Posted by: Neurobites | October 15, 2012

Getting to know NOLA


Neuroloves, as promised I want you guys to get a feel of NOLA with us. Neuroscience is awesome and all (obviously we loves it) but there is more to the world then just Neuroscience (I know I know we are just wrapping our head around that concept too;)) So be forewarned. There. Is. NO. Neuroscience in this post. But there is sheer awesomeness;) A picture they say is worth a thousand words, so there will be plenty of that.

Let’s get right to it.

I don’t know about everyone else, but I am finding it exteremly difficult to describe New Orleans to anyone. The feel, the vibe, the atmosphere, the culture, the look or the people. It just blows my mind. I think the first thing that comes to anyones mind when they think New Orleans is the infamous Bourbon St. Rightly so, this street has earned it’s rep as being the street of sin. Bars, clubs, drinks, beads and intoxicated individuals can be found on every meter of this street. But as a non-drinker, non-partyer (shocked?!?! ) I took in the atmosphere and moved on, so the NOLA that I am getting to know is focused on the enviorment, the people and their incredible stories. Without a doubt there is more talent (musicians, singers, dancers, artists ect.) In one city block here then there are in entire cities anywhere else. It just blows my mind. Close your eyes and just feel I still stop at every single singer, musician and just stare with my jaw on the floor. It’s totes non-classy, not gonna lie.
First thing off the bat that you need to know, is the sheer amount of niceness, politeness and southern attitude/charm here is amazing. And this is coming from Canadian, we know polite. Construction workers tip their hard hats at you as you jog past them in the French Quarter, random individuals on the street look you in the eye and say how are you. Your barista, your bartender, your waitress, your random individual on the street “Hey Baby”,”Hey Sugar”, “Hey love” you. They call you beautiful, compliment you noncholantly and are very comfortable. Personally, I love this level of comfort with people, if you go through a day without meeting someone new or making someone blush/smile, seriously,to me that is a day wasted.
But going back to the Southern thing, people here move slow. I am telling ya, it drives me banana’s. I don’t know how to relax or walk in sedate lesuirely way, so I am baised when I say that people take their time doing anything here! I even had one of the construction workers telling me who I was racing as I waited for their truck to move out of my way. So I am learning to slow down. Somewhat;)
I know what you’re thinking now, tell us about the food! Man oh man. Let’s just say that I will be living at the gym when I get home. Unreal food. That is all I can say about it really. Spicy, loads of character and tons of fried food. By tons, I mean everything is fried here. I haven’t had something fried in years and NOLA just reminded me why. You can’t stop once you start:P


I don’t want to even talk about my beignet addiction. I am thinking of going into therapy.


Just a three man, no hands pyramid. No biggie.


I think this is some sort of palm plant..I failed first year plant bio (really who cares how plants make babies?!?!) *EDIT* one of our lovely lovely readers has idenified this beast as a cycad Thanks Sarcozona!


I want to live here.

If you’ve been to NOLA before and if you want us to eat, drink or dance somewhere for you..let us know. We aim to please;)

Stay amazing,

Posted by: Neurobites | October 13, 2012

SFN Day 1

Day 1 of SFN started off a bit off centre, three hours of sleep, coffee dropping, registration missing, wrong shoe choice, getting lost, getting found, high levels of ghrelin & cort.


IT got better:)

I registered to “Meet the Expert” who just happened to be Eric Nestler, whose talk Toward a Molecular Psychiatry: Studies of Biological Basis of Addiction and Depression included some personal information and perspectives. Dr.Nestler’s lab has garnered a reputation of being forerunners in the area of in vivo experssion of Addiction and Depression. His funny, humble and honest talk highlighted his and his lab’s work looking at C-FOS and Delta FOS B induction in the Arcuate Nucleus. I love talks like this, where someone who you read, cite & look up too are actually charming, generous and remind you that science isn’t about “proving” a hypothesis rather about “ah-well that’s unexpected” moments. I will be doing an inspired blog post about Dr.Nestler after SFN to do his work justice.

I spent the afternoon in a NanoSymposium Mood Disorders: Animal Models of Stress & Depression. There were defiantly alot of great talks in this block, the ones that I was particularly fond of were
Pubertal shifts in stress reactivity: The Role of  peripheral glands in modulating  neuroendocrince responsiveness. Presented by R.D.Romeo
Adolscent stress interacts with high fructose diet to alter cerebral glucose transporters. Presented by G.N. Neigh

I am really loving the attention on age and gender in these talks. More on them soon!

What I wish I could have also seen was the Dialogue between Neuroscience and Society, My life as a Rolling Neurological Clinic By Chuck Close and the Fred Kavli Public Symposium The Societal Impact and Biology of the Overt and Hidden Dysfunctions Resulting from Traumatic Brain Injury.

That was it for my SFN day. I finished off the day right with beignets from Cafe du Monde 😉

Stay Neurolicious!

Posted by: Neurobites | October 13, 2012

Extra Extra!!!

Fellow Neuronerds!


And I know I speak for the both of us when I say that we have missed you and missed dissecting knowledge with you! Yes it has been awhile and we can go into how we lack commitment, but we won’t dwell on that. We have had some soul searching, some individuals chirp us (this includes our supervisor..seriously) and we just simply couldn’t stay away.

MOVING ON (we hate emotionally charged confessions)

We are in gorgeous, laid back, hot, sexy New Orleans for the Society for Neuroscience conference! Get ready for daily posts, doubles and even triples! We will be covering the conference from talks to posters, encompassing any topic that catches our fancy. We (probably just me really) will blog also about the culture, food, and general awesomeness of NOLA.

Posts to look for
SFN day #
A Day in NOLA
Special Features.

If you would like us to attend a talk or poster or even if you want us to stalk,ahem, I mean find an expert for ya let us know!

Thank you for sticking with us. We promise we are worth it.
As always stay neurofabulous,
Rim & Harry

Posted by: Harry | December 15, 2011

Treating Hypothalamic Amenorrhea with Leptin
Hypothalamic amenorrhea (HA) is a one of the main causes of functional reproductive disorder in females. The condition involves the cessation of menstrual cycles in pre-menopausal women in the absence of any specific organic failures (no ovarian cancer, pituitary tumors, etc.). HA can be caused by many environmental factors, but the three leaders are: stress, strenuous exercise, and chronically reduced food intake (individuals with anorexia nervosa often have HA). To a certain extent, these environmental triggers do have some utility – it’s probably not a great bargain to devote energy to maintaining the reproductive system when times are tough and food is apparently scarce. That is, at least, the usual evolutionary view of things.

Lately I’ve been looking at HA and how its development and course may be altered by psychological stress, but I’ve already written about that in a term paper, so instead I’m going to write a bit about HA and energy deficiency. As suggested, the menstrual cycle often stops in the face of severe energy deficit, or as a result of strenuous exercise. Not surprisingly, the condition is seen from time to time in female athletes. Many, but not all cases of HA have hypoestrogenemia as a symptom. Estrogen is produced by the ovaries in a cyclic manner under stimulation by gonadotropic hormones arising from the pituitary gland. When this stimulation ceases, estrogen production drops off. This is an undesirable state of affairs for a number of reasons, among them osteopenia and osteoporosis, not to mention the inability to conceive.

So if HA is caused by nutritional deficit, we might guess that some of the hormonal signals that the body uses to communicate energy balance might also be used by the reproductive system for the same reason. It turns out that this is a very good guess. In the paper I am covering today, the authors took women suffering from HA and assigned them to receive either recombinant leptin or a placebo. After the treatment period elapsed, 7 out of 10 women had seen their menstruation return, compared to just 2 out of 9 for the placebo group. There was also an increase is estrogen and progesterone among leptin treated women. There was not, on the other hand, any chance in bone mineral density did not improve significantly over the treatment period, though perhaps the 36 week observation period was not long enough to detect these differences.

This treatment offers an interesting proof of concept for the use of metabolic hormones in the treatment of female reproductive dysfunction. Leptin treatment is not the perfect therapy. To begin with, it has to be injected (peptide hormones like leptin and insulin are destroyed by digestion, precluding oral administration). It also carries the risk of causing weight loss and loss of fat mass. It also doesn’t seem to help bone restoration, which is a notoriously tricky thing for any treatment to do (it’s enough, perhaps, to simply halt decay). Under normal conditions, leptin is interpreted by the brain as a signal of adequate fat stores, leading to a decrease in food intake. Applying exogenous leptin may also trigger these mechanisms, leading to unnecessary and potentially unhealthy weight loss (remember, women with HA are often underweight to begin with). Likely the optimal treatment for HA will comprise psychological interventions to deal with the stress related problems and maladaptive coping that may give rise to HA. Similarly, replacement of estrogen with oral contraceptives may also form a useful adjunct. But these more complicated therapies would likely require more sensitive and larger-scale study, and papers like this are a necessary prerequisite.

Chou SH, Chamberland JP, Liu X, Matarese G, Gao C, Stefanakis R, Brinkoetter MT, Gong H, Arampatzi K, & Mantzoros CS (2011). Leptin is an effective treatment for hypothalamic amenorrhea. Proceedings of the National Academy of Sciences of the United States of America, 108 (16), 6585-90 PMID: 21464293

Posted by: Neurobites | November 24, 2011

SfN 2011, Talks that inspired – Martin Myers on Leptin

My neurolovers!

I have missed you! I have missed the constant stream of awesome science! I have missed SFN and its craziness! A lot of missing is happening folks. Now that we are back, we are trying to digest the insurmountable amount of information that was dumped on us and trying to integrate some awesome ideas into our research. As I mentioned in our Daily Diaries’ that we attended quite a number of lectures, and from these lectures we have been oh so inspired! So for a couple of upcoming posts we will be using these lectures as a foundation of the blog posts.

Leptin. The hormone that was thought to be the answer to obesity when it was discovered via ob/ob mice in 1994 by Jeffrey Friedman’s lab. Characterized by studying a mouse model that had a recessive genetic obesity, called the ob/ob mice which were sterile mice which over 50% body fat (Google Image ob/ob mice, you know how we feel about being trouble for using someone else’s picture)Leptin has put researchers, clinicians and pharmaceutical companies through the ringer since its discovery. Initially touted as being the be all end all of controlling obesity, due to it decreasing body weight & increasing energy expenditure, it was soon realized that it was not as simple as that (more on leptin and obesity in another post).

Leptin, predominately synthesized by your adipose tissue (fat cells), is central to the regulation of energy intake, energy utilization, & metabolism (pretty much everything relates to it). When humans are in a neutral energy balance (basically that the number of calories consumed are just enough to satisfy their metabolic needs) the levels of leptin expression and secretion is representative the amount of body fat mass. Leptin levels are elevated in humans days after over eating, and are decreased in hours after fasting is initiated.

It’s important to note that leptin receptors are widely expressed not only in the periphery of the body but also the brain, making it difficult to study specific regions.

Dr. Martin Myers, from the University of Michigan, talk largely covered a paper, which he and his group have recently published in Cell Metabolism. I am gonna give you lovelies, a brief (very brief) snippet of the paper. Through a series of elegant experiments they haves specifically looked at leptin receptors expressed in the lateral hypothalamus which contain neurotensin (LepRbNts), a neuropeptide that interacts with the dopaminergic system. These neurons are activated by leptin and are part of network that is connected to a population of orexin (also known as hypocretin, are implicated in wakefulness, food intake and energy expenditure) neurons and the ventral tegmental area (VTA, we will look into the wonderful world of the VTA in another post). The researchers found that these neurons are regulating orexin expression and the activity of these neurons. This suggests that LepRbNts neurons may be involved in the physiologic leptin action of the orexin neurons.

They generated a strain of mice that were without leptin receptors on the neurons that expressed neurotensin (Nts-LepRbKO) this resulted in the mice exhibiting early-onset obese phenotype, increased feeding and decreased locomotor activity. This strain revealed to have altered regulation of the orexin neurons and the mesolimbic dopamine system. Their overall take home message, is that there are important roles in which leptin action ‘s on LepRbNts neurons in relation to controlling energy balance and neurophysiology.

If you even have a remote interest in leptin, energy metabolism, interesting methods, or just really really pretty pictures, I highly recommend checking the paper out. It is published in Cell Metabolism, which may make it difficult to get, however hustle your librarians, supervisors, fellow bloggers, nerdy friends and if all else fails, shoot as an email and we will hook you up;)

coughsuperstarcough → Dr.Myers portfolio

ResearchBlogging.orgLeinninger GM, Opland DM, Jo YH, Faouzi M, Christensen L, Cappellucci LA, Rhodes CJ, Gnegy ME, Becker JB, Pothos EN, Seasholtz AF, Thompson RC, & Myers MG Jr (2011). Leptin action via neurotensin neurons controls orexin, the mesolimbic dopamine system and energy balance. Cell metabolism, 14 (3), 313-23 PMID: 21907138

Because the conference is so busy, and because it imposes so many conflicting demands on my time, it was impossible to make every talk and poster. For the next little while, I will blog about things I wish that I saw at Neuroscience, but for various reasons did not.

Epigenetics is a very interesting field, though for whatever reason, some find it unapproachable and intimidating. This could be due to the fact that the field is just so darn inclusive. If you dissect the etymology of the word, you see the prefix epi- which simply means “above” or “upon” and -genetics, which means, well genetics. So in the broadest sense, epigenetics concerns things that relate to genetics (in practice: how genes are expressed) that exist over and above the genetics themselves. Since the field is so broad, and constitutes yet another layer of molecular complexity on top of our already confusing genetic code, it may seem difficult to apprehend.

Your genes are, after all, fixed at conception. But clearly that is not the entire story, as gene expression is regulated in a tissue dependent fashion (your liver expresses liver genes, your brain expresses brain genes, etc., in spite of the fact that each of them possesses a nucleus containing the same DNA). Gene expression is also regulated by experiential factors. Environmental factors during development, or even in adult life can affect the expression of genes in a long-term fashion. What’s interesting, from the point of view of scientists studying these phenomena, is that the changes tend to last much longer than the initial stimulation (whatever it was). So the question we’re dealing with is the following: what types of molecular changes underlie these long-term effects, and how do they relate to illnesses we face?

Researchers from the Mt. Sinai School of Medicine in NY discussed this topic in a minisymposium. Mental illness is an important topic for epigenetic studies, since often times the most challenging illnesses persist for long periods, perhaps indefinitely. It is possible, then, that epigenetic factors are involved in this persistence. The series of studies here took an interesting approach by focusing on models of depression that only affected female animals (this is a topic that Rim is quite interested in, but I’m blogging about it, so too bad for her). This is a very sensible approach, since depression is actually more common in females (though I dislike making sweeping generalizations, this does seem to hold up). In this model, mice were subjected to various mild stressors given at various, unpredictable times during the day. This treatment induced behaviors reminiscent of depression and anxiety in female, but not male mice.

After this treatment they found that stressed females showed an upregulation of two proteins involved in “stamping in” epigenetic marks in DNA. These proteins (one is an enzyme, the other a DNA binding protein) are crucial in DNA methylation, a type of epigenetic mark that involves attaching methyl groups to the points on the DNA thereby reducing transcription of nearby genes. To further cement this case, the authors used various techniques to artificially upregulate these methylation related genes, thereby mimicking the effects they saw in the stressed animals. Indeed, this manipulation actually made males more like females in their response to stress. On the other hand, blocking these seemed to have anti-depressent effects in females. The implication of all this, I suppose, is that since methylation is presumably being increased, genes that are protective against stress induced depression are being silenced, leading to the depressed phenotype.

What’s interesting about this study is that it addresses the very important issue of sex differences in mental illness. Well actually sex differences exist in practically everything, and more should be made of it. But since mental illnesses are particularly sexually dimorphic, studies that bring sex into the picture should hopefully be getting more and more common.

Posted by: Neurobites | November 16, 2011

Daily Diary SFN11 Day 5

My Dearest most beloved Neuroloves,

Day 5 of the epic SFN 11. Harry took a well deserved day to actually “see” Washington beyond 7th Street and Independence Ave. He hit up the Aquarium and the Natural History Museum. I on the other had could not bring my self to miss two talks that I just had to go to.

The first one was The Molecular Dissection of Leptin by Dr. Martin Myers. Oft. There are just so many things that were right about this talk I don’t know where to begin or how to do it justice. The best I can do is actually right up an overview post of leptin and review some of his papers. Such a clean, crisp, story teller of a presenter.

The second lecture I attended was the Neurobiology of Mood by Huda Akil. This combined what I love (mental disorders) with something I dislike (genetics:P). Her presentation style was straightforward and clear. I felt like I was getting alot of information but in such a systematic way that it all made sense.

Walking away from the Walter E Convention Center with the sky pouring rain, I felt both a sense of relief and sadness. We will update you guys about our experience, about attending the conference for the first time, getting to blog/tweet about it, and experiencing D.C.

Will update you as soon as we get back home.
Stay nerdfabulous,

Posted by: Neurobites | November 16, 2011

#SFN11 Daily Diary Day 4


I hope you guys finished up day 4 of SFN feeling gooooooood! I spent the morning presenting my research on the poster floor:) after knocking down one of the presentation boards and giggling uncontrollably for half an hour:P

During my poster presentation I met some amazing people, people who I read their work and want to marry their brains. One of them was Caroline Escobar. Yes THAT Caroline Escobar. She was NOTHING like I would have expected! Petite, gorgeous, gracious, funny and kind. Legit. She gave me tips on how to improve the study from everything in methodology to how to present my graphs:) It was Awesome:) I was in love:p

After the poster presentation I had rush to women’s luncheon, which was nice:) it’s inspiring to hear the stories, triumphs and tribulations of these insanely talented ladies!

I headed back to check out the posters, and hustled some exhibitors (I’m looking at you JOVE:p)

I finally had the opportunity to check out National Geographic!

How was your day 4?

As always, stay nerd fabulous lovers,

People with PD suffer from a variety of movement related symptoms (among other things), and while the disorder can be controlled to a certain extent by drugs such as levodopa, it remains progressive and ultimately uncurable. Deep brain stimulation (DBS) is an interesting approach to treating Parkinson’s disease (PD). This technique is being used in humans, and it involves implanting a small electrode in one or another areas of the motor pathways that are affected by PD and its treatments. In clinical scenarios, DBS in the subthalamic nucleus is a common treatment. It seems that this treatment not only reduces the motor symptoms of the disorder itself, but also some of the side effects of the medication used to treat PD.

One of the big questions here concerns what the downstream effects of this procedure might be? In a talk I saw today, Min and company presented a new model to study this treatment. To do this, they implanted electrodes in the pig subthalamic nucleus, and scanned their brains using a specialized functional MRI machine. They found that electrical stimulation resulted in increases in activity in the motor and premotor cortical areas, as well as the basal ganglia and cerebellum. The idea here, I think, is that while this form of stimulation is of therapeutic value, how it works is somewhat mysterious. By working with this pig based model, we can hopefully determine how it works in humans.

In other SfN related news, I spent some time jumping on the various structures outside the conference centre. I think Rim posted a video on the youtube.

Posted by: Neurobites | November 15, 2011

#SFN11 Daily Diary Day 3

Day 3. DONE. Oh man was it just packed!! Harry started off his day presenting his research, while I had a full day of lectures to attend

1) In the morning I made my way to the Special Lecture Rapid Synaptic Actions of Estrogens by Dr. Catherine Wooley. This was one of my favourite talks so far. Terrific research of course, and she’s such a cool chill person. I wish she was there at the Perils of Sex differences symposium;)

2) In the late morning I attended the Special Lecture, Protein Synthesis and Degradation at Synapses by Dr. Erin Schuman. Again, great talk but it made me feel that I need to brush up on my protein education 😛

3) In the afternoon, I attended the Symposium Genetically Driven Manipulation of Hypothalamic Circuitry Controlling Behavior. The panel included, Anderson, Sternson, Elmquist, Saper, & Elias. I missed the first talk but out of the ones that I did see, I really really enjoyed the talk by Elmquist and the one by Saper.

After taking some time to eat, get caffeinated I headed over with Harry to #sfnBANTER, a meet up for the neuroscientists that are tweeting and blogging. It was organized by the lovely @doc_becca . It was so surreal to meet people, who we both read,dissect and aspire to be:) It was such a relief to discover how nice they were! As relatively new bloggers and blogging for SFN, we both understand that there are expectations for us to reach within the blogging community. However, we found that the people we met were nothing short of welcoming and sweet. We did spot some bloggers/tweeters that we knew who they were, but neither one of us had the guts to approach them and say hello..

We are both total chickens.
Don’t judge.

But, we did meet some superstars, so a shout out to our now blog homies 😉

Our gorgeous host Doc_Becca
The incomparable & hilarous Scicurious
The beautiful social butterfly Braininteresting
The charming gentleman ThatBS

It was such a pleasure meeting them! GROUP HUG!

Stay neruolicious loves,

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