Age-related modifications of potassium homeostasis and synaptic transmission during and after anoxia in rat hippocampal slices

NADH hyperoxidation correlates with enhanced susceptibility of aged rats to hypoxia

“…A similar result was obtained in which recovery of orthodromic spike activity and homeostasis following hypoxia in slices from aged rats was delayed, compared to slices from 6 to 7 months old rats (Roberts et al, 1990). The delays in recovery of synaptic transmission in both studies may have been the result of agerelated decreases in energy metabolism, particularly glycolysis, as opposed to oxidative phosphorylation and/or less effective pH buffering (Roberts and Chih, 1998).…”

“…Since the aged brain has shown increased vulnerability to hypoxic/ischemic damage Chih, 1995, Roberts andChih, 1998;Roberts et al, 1990), it is conceivable that injury to the aged brain will be exacerbated by the combined effects of changes in calcium buffering, prolonged hsd and resulting NADH hyperoxidation. To answer this question, a hippocampal tissue slice preparation of rats across the lifespan was used to test the following hypotheses: (1) NADH hyperoxidation following hypoxia is exacerbated in aged animals and is associated with diminished neuronal recovery compared to other age groups; (2) the removal of calcium during hypoxia in aged rats will decrease NADH hyperoxidation and improve neuronal recovery.…”

Age-related resistance to ?-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-induced hippocampal lesion

“…Altered calcium (Verkhratsky and Toescu, 1998) and potassium (Roberts et al, 1990) homeostasis have been proposed to underlie increased neuronal vulnerability associated with aging in several structures (Wozniak et al, 1991;Brouillet et al, 1993). However, and in agreement with authors who worked with toxins other than AMPA (Kesslak et al, 1995), our results indicate that aging between at least 3 and 15 months may reduce hippocampal vulnerability to excitotoxicity; a similar decrease has also been found in other brain areas, such as the nucleus basalis magnocellularis (Luiten et al, 1995;Wenk et al, 1996) or the striatum (Finn et al, 1991).…”

Hypoxic changes in rat locus coeruleus neurons in vitro.

“…During long-term hypoxia (> 5 min) the HH changed into depolarization which was initially slow and moderate but subsequently accelerated (Hansen et al 1982;Fujiwara et al 1987;Grigg & Anderson, 1989). This depolarization was due to a large increase of the extracellular K+ concentration similar to changes during spreading depression (Hansen et al 1982;Roberts, Rosenthal & Sick, 1990).…”