Journal
JOURNAL OF NEURAL TRANSMISSION
Volume 113, Issue 4, Pages 497-519Publisher
SPRINGER WIEN
DOI: 10.1007/s00702-005-0406-1
Keywords
hyperthermia; brain injury; naloxone; blood-brain barrier permeability; brain edema formation; cell injury; glutamate; GABA; glycine; aspartate; amino acids; neurotransmitters; Evans blue; lanthanum; motor function; foot print analysis; rota-rod performances
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Role of excitatory amino acids, glutamate, aspartate, and inhibitory amino acids, gamma aminobutyric acid (GABA) and glycine in brain damage caused by heat stress was examined in a rat model. Subjection of rats to 4h heat stress at 38 degrees C in a biological oxygen demand (BOD) incubator resulted in a marked increase in glutamate and aspartate in some brain regions, whereas a significant decline in GABA and glycine was observed in several brain areas. Profound behavioural alterations and impairment of motor and cognitive functions were seen at this time. Breakdown of the blood-brain barrier (BBB), reduction in regional cerebral blood flow (CBF), edema formation and cell injuries are prominent in several parts of the brain. Pretreatment with multiple opioid receptor antagonist, naloxone (10mg/kg, i.p.) significantly restored the heat stress induced decline in GABA and glycine and thwarted the elevation of glutamate and aspartate in various brain areas. The motor or cognitive deficits were also attenuated. A significant reduction in BBB permeability, cerebral blood flow abnormalities, edema formation and cell injuries was evident. These novel observations suggest that (i) glutamate, aspartate, GABA and glycine are involved in the pathophysiology of heat stress, and (ii) a balance between excitatory and inhibitory amino acids in brain is crucial in hyperthermia induced brain injuries or repair.
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