Sunday, October 28, 2012

Dopamine and GABA working together

Until recently, the neurotransmitters of the brain have thought to be generally separate. That is, if a neuron is inhibitory, it releases GABA, and if it is neuromodulatory, it releases something else, dopamine perhaps.  But two new papers show that specific neurons release both GABA and Dopamine. I briefly mention these new findings here.

Dopamine and GABA together forever (source)
First a subset of cells that were mainly thought to be GABAergic turn out to release dopamine as well. In 2010, Ibanez-Sandoval et al. found that there are interneurons in the striatum that stain positive for Tyrosine Hydroxylase. Tyrosine Hydroxylase is a precursor molecule needed for the creation of dopamine, and is a telltale sign of a neuron that can make and release dopamine. The authors found that these neurons release GABA and inhibit nearby cells. In this paper they did not confirm that the cells actually release dopamine, just that they have the machinery for it.

This is weird for a few reasons. 1. Why would the striatum need dopamine in its interneurons? The main source of dopamine to this brain region is the substantia nigra pars compacta, and it pretty well covers the entire striatum with dopamine when it wants to. 2. Why would a cell release dopamine and GABA at the same time?  

Second the canonical dopaminergic neurons of the substantia nigra turn out to release GABA as well. In 2012, Tritsch et al., found that when stimulated with light, the dopaminergic neurons of the substantia nigra cause inhibitory responses in the cells in the striatum.

The authors did extensive control experiments to make sure that they were indeed seeing GABA release from dopaminergic axons. They used carbon fiber amperometry to measure dopamine, and confirmed that dopamine was being released, and they blocked GABA receptors to make sure that it was GABA that was causing the inhibitory response. Finally they tested whether these cells were directly releasing GABA or perhaps stimulating other cells that released GABA. They did this by adding TTX, a sodium channel blocker, to prevent action potentials. In this condition, they could still evoke neurotransmitter release by light-based activation of these axons, confirming that these neurons directly release both dopamine and GABA.

So what's with this mash up?

Within two years it's been shown that GABA cells might release dopamine and dopamine cells do release GABA. Why? Neither paper speculates much on why GABA and dopamine might be co-released, or what the consequences of such a partnership might be.

© TheCellularScale
Ibáñez-Sandoval O, Tecuapetla F, Unal B, Shah F, Koós T, & Tepper JM (2010). Electrophysiological and morphological characteristics and synaptic connectivity of tyrosine hydroxylase-expressing neurons in adult mouse striatum. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (20), 6999-7016 PMID: 20484642

Tritsch NX, Ding JB, & Sabatini BL (2012). Dopaminergic neurons inhibit striatal output through non-canonical release of GABA. Nature, 490 (7419), 262-6 PMID: 23034651

Tuesday, October 23, 2012

Can you turn a rat gay?

What does it take to 'turn a rat gay'? This question may have crossed your mind, but a group in Mexico actually did the experiments to test it.

A weak first attempt (source)
Triana-Del Rio et al., 2011 used a co-habitation conditioning paradigm to see if they could condition a male rat to prefer a male partner.
The basic paradigm was to house the 'experimental rat' to the 'stimulus rat' (who was scented with almond) for a full day every 4 days. Under these conditions, the experimental rat did not show any preference for the almond-scented stimulus rat later on.  However, if the experimental rat was injected with quinpirole, which stimulates dopamine D2 receptors, he did develop a preference for the almond-scented rat. This preference was not sexual in nature. Preference was measured by time spent together, and these guys just wanted to hang out.

Triana-Del Rio et al., 2011 (figure 1)

The authors then did a separate experiment where instead of using 'sexually naive' rats as the stimulus rats, they used 'sexually expert' rats.  They created these Cassanovas by riling them up with very 'receptive' female rats at least 10 separate times. They refer to this as 'sexual training.' When the sexually expert rats were used as stimulus rats, the experimental rats developed a sexual preference when injected with quinpirole. These experimental rats strongly preferred their almond-scented partners as measured by time spent together, mounting, and 'genital investigation.'

So what does this mean? First of all, even the most drastic change was not permanent, partner preference dissipated after 45 days. And as I mentioned in my SfN summary, this protocol did not have the same effect in female rats. I do not think that the researchers here 'turned a rat gay.' While they did succeed in biasing the preference of the experimental rat for the guy he was housed with, they certainly didn't change the rats sexual preference in a deep or universal way. There is no evidence that the experimental rat preferred males in general over females, just that he really likes the one guy he was hanging out with.

So this study does not really tell us anything about the biological basis of homosexuality, and it certainly does not tell us how to make a gay bomb. The most interesting implication for this study is in the activity of the D2 dopamine receptor, which may be involved in pair-bonding. I would be interested to see what some ex vivo cellular studies revealed about this treatment. Does quinpirole application cause a change in the number or location of the D2 dopamine receptors or the activity of the neuron?

© TheCellularScale

ResearchBlogging.orgTriana-Del Rio R, Montero-Domínguez F, Cibrian-Llanderal T, Tecamachaltzi-Silvaran MB, Garcia LI, Manzo J, Hernandez ME, & Coria-Avila GA (2011). Same-sex cohabitation under the effects of quinpirole induces a conditioned socio-sexual partner preference in males, but not in female rats. Pharmacology, biochemistry, and behavior, 99 (4), 604-13 PMID: 21704064

Friday, October 19, 2012

SfN Neuroblogging 2012: The Recovery Period

SfN 2012 is finally over, and now I can get back to answering your questions and teaching you how to build a neuron. Things will simmer down and neuroscientists will go back to their research and smaller more specialized conferences. Until May that is, when abstracts of SfN 2013 will be due!

SfN 2013 in San Diego, CA
Here are just a few final tips to cope with the post-SfN feeling.

1. Sleep. Consolidate all that knowledge and decompress. 

2. Consolidate your notes.  Do this right away or else you will completely forget where all those little scraps of paper went with scribbled citations and email addresses. Put them all in one notebook or type them up.

3. Email those people. Whoever they are, you probably got someones email address and told them you would be in contact. Maybe to send them the PDF of your poster, or maybe to get theirs.  Maybe because you had an ACSF recipe to send them, or they were going to tell you the super-secret voodoo chant that they do to get their in situ hybridizations to work every time.  Whatever it was, email them right now. Don't lollygag on this. You might forget to email, or they might forget who you are.

4. Do your receipts. If you are lucky enough to have your conference trip paid for, get all the reimbursement stuff together right away. Some universities (mine included) require that you get all this in order and turned in within a week of returning from the conference.

5. Make use of your motivation. You hopefully came back from SfN full of ideas! Use that excitement: set things up to start that new experiment. Order that new reagent. Write out that new idea for a grant proposal. Read those new papers you hadn't heard of before.

© TheCellularScale

Tuesday, October 16, 2012

SfN Neuroblogging 2012: Implicit and Explicit Gender Bias

Today I am going to talk about just one thing rather than poster highlights from the whole day.
As always, all the SfN Neuroblogging posts can be found here. Other posts on gender and neurosexism can be found here.

Today was the annual "Celebration of Women in Neuroscience Luncheon." This is one of the highlights of SfN for me each year. There is always a fantastic speaker (Phyllis Wise this year) and the lunch is delicious.

Phyllis Wise brought up the 'exact same resume study' in her speech and it got me thinking. The 'exact same resume' study is where researchers construct a fake person and write up their resume, and then submit it in application for various jobs. However, sometimes they put a woman's name at the top and sometimes they put a man's name at the top. 

The study found that the male names received more and higher paying job offers and were judged to be more qualified. And it wasn't just that men thought women less capable. The females who judged the resumes were just as biased as the males who judged resumes. This is pretty depressing. I mean this isn't the middle ages, or even the Victorian era, aren't we past this bias?

But that's exactly the problem. We think we are past this bias. Even though people (both women and men) don't think they have a bias, they actually do. Even you. Just like you probably think you are smarter than average, or a better driver than average, you also probably think that you are less biased than average. That. is. the. problem. People have an implicit bias towards thinking men are smarter, better and more capable even when faced with the exact same description of the person. And they don't acknowledge this bias.

How can you combat or fix a bias that people don't even think they have? A gender blind resume process could be implemented in the initial application process for a jobs. But as soon as the applicant arrives for an interview, the gender bias would rear its ugly head. Should faculty or hiring committees develop an explicit bias towards women in their hiring and salary negotiation process?

I do not know the answer to this question. I can't think of a better way to combat implicit bias than with explicit bias, but it's hard to argue that implementing an explicit bias is 'fair' (It is a bias after all). It would especially seem unfair to those who don't think that they are implicitly biased (which we have established is basically everyone). But is there a fair way to handle this problem?

UPDATE (10/19/12): Thank you to Dario Maestripieri for helping me think about this problem in a new way. Perhaps the best way to start addressing an implicit bias is to make it explicit. When someone makes an idiotic or sexist comment, it should be made public. When someone gets grabby, it should be made public. The whole point of this post is that one of the biggest problems with gender bias in science is that people don't believe it is there. If it is made clear that it is there, people can more easily fight against it.

© TheCellularScale

ResearchBlogging.orgMoss-Racusin CA, Dovidio JF, Brescoll VL, Graham MJ, & Handelsman J (2012). Science faculty's subtle gender biases favor male students. Proceedings of the National Academy of Sciences of the United States of America, 109 (41), 16474-9 PMID: 22988126

Monday, October 15, 2012

SfN Neuroblogging 2012: ketamine in neurogenesis and dopamine in obesity

SfN day 3, exhaustion setting in, but the science doesn't quit! Here are some highlights:
ketamine for depression? (source

1. Ketamine and the neurogenesis theory of depression. At a nice poster (324.28) R.M. Carter explained that ketamine has fast anti-depressant effects. Some people think that depression is caused by neurodegeneration and cured by neurogenesis (the growth of new neurons). So this group wanted to test whether ketamine could affect the growth of new neurons on the same timescale that ketamine affects depression (a few hours). And it does! Ketamine increased the rate that newly generated neurons in the dentate gyrus became synaptically mature. It will be interesting to see where this theory of depression goes. I would love to see a possible mechanism of action by which an NMDA antagonist could speed up neuron maturity. (Intuitively I would guess it would do the opposite.)

UPDATE 11/5/12: More on mechanisms of ketamine in synaptogenesis.

2. Fat and dopamine. In a nanosymposium (420.06) J. Carlin explained that rats fed a high fat diet from birth had lower dopamine than controls. This goes along with the idea that obesity can be related to a lower sensitivity to reward. The good news is that when the rats were put on a normal diet, the dopamine went back to normal. HOWEVER, this was only true for the males! The female rats did not go back to normal dopamine levels. Yikes, right? Carlin explained that maybe the females do go back to normal dopamine, but just not within the time frame that they tested. As always, more research is necessary.

© TheCellularScale

SfN Neuroblogging 2012: drunk birds, worms, and robot noses

After a distressing night of not having wifi in my hotel, I am finally able to put this post up.  All of the previous "SfN Neuroblogging" posts can be found here.

And now 3 more highlights from day 2 of SfN:

a bird and his beer (source)
1. Can songbirds be a good model organism in which to study the effects of alcohol? Well yes and no. A poster (207.14), presented by C.R. Olson explains that songbirds don't seem to get addicted to alcohol, so they might not make good subjects for alcoholism studies. But alcohol does effect their song learning. Basically when low levels (below the legal human driving limit) of alcohol were maintained in the songbird's bloodstream while the bird was learning its song, the bird crystallized its song earlier.  That is it stopped practicing and settled on a song faster that the sober birds. The meaning of this is still unclear, as the researchers still need to analyze how 'good' the songs are.

2. What can worms tell us about the relationship between voltage and calcium?  A poster (174.03) directly compared a voltage sensitive dye to a calcium sensitive dye it the C. Elegans nematode. H. Shidara's poster explains that the calcium and voltage signals in the AIY neuron do not necessarily correspond. When the voltage was elevated in the soma and dendrites, the calcium was really only elevated in the dendrites, not the soma. I didn't quite catch the putative explanation for this from the researchers, but I suspect the huge surface to volume difference in a cell body compared to a dendrite might have a strong effect on the calcium dye, but not the voltage dye.

3. Finally, a poster (174.06) explains a new method for making an odor sensor. C. Pickford explains that the drosophila larva (commonly referred to as a maggot) has only so many odor receptors but can detect gazillions of different odors (I don't have the exact numbers here). So basically he is trying to make an odor sensor modeled off of the actual larva nose. This would serve two main purposes: 1. to create an odor sensor that can sense many odors and 2. to actually understand how the larva might be processing the information from its few odor receptors to detect many scents. 

© TheCellularScale

Sunday, October 14, 2012

SfN Neuroblogging 2012: weird receptors

Day 2 of SfN was so packed with awesome science that I have too much to blog about.

here are two highlights:
NMDA receptor (source)

1. A great special lecture by C. Luscher about drugs and synaptic plasticity introduced me to the concept of a calcium impermeable NMDA receptor. As far as I was concerned, calcium permeability was a defining characteristic of the NMDA receptor. Luscher explained that after cocaine exposure (I don't remember how much or how long an exposure), there was a shift in AMPA receptor type from calcium impermeable to permeable. AND a corresponding shift in NMDA recepter type from calcium permeable to impermeable.

2. A poster (236.14) presented by M. Markham on the weakly electric fish introduced me to the sodium activated potassium channel. I was familiar with calcium activated potassium channels, but a sodium activated potassium channel allows the action potential in the electric fish to repolarize super quickly to facilitate very high frequency firing.  Other species of electric fish do not have these channels and do not use such high frequencies.
But here's the really interesting thing: People (and mammals in general) do have these channels (236.17). In fact a mutation in this channel in humans leads to serious serious central nervous system problems.
And here is the even more interesting part. In humans these channels aren't used to create super fast firing frequencies. It is more likely that they trigger essential intracellular signaling cascades.

UPDATE 11/13/12: for more on the sodium-activated potassium channels (SLICK and SLACK) and how they help the auditory system fire precisely, see this new post.

Again, more details will follow SfN and I will post more highlights from today tomorrow.

© TheCellularScale

Saturday, October 13, 2012

SfN neuroblogging 2012: confusion, dopamine, and gay rats

First poster session of SfN. Here are the 3 highlights:

You use too many of them. (source)

1. The worst poster ever. No graphs only words (well one picture of a whole brain) and TABLES! Oh the tables that should have been graphs! But it wasn't just the layout, the presentation was rambly and confusing. I gave them a fair chance to explain their work, asking more than once "what is the main point?" And when they finally got to the point, I said "oh, I see. I didn't get [the main point] until just now." But instead of realizing that the presentation was unclear, they made a bad joke about how neurotransmitter x must not have been working in my brain. um no, just no.

2. Dopamine neurons might not only release dopamine, new research from the Sabatini lab at Harvard suggests that they also release GABA, the main inhibitory neurotransmitter in the brain. This has interesting implications for Parkinson's Disease because the dopamine neurons die. Instead of only thinking about dopamine imbalances, maybe researchers should investigate GABA imbalances in PD.

 UPDATE 10/28/12: Here is a more detailed look at dopamine and GABA

3. Turning rats gay. you heard me right. A group in Mexico can make a male rat gay for another male rat by injecting him with a dopamine D2 agonist Quinpirole when he is around the other male. Eventually the quin-treated male will prefer the  other male even over a 'receptive' female.
The poster I went to today was presenting an extension of this research, inducing same-sex preference in females. This requires oxytocin in addition to quinpirole.
I didn't get a chance to ask about the further implications for this research because the poster was pretty well attended. mostly by young men.

UPDATE 10/23/12: Here is a more detailed look at turning rats gay.

I will post a more detailed analysis of both of these studies after SfN is over. As I've said already, I'll post brief summaries of the daily highlights, and more in-depth posts later.

© TheCellularScale

SfN Neuroblogging 2012: The long hard road to the Big Easy

You want to get to SfN on time, so here's a pro tip about how airlines work. 

How do airlines work?
I know it's a little late for this, but maybe you can take heed of this advice for next years SfN.

Airlines oversell their flights, ALWAYs. Especially if everyone in the universe is trying to get to the same place for a gigantic conference. So just because you bought a ticket, you don't actually have a guaranteed seat on that flight.

I witnessed the horrible tragedy of a woman not getting to her satellite event talk because she didn't have a seat on a plane for which she had bought a seat. They asked my flight for 8 volunteers to bump to another flight to New Orleans. 8 people! That means that 8 people who BOUGHT tickets did not have seats on the plane. 

They didn't have enough volunteers so some people were involuntarily bumped! Including our noble heroine who bravely decided to drive from our connecting city all the way to New Orleans to at least get there the same day, but unfortunately not in time to give her talk. (7 hour drive)

Ok so how can you avoid being in this situation?

As far as I can tell, the best way to lock in your seat is to actually check into your flight as early as possible. That usually means going online and printing your boarding pass. But that alone is not good enough. The online checkin process usually opens 24 hours before the flight, so my advice is to set an alarm exactly 24 hours before your flight and checkin online right then.

One of the airlines I ended up taking doesn't even automatically give boarding passes to the last 15 people who check in.  They give 'security passes' so you can get through security and to the gate but you do not have official permission to board your flight. 

So check in early and if you are presenting on Saturday afternoon get a flight on Friday. DO NOT count on everything going smoothly at the airport.

What I have just described is pretty much a worst-case scenario, and obviously plenty of people made it to New Orleans without much trouble (check out the #SfN12 tag to read about all the fun things people are doing there).

So yeah, I am writing this at the airport...but at least I'm not driving. And thank goodness my poster is not until Wednesday.

© TheCellularScale

Wednesday, October 10, 2012

SfN Neuroblogging 2012: unofficial rules

SfN gives some official rules for presenting posters. These are great and all, but there are some unofficial rules that you should follow as well.

Poster presenting should look like this (source)
Here are the official rules from the SfN website.
  • Poster Dimensions Authors scheduled in poster sessions are assigned posterboard space (six feet wide x four feet high or 1.8 m x 1.2 m) for displaying illustrative material (graphs, charts, and tables). Posters cannot exceed these dimensions.
  • E-mail Confirmation Authors will receive e-mail confirmation listing session title, session date, and location in late June. Authors will receive another e-mail with board numbers and presentation times in late July. This e-mail will also ask presenters for audiovisual equipment requests.
  • Author Presence Presenters are required at poster boards during a scheduled one-hour presentation time, and posters are to be mounted for the duration of a four-hour poster session. No presentation may be given by an individual who is not an author on the abstract.
  • Photography
    Photography is prohibited on the poster floor.

And here are some unofficial rules:

  • Be at your poster the whole time: They say you only need to be there during the one hour that you are scheduled, but it's a good idea to be there basically the whole time. If there really are posters you want to see during your 4 hour poster-slot, then have a co-author stay by your poster during that time. If you're lucky, you will be talking non-stop for the full four hours, and won't have time to even think about leaving.

  • Groom yourself: Nothing makes me want to get away from a poster faster that BAD BREATH. You don't need to look like a supermodel and you certainly don't need to wear a suit. But please brush your teeth, and then when you have that all important mid-morning coffee, chew some gum for a minute afterwards (then spit it out, because you don't want to smacking gum in someone's face either).

  • Engage your audience: If some one stares at your poster for more than 30 seconds, say something to them.  "Would you like me to take you through it?" or "Do you have any questions?" are perfectly fine things to say. If they say no, then let them read the poster. Though it's their loss. 

  • Don't waste your audience's time: If there are only one or two people at a time at your poster, ask them about themselves. "Are you familiar with grid cells?" or "Do you know how the striatum works?" are a great way to get a feel for what you should be telling them. You might have someone who barely knows anything about neuroscience, and for them you should start simple. But it is equally likely that you will be talking to some experts in your field. They will only want to know the newest most interesting aspect of your project. And they are probably busy and don't want to spend more than 5 minutes hearing about your poster. You shouldn't start explaining that a neuron is a cell in your brain to these people.

© TheCellularScale

Monday, October 8, 2012

SfN Neuroblogging 2012: Preparation

So you are going to a big scientific conference, congratulations!

Maybe you are going for the very first time and not presenting anything.  Maybe you are presenting your very own first author poster for the first time.  Maybe you are presenting yet another small update in your ongoing project. Maybe you are presenting a nanosymposiom or minisymposium talk. Maybe you are a PI and have a whole labs worth of posters presented by your students and post-docs. 

Whatever your situation, you need to do some preparation. 

for N00Bs:

If you are just attending the meeting, but not presenting anything, you need to do some pre-planning to get the most out of the conference. We are basically talking about the Society for Neuroscience annual meeting here.  And this conference is HUGE.

There are a ton of presentations and you literally cannot see them all (probably not even a quarter of them). So you have to do some preparation.  You can use the SfN meeting planner to search for topics you want to read about and to make an itinerary. You can also use the Hubbian app ( to browse abstracts and plan your SfN schedule. 

The absolute worst way to 'do SfN' is to just walk through the posters stopping at whichever ones catch your eye. You will miss the ones you are interested in, and will waste a lot of time.

for the poster presenter:

So you are presenting a poster. You are probably (hopefully)  finished or almost finished creating it at this point in time. If you are still working out the layout, you might want to check out Dr. Zen's blog Better Posters. It gives some helpful insights into those important questions like 'what font should I use?' and 'where should my acknowledgements go?'

Now after your poster is made, you will want to practice actually presenting it.  You can do this alone, just going through the explanation of what you did and why you did it. Or you can present the poster to an actual person. This is a better option because then you can get some feedback and practice answering their questions. But no matter what, PRACTICE your poster presentation.

You took so much time and effort to collect the data, run the simulations, analyze everything and layout out your poster. But all that work will be basically for nothing if you can't quickly and concisely communicate your results. You don't want 'Dr. Big Shot' leaving your poster confused and irritated because she couldn't understand the jumble of words you were throwing at her. 

for those presenting a talk:

It's more obvious to people that they need to practice a talk than that they need to practice the poster presentation. But there are a lot of bad presentations out there, and there is a lot of good advice online. I have proposed one single golden rule for presentations, but others have gone into much greater detail. I highly recommend Scicurious's "And Now, A Powerpoint Presentation" for some excellent tips on presenting scientific findings at a conference. 

For the lab head: (PI):

Not being a PI myself, I turned to twitter, asking 'What is the main role for a PI at a scientific conference?'

It basically came down to:

1. Communicate your research as a whole, as in: "Tell your lab's science story" (@Oldsjames) or "talk up lab work" (@GertyZ)

2. Networking, as in: "being the honey bee in the pollen-rich garden" (@neuropolarbear)

3. Help your students out, as in: "Introducing peeps to folks" (@GertyZ) or "pay for lab dinner" (@jsnsndr)

You also might want to take a stroll down 'NIH row' to do some schmoozing as recommended by Drugmonkey

So there you have it, tips for SfN attendees at all levels. Now go prepare, people!

© TheCellularScale

Friday, October 5, 2012

SfN Neuroblogging 2012: Introduction

The Cellular Scale is one of the official NeuroBloggers of the Society for Neuroscience annual meeting this year. You might have some questions, so let me answer them:

What is the Society for Neuroscience meeting?

The Society for Neuroscience annual meeting is the biggest neuroscience conference ever.  It is attended by about 30,000 people each year, and there are about 20,000 presentations (including posters).  It's like a gigantic science fair. 

one tiny corner of SfN
How often will I be blogging?

I am planning to post at least once a day about interesting posters or talks I see or events I attend during the actual meeting (October 13th-17th). These posts won't be super in-depth in terms of the science, but I plan to write a whole bunch of follow up posts after the meeting delving deeper into the most interesting science.

What will I be blogging about? 

SfN is divided up into themes. I don't know about you, but I have never put much thought into the 'theme' I wanted to visit during the meeting. In fact I am not quite certain which theme my own poster is in.  But regardless, the official bloggers are also organized by theme and The Cellular Scale will be covering themes B and D.

Theme B: Neural Excitability, Synapses, and Glia: Cellular Mechanisms.
   This is a good match for this blog because I've already discussed many of the sub-topics in this theme, such as synaptic plasticity, glia-neuronal interactions, and other weird things about cells.

Theme D: Sensory and Motor Systems
    This is also a good match because I love to blog about the senses at a cellular level. See these links for posts about the cells involved in vision, hearing, taste and smell.

So these themes are what I am 'officially' covering, but I plan to blog about the most interesting science even if it falls under another category.

What else?

I am going to index all the "SfN Neuroblogging" posts in a tab at the top of the page so you can easily get to all of them.

I will also be tweeting the meeting as they say, so follow me @cellularscale on twitter for up-to-the-minute updates.

If you have any questions that I didn't answer here, add a comment and I will try to answer it.

© TheCellularScale

Wednesday, October 3, 2012

Bomb Dogs or Bomb Cells?

It's about to get really neuro-heavy here at The Cellular Scale because of the impending Society for Neuroscience annual conference. So before that onslaught of neuroinformation, lets step back and talk about two of my other favorite things: smell and beer.
Dogs are good at Smelling Things... (I took this picture)
But could beer yeast eventually be better at it? 

In 2007, researchers genetically engineered Saccharomyces cerevisiae (beer yeast) to express a rat olfactory receptor. But not just any old fully functioning olfactory receptor. Radhika et al. (2007) made a lovely franken-protein by using bits of dna from all over the place. They basically end up with a dna sequence coding for a receptor that expresses GFP (green fluorescence protein) when it is 'triggered.' The key here is that this 'trigger' could be easily changed. 

They first demonstrate that they can replace the trigger part of this receptor, making it sensitive to the scent of vanillin or cintronellal. While yeast that can turn green in response to the relaxing scent of vanilla might make for great advances in home decorating, the authors actually wanted to make a yeast strain that would fluoresce in response to the scent of bombs.

Specifically, they wanted the yeast to respond to DNT, a mimic of TNT. To do this, they had to conduct a large assay on a 'library of cDNA inserts.' That basically means they had to switch in different 'triggers' for the receptor based on known strings of olfactory receptor dna and test each one to see if it responded to DNT. Lucky for them, they happened to find one. 

Radhika et al., 2007 Figure 4A: yeast glows in response to DNT

And voila! a strain of bomb-sniffing yeast!

While I don't think we'll be replacing bomb-sniffing dogs with petri dishes of glowing yeast any time soon, this is a significant step toward cellular level bomb-detection.  More importantly, this study developed a new way to screen dna. They have created a versatile receptor 'cassette' into which they can place a string of dna and test which ligands or odors 'trigger' that section of the protein.

© TheCellularScale

ResearchBlogging.orgRadhika V, Proikas-Cezanne T, Jayaraman M, Onesime D, Ha JH, & Dhanasekaran DN (2007). Chemical sensing of DNT by engineered olfactory yeast strain. Nature chemical biology, 3 (6), 325-30 PMID: 17486045