Cataplexy? August 30, 2009

This pathology is not a cousin to dyslexia, but rather a “hidden” side effect of narcolepsy. Even the biologically-versed creator of Montegraphia.Nonsense did not know about symptoms of cataplexy or that it is solely associated with narcolepsy, which means: does the general public have any idea?

Cataplexy is characterized by a sudden loss/paralysis of muscle tonus seen during REM sleep. It is triggered by intense emotional states, including humor and anger, and is proceeded by a transient entrance into REM sleep (i.e. the victims immediately fall asleep). Orgasms also trigger cataleptic/narcoleptic episodes, which I imagine are often mischaracterized as the “post-coitus stupor.” Humans are not the only cataleptic mammalian species. Dr. Bill “The Crusader” Dement and the Standford Sleep Medicine crew have bred narcoleptic dogs for decades.

The etiology of narcolepsy and associated cataleptic episodes manifest from the destruction of hypocretin/orexin-expressing areas of the brain, which are wake (and hunger)-promoting.

For more information on narcolepsy and/or for philanthropical contributions to narcolepsy research and public awareness about the disorder see the Center for Narcolepsy at Stanford.

Below is a video of a child and dog who both suffer from cataleptic/narcoleptic attacks.

My My My My V-V-VLPO August 28, 2009

As a side note, I happen to be listening to a remix of Lady Gaga’s “Poker Face” while writing this entry, and hence the random title. Over my tenure of blogging, I have neglected to mention another critical structure involved with the regulation of sleep/wake. There have been plenty of discussions about the SCN this and the SCN that, but it isn’t the only master control center.

Without further ado, I introduce the ventrolateral preoptic area (VLPO) photomicrographed below.

It’s not a coincidence that this structure is in the hypothalamus and anterior to the SCN. Lot’s of cross-talking within that region. The VLPO has GABA and galanin-ergic projections that extend onto wake-promoting areas including the serotonin-expressing raphe nuclei of the midbrain, the histamine-expressing tuberomammaliary nuclei (reason why antihistamines cause drowsiness), and dopamine-expressing mesolimbic areas.

Yesterday, an article in the European Journal of Neuroscience was published on the role of the VLPO in REM and NREM rebounds following a period of sleep deprivation.

More tidbits for cocktail hour.

National Sleep Foundation Back to School Tips August 25, 2009

Next week is the most anticipated time of the year; the pee-wees return to campus nagging about early rise times for that 7:45 AM lab, chatting loudly in the hallway next to the lab, and with no apple for the teacher(s).

Today, the National Sleep Foundation published a list of “Back To School” sleep tips that should already be incorporated into our daily schedules, particularly those of the early-rising naggers with no apple for the teacher.

• Gradually adjust to earlier sleep and wake schedules 10 days to two weeks before school begins. This will set biological clocks to the new schedule. OOPS! Does this mean I can delay teaching for 2 weeks. My students need to entrain in order to have superior lab reports and grades, and consequently, to give the T.A. an outstanding recommendation : )
• Keep a regular sleep schedule, and avoid extremes on weekends. Having a regular bedtime increases the likelihood that kids – including teens – will get optimal sleep.
• Establish a relaxing bedtime routine. Reading before bed is a good choice for kids of all ages and for parents. That’s right, students, you better be reading that lab manual every night.
• Create a sleep environment that is cool, quiet, dimly lit and comfortable.
• Keep television, video games and other electronics out of the bedroom. National Sleep Foundation’s 2006 Sleep in America poll revealed that having electronic devices in the bedroom is associated with an increased risk of falling asleep in class and while doing homework. Eliminate exposure to electronic media (television, video and computer games etc.) within an hour of bedtime.
• Limit caffeine, especially after lunchtime. I break this rule every day. It’s a manifestation of once living in New England.
• Eat well and exercise.

If Only I Had A Mutation of DEC2 August 25, 2009

A group of researchers from the West Coast have discovered a gene mutation responsible for the short-sleeping phenotype; that’s one gene mutation we all wish to have engended. Individuals with a mutation of DEC2 sleep for an average of 6 hours a night. I’m not certain, however, whether these individuals’ short-sleeping times complement objective measures of restfulness. Time to whip out the MSLT….

Ye Drunken’ Vervets….. August 22, 2009

“12% are moderate drinkers and 5% drink to the very last drop.”

Vervet monkeys residing in the Carribbean Islands are alcoholics, according to the BBC. These monkeys, brought to the area via human intervention, once relied on fermented sugar cane for sustenance and nutrition, but have “resorted” to other means; stealing sweetened, fruity alcoholic drinks from the tourists at resorts. Take that humans.

I wonder if these vervet monkeys prefer 99 Bananas to other alcoholic drinks?

The commentator suggested that these predisposing signs of alcoholism in Vervet monkeys are other putative links of a shared ancestry. Wrong! It may be a link, but I assure you it’s the weakest one. How do you explain high alcohol consumption and preference in other mammalian species, such as the Syrian hamster, which has been shown by our lab to consume 50 times more alcohol than the average human? They have extremely high levels of alcohol dehydrogenase, and there is almost no detectable damage to their livers following long-term, chronic alcohol consumption. Why? In their natural environment, these desert-dwelling creatures bury fruit, and subsequently uncover and eat this fruit once fermented. The pungent smell of fermented fruit navigates them to the burying site. MMMM, pomegranate liquor.

William C. Dement Retreat 2009: SHY, PVT, mTOR, and PPD August 21, 2009

The 3 day sleep/circadian retreat held in the scenic W. Alton Jones Campus was “acronymonyous.” In addition to the impressive 10 minute presentations given by the Dement fellows, including discussions on the evolution of sleep and sleep in autistic children, the young investigators were off the hook. Dr. Erin Henlon, a post-doc in Ciara Chirelli and Julio Tuononi’s lab at Wisconsin-Madison, nicely summarized the role of BDNF in the learning process, and the SHY theory of synaptic plasticity across sleep and wake; during the waking day, there is incredibly high synaptic potentiation (LTP), and rewiring of synapses that are facilitated through mGlu1 activity. During sleep, LTP across wake is counterbalanced by synaptic depotentiation (LTD) mediated through the phosphorylation of serine. This suggests that sleep resets neuronal processing, serving as a protective mechanism against overstimulation and subsequent neuronal death.

Dr. Dan Mollicone from Pulsar Informatics in Philly uses mathematical modeling to explain detriments in performance related to sleep debt and shifted circadian phases. His model is incredibly reliable; he assured us that he could spend a day in the international terminal at JFK, and know which time zone the sleepy, jet-lagged traveler had arrived from based on his/her performance on the psychomotor vigilance test (PVT); a simple, Gameboy-esque device used to test reaction times. The bottom line is that even though a sleepy traveler may objectively appear alert after taking the PVT at one time of the day, this above-average performance can drastically change within 2 hours. Hence, the circadian timing system is a potent mediator of wakefulness and sleepiness.

Dr. Jonathan Lipton from Harvard Medical School is a neuroscientist/neurologist (M.D./Ph.D.) who balances research and clinical practice. He spends most of his week studying the circadian expression of mTOR, the mammalian target of rapamycin that mediates cell growth and apoptosis, and possibly responsible for the etiology of cancer, and one day diagnosing pediatric sleep disorders . His clinical passion is the role of sleep in the onset and perpetuation of autism.

Finally, Dr. Hawley Montgomery-Downs (bonus points for the awesome name) studies sleep in women post-child birth. Poor sleep following child birth is independent of time in bed and total sleep time. It’s sleep fragmentation across the night that leads to severe sleepiness. As Dr. “The Crusader Dement” has recapitulated over and over again…SLEEPINESS IS RED ALERT! This retreat he even brought us mini squirt guns with his motto engraved on the side. Handy for rest stops…..

3 Day Haitus for a 3 Day Retreat August 17, 2009

You will notice an absence of new posts within the next day or two. I will be spending the next 3 days at the W.Alton Jones Campus in West Greenwich, Rhode Island for the annual Dement Fellowship sleep/circadian rhythm retreat. The retreat is at the scenic ecological wetland reserve owned by the University of Rhode Island. In addition to hanging out with Dr. D, the discoverer of REM sleep, I will be preoccupied with finding turtles, water snakes, and other native Rhode Island flora and fauna.

Evolution of Humans = Monkey Fish Squirrel August 14, 2009

“You’re the retarded offspring of five monkeys having butt sex with a fish squirrel.” Mr(s.) Garrison, South Park.

Mr(s.) Garrison’s outlandish teaching of evolution is comparable to other documentated cases in American school systems. It’s a touchy subject. To be brief, and to not steal the limelight of  a fellow graduate student more versed in evolution, Mr(s). Garrison refused to teach evolution to the class, but since he’s not Principal Victoria, he presented an abridged version.

Later in the episode, he has an epiphany and realizes, through the guidance of Richard Dawkins, that evolution is not a bunch of “bullcrap.” If you have 30 minutes to kill, the episode is ROFL.

No Crash Pads for Pilots August 13, 2009

This post is not about the tragic plane crash over the Hudson river, killing 9 people. This post is about the efficacious of crash pads; small-scale dormitories supplanted in metropolis and designed to provide trans-America pilots with some “decent” shut-eye. I applaud the Federal Aviation Administration for realizing that sleep is vital and incredibly dangerous without; sleep-deprived drivers, pilots, doctors, and laborers make more errors and have more lapses of attention than drunken ones.

As for the crash pads, the Washington Post recently critiqued their efficacy, and didn’t have a Siskel and Ebert approval of two thumbs up. This is not surprisingly, since; 1) most required co-in habitation with other pilots, which can certainly be a hindrance of sound sleep (i.e. spouses); and 2) the dorms were not equipped for minimizing sunlight.

Back to the drawing board FAA. In the meantime, disrupted, shortened sleep has to be better than no sleep, right?

Climate Change Does Not Affect The Timing of Bird Migration August 11, 2009

Yesterday, I attended Science Cafe Cleveland, an international monthly science colloquium sponsored by Sigma Xi. The topic of burning interest this month was bird migration.  Though a general overview of the vast and profound physiological processes required for migration were narrated by Dr. Sarah Nabey of Hiram College and Harvey Webster of the Cleveland Museum of Natural History, the audience was nonetheless concerned with an assumed looming issue: the effect of global climate change on the timing of bird migration.

As a chronobiologist, I would argue that global climate change does not affect the timing of bird migration. Emphasis on timing. Sarah agreed. Why? Migrating bird species have adapted to plastic weather, climate, and food availability by relying on the single, least plastic, most constant, reliable phenomenon on mother Earth; the hours of light (photoperiod) and dark (scotoperiod) in a given day. Of course, we all know that the lengths of photo and scotoperiods vary seasonally due to the Earth’s tilt. Unless global climate change alters the Earth’s tilt, then the timing of migration and return home will not change. Yes, the suprachiasmic nuclei’s abilities to integrate photic information and modulate behavior and physiology accordingly are that awesome.

Another intriguing question was whether the length of the photo or scotoperiod is a more important determinant of the timing of migration. From a chronobiological perspective, I would postulate that the scotoperiod is more influential. Why? The onset of all reproductive phenomena and related physiological stress,  which is highly important for the mobilization of energy resources during the migratory process (on average, an 80 hour, non-stop flight, with no meals, drinks, and in-flight entertainment), are mediated by melatonin, the hormone of darkness. In mammalian species, the pineal gland, responsible for nocturnal melatonin secretion, is indirectly wired to the retina, the locus of photic integration, via the spinal cord. In avian species, the pineal gland is directly wired to the retina, minimizing interferences of transmitted photic information from other indirectly projecting brain areas. This suggests that melatonin secretion from the pineal gland in avian species is critically involved in the timing and onset of physiological phenomena influenced by the lengths of daylight and/or darkness.

For trivial purposes: The two prominent killers of birds, migratory and non-migratory, are felis catus (the domestic cat) and illuminating, ambient lights of skyscrapers.

Below is a picture from www.montegraphia.com of a migratory Copper’s Hawk, we saw in Letchworth State Park near Rochester, New York.