diet soda has adverse effect on the cerebellum of adult female albino Wistar rats.

show abstract

Section: Discussionsupporting

confidence: 92%

A comparative study of the effect of diet and soda carbonated drinks on the histology of the cerebellum of adult female albino Wistar rats

Eluwa

Inyangmme²,

Akpantah³

et al. 2013

Afr H. Sci.

View full text Add to dashboard Cite

show abstract

“…NMDA administered systemically can act directly on the specific receptors located in the brain after passing through the blood-brain barrier [39]. The mechanisms by which chronic NMDA increased the mRNA levels of IL-1β, TNFα, GFAP and iNOS in the rat frontal cortex remain to be clarified.…”

Section: Discussionmentioning

confidence: 99%

Chronic NMDA Administration Increases Neuroinflammatory Markers in Rat Frontal Cortex: Cross-Talk Between Excitotoxicity and Neuroinflammation

et al. 2008

View full text Add to dashboard Cite

Chronic N-Methyl-D-aspartate (NMDA) administration, a model of excitotoxicity, and chronic intracerebroventricular lipopolysaccharide infusion, a model of neuroinflammation, are reported to upregulate arachidonic acid incorporation and turnover in rat brain phospholipids as well as enzymes involved in arachidonic acid metabolism. This suggests cross-talk between signaling pathways of excitotoxicity and of neuroinflammation, involving arachidonic acid. To test whether chronic NMDA administrations to rats can upregulate brain markers of neuroinflammation, NMDA (25 mg/kg i.p.) or vehicle (1 ml saline/kg i.p.) was administered daily to adult male rats for 21 days. Protein and mRNA levels of cytokines and other inflammatory markers were measured in the frontal cortex using immunoblot and real-time PCR. Compared with chronic vehicle, chronic NMDA significantly increased protein and mRNA levels of interleukin-1beta, tumor necrosis factor alpha, glial fibrillary acidic protein and inducible nitric oxide synthase. Chronic NMDA receptor overactivation results in increased levels of neuroinflammatory markers in the rat frontal cortex, consistent with cross-talk between excitotoxicity and neuroinflammation. As both processes have been reported in a number of human brain diseases, NMDA receptor inhibitors might be of use in treating neuroinflammation in these diseases.

show abstract

“…More examples include excitotoxin, NMDA, and immunosuppressants (cyclosporin A and tacrolimus). Although structurally different, all of these chemicals can induce apoptosis in brain capillary endothelial cells prior to their initiation of neuronal lesions (7,8).…”

Section: Neurotoxicity Due To Injured Barrier Structures: Nitrobenzenmentioning

confidence: 99%

Neurotoxicology of the Brain Barrier System: New Implications

Zheng

2001

Journal of Toxicology: Clinical Toxicology

105

View full text Add to dashboard Cite

The concept of a barrier system in the brain has existed for nearly a century. The barrier that separates the blood from the cerebral interstitial fluid is defined as the blood-brain barrier, while the one that discontinues the circulation between the blood and cerebrospinal fluid is named the blood-cerebrospinal fluid barrier. Evidence in the past decades suggests that brain barriers are subject to toxic insults from neurotoxic chemicals circulating in blood. The aging process and some disease states render barriers more vulnerable to insults arising inside and outside the barriers. The implication of brain barriers in certain neurodegenerative diseases is compelling, although the contribution of chemical-induced barrier dysfunction in the etiology of any of these disorders remains poorly understood. This review examines what is currently understood about brain barrier systems in central nervous system disorders by focusing on chemical-induced neurotoxicities including those associated with nitrobenzenes, N-methyl-D-aspartate, cyclosporin A, pyridostigmine bromide, aluminum, lead, manganese, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and 3-nitropropionic acid. Contemporary research questions arising from this growing understanding show enormous promises for brain researchers, toxicologists, and clinicians.

show abstract

Neurotoxicity, Blood-Brain Barrier Breakdown, Demyelination and Remyelination Associated With NMDA-Induced Lesions of the Rat Lateral Hypothalamus

Cited by 39 publications

References 36 publications

A comparative study of the effect of diet and soda carbonated drinks on the histology of the cerebellum of adult female albino Wistar rats

A comparative study of the effect of diet and soda carbonated drinks on the histology of the cerebellum of adult female albino Wistar rats

Chronic NMDA Administration Increases Neuroinflammatory Markers in Rat Frontal Cortex: Cross-Talk Between Excitotoxicity and Neuroinflammation

Neurotoxicology of the Brain Barrier System: New Implications

Contact Info

Product

Resources

About