Differences in Temperature Dependence of Early Development of Sea Urchins with Different Growing Seasons

Volume: 176Start Page: 96End Page: 10

Glutamate Neurotoxicity As a Mechanism of Ischemic Brain Damage: A Basic Study Using a New In Vivo Model

Ischemic brain damage is seen as a common feature in many pathological conditions such as ischemic stroke, subarachnoid hemorrhage, head injury, and prolonged seizures [1]. A number of animal studies have shown that there is a marked increase in the extracellular concentrations of glutamate under such conditions [2–7]. The neuroprotective effects of glutamate antagonists have also been demonstrated in the animal models of ischemia and head injury [1, 8], and thus it has been suggested that these conditions share a common injury mechanism, that is, glutamate neurotoxicity

Effects of mild hypothermia on cerebral blood flow-independent changes in cortical extracellular levels of amino acids following contusion trauma in the rat

The mechanism of hypothermic cerebroprotection after traumatic brain injury (TBI) is unknown. The present study was conducted to investigate the effects of mild hypothermia on the changes in cortical extracellular amino acids and cerebral blood flow (CBF) caused by cerebral contusion created in the rat parietal cortex by a weight-drop method. CBF in both normothermia (37°C) and hypothermia (32°C) groups, which was monitored using the hydrogen clearance technique, decreased significantly after contusion, but never fell below the threshold for ischemia. Cortical levels of glutamate, aspartate, glycine and taurine, which were measured by intracerebral microdialysis, were significantly increased after contusion in each group. However, these increases were greater in the hypothermic than in the normothermic rats. Normal plasma amino acid levels were high, and autoradiography following intravenous injection of 14C-labeled glutamate revealed marked extravasation of [ 14C]glutamate at the site of cortical impact. These results suggest that the post-traumatic increase in extracellular amino acids occurs independently of CBF reduction, and that extravasation of amino acids from the vascular compartment partly contributes to this increase. Hypothermic cerebroprotection in TBI is thus likely to occur through a mechanism other than reduction in interstitial excitatory amino acids. In TBI, it is postulated that the postsynaptic effects of hypothermia may be more important than the presynaptic effects, when CBF is kept above the ischemic threshold

Effects of Exogastrula-Inducing Peptides on Cell Proliferation in Embryos of the Sea Urchin Anthocidaris crassispina

Volume: 10Start Page: 793End Page: 80