Posts Tagged ‘ hormones ’

Wakefulness Cells

Certain groups of neurons determine whether light keeps us awake or not, says a new study.

Just a typical day for a hypocretin-deficient mouse. Okay, I'll wait for you to finish making that squinchy "Awww!" face, and then we'll move on with the article.

In the hypothalamus – a brain structure responsible for regulating hormone levels – specific kinds of neurons release a hormone called hypocretin (also known as hcrt or orexin). Hypocretin lets light-sensitive cells in other parts of the brain – such as the visual pathway – know that they should respond to incoming light by passing along signals for us to stay awake.

Scientists have understood for centuries that most animals and plants go through regular cycles of wakefulness and sleep – they call these patterns circadian rhythms or circadian cycles. More recently, researchers have begun unraveling the various chemical messaging systems our bodies use to time and control these cycles – enzymes like PER and JARID1a, which help give us an intuitive sense of how long we’ve been awake or asleep.

But now, as the Journal of Neuroscience reports, a team led by UCLA’s Jerome Siegel has isolated a neurochemical messaging system that dictates whether or not we can stay awake during the day at all. The team bred a special strain of mice whose brains were unable to produce hypocretin, and found that these mice acted like students in first-period algebra – even under bright lights, they just kept dozing off. However, they did jump awake when they received a mild electric shock:

This is the first demonstration of such specificity of arousal system function and has implications for understanding the motivational and circadian consequences of arousal system dysfunction.

What’s even more interesting, though, is that there’s a second half to this story – the dozy mice were perfectly perky in the dark:

We found that Hcrt knock-out mice were unable to work for food or water reward during the light phase. However, they were unimpaired relative to wild-type (WT) mice when working for reward during the dark phase or when working to avoid shock in the light or dark phase.

In other words, the mice without hypocretin stayed awake and worked for food just fine when the lights were out. So they probably have promising futures as bartenders or bouncers.

The takeaway here is that hypocretin isn’t so much responsible for enabling knee-jerk reactions as it is for helping mice (and us) stay alert and motivated to complete reward-based tasks when the lights are on. Without this hormone, we might act normally at night, but we just wouldn’t feel like staying awake when the sun was out.

And that’s exactly what Siegel’s team had found in several of their earlier studies, which linked human hypocretin deficiency with narcolepsy – a disease that causes excessive sleepiness and frequent daytime “sleep attacks.” These new results suggest that narcoleptic patients might have more success getting work done during the night, when their symptoms might be less severe.

Siegel also thinks clinically administered hypocretin might help block many effects of depression, and allow depressed patients to feel more motivated to get up and about during the day. If so, this could be a promising new form of treatment for that disease as well.

Finally, and perhaps most intriguingly of all, it’s likely that similar hormonal response “gateways” play crucial roles in other neurochemical arousal systems – like those involved in fearanger, and sexual excitement. If so, discoveries along those lines could provide us with some staggering new insights into the ways our brains regulate their own behavior.

So, I know what you’re probably wondering: am I really advocating the use of electric shocks to keep bored math students awake? Of course not – I think releasing wild badgers into the classroom would be much more effective.

Autistic Genetics

Some forms of autism seem to be linked with variations in certain genes, a new study says.

One of these chromosomes is not like the others (maybe).

The deletion of a certain cluster of 27 genes on the mammalian chromosome 16 – specifically a region known as 16p11.2 – causes autism-like features to develop in mouse brains. These mice exhibited hyperactivity, repetitive behaviors, and difficulty adjusting to new environments, much like human children with autism. (As I mention a lot on this blog, mouse brains provide pretty reliable models of certain human brain functions, which is why neuroscientists experiment on them.)

The idea that chromosome 16 might be linked to autism dates back to 2007, when Michael Wigler at Cold Spring Harbor Laboratory (CSHL) discovered that many children with autism had a deletion of a certain set of 27 genes in region 16p11.2.

Tired of acronyms yet? I sure hope not, because here come some more.

As the journal Proceedings of the National Academy of Sciences (PNAS) reports, a team led by Guy Horev at CSHL genetically engineered mice to manifest this same chromosomal copy number variation (CNV):

We used chromosome engineering to generate mice harboring deletion of the chromosomal region corresponding to 16p11.2, as well as mice harboring the reciprocal duplication. These 16p11.2 CNV models have dosage-dependent changes in gene expression, viability, brain architecture, and behavior. For each phenotype, the consequence of the deletion is more severe than that of the duplication.

In short, a deletion of those 27 genes produced autism-like symptoms, while mice with an extra copy of region 16p11.2 didn’t seem to be autistic at all.

Interestingly, half the mice with the deletion died soon after birth. The ones that survived to adulthood were physically healthy and fertile, but when the researchers studied their brains under MRI scans, they found a set of neurological symptoms that were all too recognizable:

[The mice] have alterations in the hypothalamus and exhibit a “behavior trap” phenotype—a specific behavior characteristic of rodents with lateral hypothalamic and nigrostriatal lesions.

The hypothalamus is a brain region involved in regulating our hormones, balancing our body temperature, and motivating us to perform semi-automatic tasks like eating, drinking, and sleeping. The nigrostriatal pathway connects the midbrain’s substantia nigra to the forebrain’s striatum; it’s a major dopamine pathway that’s involved in motivating movement. Abnormalities in all these regions have been linked with autism in previous studies.

The next step in this research will be to pinpoint which of the 27 genes in region 16p11.2 impact autistic development in what ways. The researchers hope future discoveries along those lines will help doctors diagnose autism early in a child’s life, or perhaps even predict its likelihood based on the genetics of the parents.

Like other predictive genetic tests, this could lead to some tough ethical dilemmas for would-be mothers and fathers – but it’s also likely to lead to more proactive treatments. And besides, even if you know your child will be born with autism, you never know if he or she might be the next Daniel Tammett or Temple Grandin.

The Splort Hormone

At the end of my last post, I promised I’d explain more about inner dialogue, and get into some practical tips on self-programming. A draft of that write-up is almost finished [SCIENCE UPDATE! It’s here.] but I came across an article today that brought up some intriguing points – and some common misconceptions – about neurochemistry. I couldn’t resist such a perfect opportunity to explain some concepts more clearly.

Eye (and nose) contact.

The article is mainly about the chemistry of eye contact, and…well, I’d better let the author speak for herself.

A loved one’s lingering look can trigger a rush of happiness, but too much eye contact with an acquaintance or a stranger can bring on sudden discomfort. How, exactly, does eye contact affect us, anyway?

Sounds pretty frickin’ fascinating so far, right? So let’s dive in. After a few introductory paragraphs, the author gets to the good part – the neuroscience. She explains that authentic expressions affect other individuals’ emotional responses differently than faked ones do – which is accurate, and backed up by some intriguing scientific research.

But the next bit was what made my Science Radar bleep a warning:

Oxytocin, also known as the “love” or “cuddle” hormone, plays a big part in [making our hearts flutter]. It’s a feel-good chemical that’s released when we feel bonded with someone, either emotionally or physically. The release is prompted by a warm hug, holding hands, falling in love, and so forth.

Well… that’s only sort of true. And sort-of-true statements often lead to confusion, which is why I want to explain the oxytocin situation as clearly as I know how.

Oxytocin is often called the “love hormone” or the “cuddle hormone.” That’s probably because it can be detected at raised levels in human blood plasma around the time of orgasm. If you Google oxytocin, most of the results will contain words like “love” or “cuddle.” You’ll also see a lot of articles asking, “Can oxytocin do [X]?” and “Does it do [Y]?” There’s plenty of speculation floating around – but the fact is, scientists are still unraveling the complex relationship between oxytocin and human emotions.

For example, oxytocin levels seem to rise during physical sexual arousal in women, and “spike” around the time of orgasm. But women’s bodies also release high levels of oxytocin during cervical dilation (i.e., expansion of the vaginal canal) during second- and third-stage labor, as well as when their nipples are physically stimulated for breastfeeding by an infant.

Meanwhile, in men’s bodies, oxytocin levels seem to just rise and then level off during sexual arousal. Some studies have found a mild spike around the time of orgasm, while others haven’t. Oddly enough, at least one study has found that oxytocin levels rise highest in men who stimulate themselves to orgasm. So we might just call oxtyocin the “splort hormone” and be done with it – but (as usually happens with science) there’s a lot more to it than that.

A sexy, naked oxytocin molecule.

First of all, who wants to know what oxytocin is? It’s a polypeptide hormone (i.e., a hormone created when a string of amino acids join together in a specific way). It’s produced in the pituitary gland of mammals. In very general terms, oxytocin is related to changes in the contractile properties of reproductive tissue. Some studies seem to show that oxytocin induces or promotes those changes; other scientists think its presence is just a reflection that they’re happening.

But even that’s just the tip of the oxytocin iceberg. Over the past few years, scientists have learned a lot about this hormone by studying some of the effects it can produce.

In mice, oxytocin in taste buds has been shown to inhibit the desire to keep eating. In the hypothalamus, it helps rodents time their birth cycles. In rats, a raised oxytocin level in the hippocampus decreases responsiveness to stress, and allows wounds to heal more quickly. In humans, it’s been shown to increase generosity toward strangers. Then again, it also makes people racist:

The love and trust oxytocin promotes are not toward the world in general, just toward a person’s in-group. It turns out to be the hormone of the clan, not of universal brotherhood.

Here’s where we finally come around to those ideas about oxytocin being a “cuddle hormone.” Oxytocin in blood plasma has been shown to spike when a person receives a friendly hug, or even an extended gaze. But whether the hormone is rising because we’re feeling loved – or if it’s just because we’re responding emotionally to the behaviors of other individuals in our species – is a question that’s still open.

So, like I said: sort of true.

To be honest, I’m glad I found that article, and I hope others do too – anything that helps get people excited about neurophysiology is awesome as far as I’m concerned. But I like to present things clearly, with plenty of specifics. I think that, as a journalist, if I can’t sit down and describe any given detail of my subject clearly and succinctly, I haven’t done enough research, and it’s time to hit the books again.

That’s just one guy’s opinion, obviously. But it’s the way my connectome is wired.


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