This article nicely complements my schedule the next few weeks; lots of work and little sleep. That’s what trying to finish up grad work, and preparing for Neuroscience will cause! Last week, The Journal of Neuroscience featured another sleep-related article of which I’ve seen tidbits of previously at SLEEP and Neuroscience poster sessions.

Harvardian researchers have identified increases in nitric-oxide activity concomitant with acute sleep deprivation. First, a fluorescent dye targeting nitric-oxide producing cells was injected into the lateral ventricle of rodents. It was followed by 6 hrs of sleep deprivation (or undisturbed controls) achieved by gentle handling and air puffs. Here’s a cool schematic detailing the procedure.

While general nitric-oxide concentrations increased in the basal forebrain in lieu of sleep deprivation, it did not increase in brain areas mediating stress such as the paraventricular nucleus (PVN) of the hypothalamus and the amygdala. This is surprising given that any type of handling freaks animals out. I have lots of experience with this.

ResearchBlogging.orgWe know that nitric oxide activity mediates many physiological pathways aside from its presence during short-term sleep deprivation.  The regulation of phase-shifting of behavioral rhythms by light,  severity of alcohol withdrawal and relapse, and erectile dysfunction are a few of many important physiological processes (and pathologies) guided by nitric oxide activity.

What’s the next step? Is nitric oxide activity associated with sleep deprivation-induced cognitive lapses??

Kalinchuk AV, McCarley RW, Porkka-Heiskanen T, & Basheer R (2010). Sleep deprivation triggers inducible nitric oxide-dependent nitric oxide production in wake-active Basal forebrain neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (40), 13254-64 PMID: 20926651