Pole dance: a brief history

Let's face it: calling yourself a pole dancer still raises a few eyebrows today. But with pole athletes competing in national and international competitions, and studios popping up across the globe, it's clearly moved beyond the confines of the strip club. So how did pole expand from the red light district to the fitness studio?

Pole fun :)

Pole dancing has a colorful history which long predates its presence in gentlemen's clubs. Historically, traditional gymnastic-like performances on a pole were performed in both China and India since at least the 12th century, though in both cases this was a men's sport. The Chinese art looked more or less like today's cirque du soleil (performed on sticky poles), and the Indian art, mallakhamb, (performed on wooden poles) was originally developed as cross-training for wrestlers to develop speed, stamina, and agility. Mallakhamb was revived in the 19th century, and youtube offers a wealth of examples, like this one.

It should come as no surprise that cultures across Europe and Africa have also incorporated poles, as phallic symbols, into various fertility dances, perhaps the best-known of which is the maypole dance.

Most sources agree that modern western pole dance began around the turn of the twentieth century. One source traces its origins to the 1893 World's Fair in Chicago, in which Egyptian women performed a sensual, hip-gyrating dance called the "hoochie cooch." This style of performance was soon incorporated into traveling circuses as a regular sideshow act by the 1920s, performed around the pole that held up the side tent, which soon became a prop. From there, pole dancing was incorporated into the burlesque scene in the 1950s. A woman by the name of Belle Jangles performed the first recorded pole dance in a strip joint in Oregon called the Mugwump in 1968, but it wasn't until the 1980s that pole hit the strip club scene in full force across the US and Canada.

Just about every source I came across seemed to agree that the turning point in pole came in 1994, when Fawnia Deitrich opened the world's first exotic dance school in Canada, focusing on pole dance and fitness. From here, things snowballed. Pole studios began opening and classes were soon offered across the US, Canada, Europe, and Australia. Two decades later, you can read up on this history in official-sounding websites like United Pole Artists and the International Pole Dance Fitness Association. General news sources like mic.com even report on it. There is even a new movement led by KT Coates as an Olympic sport. Personally, I think this video from the International Pole Sports Federation does the best job summing up pole as I know and love it.

News from lab

There's some good news coming from lab. For my January science update, I'm happy to fill you in on the big publication that just came from my boss Keisuke. On January 6, the journal Neuron published his latest findings in an article entitled "Congenital Nystagmus Gene FRMD7 Is Necessary for Establishing a Neuronal Circuit Asymmetry for Direction Selectivity." Quite a mouthful. So let's break this down.

"Congenital Nystagmus Gene FRMD7 Is Necessary for Establishing a Neuronal Circuit Asymmetry for Direction Selectivity"

1. What is congenital nystagmus?
This is an inherited visual disease which occurs in approximately 1 in 1500 individuals. The symptoms of the disease include a lack of optokinetic reflex, the reflex which allows to focus on objects in a moving field, and spontaneous involuntary horizontal eye oscillations. This video does a great job illustrating the condition.

Patients with this condition have severely impaired vision and can have serious social challenges stemming from the aesthetics of the condition. The severity of congenital nystagmus varies from patient to patient, and we don't quite understand why. More importantly, we don't know what causes it, and certainly not how to treat it. (*There is one technique for eliminating the spontaneous eye movements which involves cutting and re-attaching the eye muscles, and even so, we don't know why this works.)

"Congenital Nystagmus Gene FRMD7 Is Necessary for Establishing a Neuronal Circuit Asymmetry for Direction Selectivity"

2. What is FRMD7?
FRMD7 is a gene expressed in limited areas around the body, most especially in certain retinal neurons. It interacts with a membrane-associated protein, and it is especially important during development, but its activity isn't really understood. Several genetic studies have quite clearly linked mutations in this somewhat mysterious FRMD7 gene to congenital nystagmus in humans. How these mutations were causing this condition were totally unknown, until now.

"Congenital Nystagmus Gene FRMD7 Is Necessary for Establishing a Neuronal Circuit Asymmetry for Direction Selectivity"

3. What is neuronal circuit asymmetry? And why does it matter for direction selectivity?
First, let's take a look at something called direction selectivity. This refers to the ability of certain neurons in the retina to respond selectively to the movement of objects in a certain cardinal direction: up, down, left, or right. This ability of different neurons to respond to motion in one of the four directions is what allows us to detect moving objects. These neurons develop their direction selectivity after the brain tissue has significantly developed. In mice, it happens after birth, just a few days before they open their eyes. In humans, we assume that the development is similar, though we don't know for sure.

The direction selectivity is established through "circuit asymmetry," the formation of asymmetric circuit connectivity between starburst cells and their downstream signaling partners, the direction-selective (ganglion) cells. The starburst cells are a set of cells which respond more strongly when the light signal begins at their cell body and then moves out into their dendrites. (For instance, if an image signal moves from left to right across this cell, it won't elicit much of a signal from the dendrites on the left of the cell body, but it'll elicit a big signal from the dendrites to the right of body, which it passes after passing the cell body.)

A generic picture of a starburst cell which I grabbed from Psychology Today. The big spot in the center is the cell body, from which all the dendrites emanate.

These starburst cells form stronger connections with the direction-selective cells whose directional preference aligns with the preferences of the starburst cell's dendrites. We don't really know how the starburst cells know how to pick and choose the cells whose preferences align with their dendrites, but we know that they unevenly pair-up with direction-selective cells, at least in healthy individuals...

And here comes Keisuke's contribution: his original work, which just got published in Neuron, shows that mice with a mutated FRMD7 have problems with their direction-selective circuits. Specifically, their up and down direction-selective cells are just fine, but the left and right ones, the ones you'd need to focus on a horizontally-moving object and to keep your eyes from spontaneously oscillating, are all but non-existent in mice with this mutation. And remember, we know that humans with this mutation have congenital nystagmus: they can't focus on objects in a horizontally-moving scene, and their eyes oscillate horizontally. It looks like, in this case, the mouse is probably a pretty good animal model for this life-altering human disease. Through studying this mouse, we think we have the first major breakthrough in understanding this hitherto mysterious human disease.

If our extrapolations from mice to humans are correct, as they seem likely to be, then we now understand that humans with congenital nystagmus are lacking horizontal direction-selective circuits in their retina. This is a major step in understanding the neuronal circuits underlying this disease, an important step towards being able to develop a medical treatment. And more broadly, this is an important step in linking genetic mutations to problems in neuronal circuits. As Keisuke is quoted as saying in a popular science summary of his publication, "To my knowledge this is the first time that we can link a disease to a defect in neurocomputation."

I hope this was clear, and that it gives you a good idea of what that lab and I are working on.

It will be exciting to see where our investigations into the circuitry defects of congenital nystagmus will go over the next few years. Stay tuned!

A new year, a new look

Happy new year from snowy Aarhus!

After a couple of weeks back stateside, exchanging presents, testing apple cider mimosas, and camping out with cousins,

Family Christmas 2015 (including the family trip to the Franklin Institute)

having survived a bus trip up to frosty Toronto to catch up with friends and family,

Toronto, until we meet again

and even squeezing in a day-trip through the Big Apple,

There's nothing quite like Rockefeller Center and the windows at Saks Fifth Avenue at Christmastime.

I've dived back into the Scandinavian winter, which is finally more wintery this side of the new year.

Mars couldn't quite decide if today's snowflakes needed chasing or were fierce enemies to run from.

And in keeping with the fresh starts that come along with the new year, I'm going to be striving for something new when it comes to this blog. For now I'm thinking of rotating weekly updates on my four favorite themes: science, pole dance, Aarhus, and travel. I'm not sure yet just how I'll spin it, but keep an eye out.