Dilemma of being a neuron

If you were a neuron, you would need fast excitatory transmission and fast synaptic inhibition. The first - fast excitatory transmission - is mediated by AMPA and the second - inhibition - is mediated by GABA.

Since the inhibition by GABA is mostly in the synapses and the excitation is in the body of the neuron, you will have to package them and transport them to two different destinations. Or you could just send them generally to the plasma membrane and let them settle down where they are needed. 

What will you do?

If neurons were people, the answer would have been easy. But neurons don't talk. So you have to quiz them with scientific procedures and protocols. A recent paper in PNAS, Differential vesicular sorting of AMPA and GABAA receptors, does just that. Using total internal reflection fluorescence microscopy  in combination with immunocytochemistry, electrophysiology, and electron microscopy methods they confirm what method neurons use to distribute the receptors in different parts of the cell membrane.

Here is a short video from the report:

It appears that neurons are rather sensible. They package the goods into vesicles in golgi bodies and transport them separately to different destinations as per the need.

Does Winning an Election Increase Corruption?

Winning a competition contributes to subsequent unethical behavior, claims a paper in PNAS, based on a series of studies. Winners behave more dishonestly than competition losers.

The paper by Amos Schurra and Ilana Ritov from Israel provides evidence to show that winning a competition increases the likelihood of winners stealing money from their counterparts in a subsequent unrelated task. But the effect holds only when winning means performing better than others and not when success is determined by chance or in reference to a personal goal. The results also show that a possible mechanism underlying the effect is an enhanced sense of entitlement among competition winners.

Now I understand why, with each election, corruption grows.

PNAS 113  (7): 1754–1759 (2016)      doi/10.1073/pnas.1515102113

Terrestrial Biodiversity hotspots and marine populations

I read a General Article in Current Science twice. I was to write an invitation to read it. The content was significant. But the style was horrible.
Anyway, what fascinated me about the article was a map of biodiversity hotspots in the world. I kept looking at it again, to distract myself from the painfully didactic text and kept wondering - what is common between these sites, so far apart geographically?
I could not take the picture from the article. So here is one from commons.wikimedia.org/

One hypothesis presented itself - these are new kinds of land forming...
After I finished writing the page in Current Science, I sat back to relax. And then I come across this paper in PNAS - "Geomorphic controls on elevational gradients of species richness" by Enrico Bertuzzo et al. in  PNAS  vol. 113  no. 7  1737–1742  February 16, 2016.
Not bad. My instincts were right when I wrote the invitation to read the paper on Biodiversity in Current Science.
Another paper that I had to introduce in the next issue of Current Science dealt with fish populations in the sea. So I could not help wondering whether the claims of this PNAS paper  - based on simulations - is true for the sea also.
So I went back to look at the PNAS paper again. At the end of the paper there is acknowledgement of funds received from... - the Swiss Federal Institute of Aquatic Science and Technology!
Not bad. The way content from diverse papers connect up. 

A sigh of relief: peptide that controls sighs found

It is not only relief, but often sadness or exhaustion may also cause sighing - a long breath. And, of course, there are also sighs without any of these - a spontaneous sigh that helps to reinflate the alveoli of your lungs. So what is the most proximal cause of sighing?

The center in the brain that controls breathing (retrotrapezoid nucleus) sends signals to the respiratory rhythm generator in the brain (preBötzinger Complex). These signals consist of two peptides: neuromedin B and gastrin-releasing peptide. A shot of these peptides elicits sighing. Blocking either of these peptides reduces sighing and blocking both peptides eliminates it altogether.

Whether it is relief from tension, emotions, tiredness or any other distal causes, this is the peptide that ultimately sets off a sigh.

A report in the recent issue of  Nature - 8th February 2016 - looks into the peptidergic control circuit for sighing.

Are you a morning person or a night owl?

Sleep researchers have been identifying genes that determine whether you get up early and go to bed early or lead a hectic life late at night, finding it easier to sleep into the morning hours. The first clock gene found was per in drosophila a few decades ago. The gene influences the circadian rhythm. And then a few more followed, one by one. Now in a fell swoop, using genome wide association studies, of self reported morning persons, scientists have identified 15 loci that contribute to the habit of rising early in the morning.

Interestingly, getting up early and going to bed early does not necessarily make you healthy, wealthy and wise. Excess body weight, depression etc have also been implicated for the tendency to rise early. But these factors do not seem to figure in the genetic analysis. Yet.

Nature Communications has open access report. Take a look.

http://www.nature.com/ncomms/2016/160202/ncomms10448/full/ncomms10448.html

New clues in the genetics of Schizophrenia

There is a paper in the latest issue of Nature that spells the development of a new perspective on schizophrenia. The paper by Aswin Sekar and others identifies the genetic risks for schizophrenia.

It was well known that the Major Histocompatibility Complex (MHC), the genetic system that forms the basis for the distinguishing of self and the other by the immune system, has a strong association with schizophrenia. But the genes and molecular mechanisms for this had not been identified. The recent paper in Nature does exactly that.

There are many structurally diverse alleles of the complement component 4 (C4) genes of the Major Histocompatibility Complex in Chromosome 6. These alleles produce widely varying levels of C4A and C4B proteins in the brain. In schizophrenia, there is more of the C4A protein.

The C4 proteins are localized mainly in neuronal synapses, dendrites, axons, and cell bodies. They are responsible for synapse elimination during postnatal development. The over expression of C4A proteins thus explains the reduced numbers of synapses in the brains of individuals with schizophrenia.

The findings are significant since now one can focus on genetically modifying the expression of the C4A allele. I predict that there will be more papers in this direction this year itself.

Aswin Sekar et. al. Schizophrenia risk from complex variation of complement component 4, 

Nature (2016) doi:10.1038/nature16549