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Neurochemical Aspects of Excitotoxicity provides extensive insight into glutamate with other neurochemical parameters in excitotoxicity, and possible treatments.
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This occurs when receptors for the excitatory neurotransmitter glutamate glutamate receptors such as the NMDA receptor and AMPA receptor are overactivated by glutamatergic storm. These enzymes go on to damage cell structures such as components of the cytoskeleton , membrane , and DNA.

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Excitotoxicity may be involved in spinal cord injury , stroke , traumatic brain injury , hearing loss through noise overexposure or ototoxicity , and in neurodegenerative diseases of the central nervous system CNS such as multiple sclerosis , Alzheimer's disease , amyotrophic lateral sclerosis ALS , Parkinson's disease , alcoholism or alcohol withdrawal and especially over-rapid benzodiazepine withdrawal , and also Huntington's disease.

Persons in excitotoxic shock must never fall into hypoglycemia.

2-Minute Neuroscience: Glutamate

Treatment is administered during the acute stages of excitotoxic shock along with glutamate antagonists. Dehydration should be avoided as this also contributes to the concentrations of glutamate in the inter-synaptic cleft [5] and "status epilepticus can also be triggered by a build up of glutamate around inter-synaptic neurons. The harmful effects of glutamate on the central nervous system CNS were first observed in by T.

Hayashi, a Japanese scientist who stated that direct application of glutamate to the CNS caused seizure activity, [7] though this report went unnoticed for several years. Lucas and J.

Neurochemical Aspects of Excitotoxicity | SpringerLink

Newhouse , after noting that "single doses of gm [of sodium glutamate in humans] have He also assessed that cell death was restricted to postsynaptic neurons, that glutamate agonists were as neurotoxic as their efficiency to activate glutamate receptors, and that glutamate antagonists could stop the neurotoxicity.

Excitotoxicity can occur from substances produced within the body endogenous excitotoxins. Glutamate is a prime example of an excitotoxin in the brain, and it is also the major excitatory neurotransmitter in the mammalian CNS. This pathologic phenomenon can also occur after brain injury and spinal cord injury.

Within minutes after spinal cord injury, damaged neural cells within the lesion site spill glutamate into the extracellular space where glutamate can stimulate presynaptic glutamate receptors to enhance the release of additional glutamate. Ischemia is followed by accumulation of glutamate and aspartate in the extracellular fluid , causing cell death, which is aggravated by lack of oxygen and glucose.


The biochemical cascade resulting from ischemia and involving excitotoxicity is called the ischemic cascade. Because of the events resulting from ischemia and glutamate receptor activation, a deep chemical coma may be induced in patients with brain injury to reduce the metabolic rate of the brain its need for oxygen and glucose and save energy to be used to remove glutamate actively.

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The main aim in induced comas is to reduce the intracranial pressure , not brain metabolism. Opening of the pore may cause mitochondria to swell and release reactive oxygen species and other proteins that can lead to apoptosis. The pore can also cause mitochondria to release more calcium.

Inadequate ATP production resulting from brain trauma can eliminate electrochemical gradients of certain ions. For regional delivery times, please check When will I receive my book? Sorry, this product is currently out of stock. Flexible - Read on multiple operating systems and devices.

Neurochemical Aspects of Alzheimer's Disease

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Free Shipping Free global shipping No minimum order. Provides a comprehensive overview of molecular aspects of risk factors, pathogenesis, biomarkers, and therapeutic strategies for Alzheimer's disease Written for researchers, clinicians, and advanced graduate students in neurology, neuroscience, neurochemistry, and neuropharmacology Acts as the first book to provide a comprehensive description of the signal transduction processes associated with pathogenesis of Alzheimer's disease.

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These processes may be primary initiating points in neurodegeneration or they may be the end result of the neurodegenerative process itself. Neurochemical Aspects of Excitotoxicity provides extensive insight into glutamate transporters and receptors, including their role in the brain with other neurochemical parameters in excitotoxicity, and possible treatments. This book will be of interest scientists already working in the field of excitotoxicity who are interested in gaining a broader understanding of this complicated subject area, as well as graduate students and neurologists who are curious about a common cause of neuronal injury and neurological disorders.