NEURONAL ADAPTATION TO BARBITURATES

Barbiturates induce mitochondrial depolarization and potentiate excitotoxic neuronal death.

Barbiturates are widely used as anesthetics, anticonvulsants, and neuroprotective agents. However, barbiturates may also inhibit mitochondrial respiration, and mitochondrial inhibitors are known to potentiate NMDA receptor-mediated neurotoxicity. Here we used rat cortical cultures to examine the effect of barbiturates on neuronal mitochondria and responses to NMDA receptor stimulation. The barb...

Barbiturates.

Oxygen sensors and neuronal adaptation to ischemia

Hypoxia research is in the focus, as three of its pioneers receive the Lasker Prize 2016 for their discovery of hypoxia-inducible transcription factors (HIFs) and prolyl-4-hydroxlase domain proteins (PHDs) as cellular oxygen sensors [1]. HIFs are heterodimers consisting of a labile α and a stable β unit. In the presence of molecular oxygen the α subunit is hydroxylated by PHDs leading to immedi...

Comparative depression of several short acting barbiturates and spiro-barbiturates.

In an effort to develop new and possibly better types of barbiturates, suitable for intravenous use, a large number of spiro-barbiturates have been prepared by a ring closure on the 5-carbon atom of the barbituric acid and afforded for pharmacologic study. Spiro(2'-ethyl-3',5'-dimethyl cyclopentane) thio-barbituric acid appears to be the most promising product of a series of 50 analogues. Stoel...

Neuronal adaptation to simulated and optically-induced astigmatic defocus

PURPOSE It is well established that spatial adaptation can improve visual acuity over time in the presence of spherical defocus. It is less well known how far adaptation to astigmatic defocus can enhance visual acuity. We adapted subjects to "simulated" and optically-induced "real" astigmatic defocus, and studied how much they adapt and how selective adaptation was for the axis of astigmatism. ...