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Neurotoxicity is a form of toxicity in which a biological, chemical, or physical agent produces an adverse effect on the structure or function of the central and/or peripheral nervous system. [1] It occurs when exposure to a substance – specifically, a neurotoxin or neurotoxicant – alters the normal activity of the nervous system in such a ...
The progressive symptoms of anatoxin-a exposure are loss of coordination, twitching, convulsions and rapid death by respiratory paralysis. The nerve tissues which communicate with muscles contain a receptor called the nicotinic acetylcholine receptor. Stimulation of these receptors causes a muscular contraction.
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 central nervous system of mammals. [14]
Toxic encephalopathy is a neurologic disorder caused by exposure to neurotoxic organic solvents such as toluene, following exposure to heavy metals such as manganese, as a side effect of melarsoprol treatment for African trypanosomiasis, adverse effects to prescription drugs, or exposure to extreme concentrations of any natural toxin such as cyanotoxins found in shellfish or freshwater ...
This is a list of major and frequently observed neurological disorders (e.g., Alzheimer's disease), symptoms (e.g., back pain), signs (e.g., aphasia) and syndromes (e.g., Aicardi syndrome). There is disagreement over the definitions and criteria used to delineate various disorders and whether some of these conditions should be classified as ...
Olney's lesions, also known as NMDA receptor antagonist neurotoxicity (NAT), is a form of brain damage consisting of selective death of neurons but not glia, observed in restricted brain regions of rats and certain other animal models exposed to large quantities of psychoactive drugs that inhibit the normal operation of the neuronal NMDA receptor.
Neuroinflammation is widely regarded as chronic, as opposed to acute, inflammation of the central nervous system. [5] Acute inflammation usually follows injury to the central nervous system immediately, and is characterized by inflammatory molecules, endothelial cell activation, platelet deposition, and tissue edema. [6]
When this refinement is missing, symptoms such as unsteadiness and ataxia [8] will present. A potential cause of chronic alcoholic cerebellar dysfunction is an alteration of GABA-A receptor . This dysfunction causes an increase in the neurotransmitter GABA in cerebellar Purkinje cells, granule cells , and interneurons leading to a disruption in ...