So much to see… but oh so little time!!! SfN #3

Today was fantastic! But I jump ahead.

I was a bit bummed that I didn’t feel too engaged with a couple of the posters I saw yesterday. I did however enjoy the presidential lecture last night. Dr. Sudhof stressed the importance of emphasizing the complexity of the brain and indeed neuropsychiatric disorders if we are going to have any sway with the public perception of not only the disease, but also why little segway had been made on understanding the disorders. He also gave an uplifting statement, genetic understanding must be linked with function and its implications in order to even begin to understand how psychiatric disorders can be understood. Needless to say, it was a great talk!

On day 3, I went to a bunch of posters that I thoroughly enjoyed, summaries of which I tweeted about – check them out on my feed. I would write about them, however, I want to write a little reflection on something profound I learnt yesterday.

I went to a reception last night and one thing led to another in which I implemented advice a neuroscientist had given me the day before: “Ignore your shyness and get in people’s faces – you have to introduce yourself.” I did just that. I introduced myself to not just 1 but 3 scientists that I thought to myself: “It would be great to get to know these people.” I have to say, all it took was a few sentences and next thing you know, I am getting insights about an outreach program I have been trying to have ironed out, and I got encouraged to keep self-promoting. I finally realized that SfN is not just about the science, it is also about the people who do the science. I have to say this is my 5th time attending SfN, and this is the year that I have garnered the most information in terms of social capital. I have learnt that you need to find and make the connections that will not only help you stand out but will also help you push your science far! I’ve always thought, particularly when listening to talks on getting mentorship, that this was some kind of elusive advice that would never be applicable, however, I have been proven wrong. Not only is it paramount for guidance, but it also is necessary for advancement. I am definitely excited about some of the connections I’ve made and look forward to pursuing them.

Last word, shout out to whoever the awesome scientists are that sponsored the turnt up social that happened at Reggies last night! I don’t think I’ve been at such an awesome dance party since I was… maybe 23… and believe me, 23 was a few years ago!

I have recovered and ready to finish SfN with a bang! Whooohoooo day #4  – let’s do this!

P.S., if you’ll still be here tomorrow afternoon, come check out my poster – R7, Wednesday afternoon session 1-5 p.m.


SfN Day #2 – the A.M.


I didn’t get to do much poster observations this morning. I did however spend sometime at the diversity mentoring breakfast and listened to an awesome talk from Eve Marder, Ph.D. The one thing I took away from the talk was the importance of being  true to yourself especially when it comes to your topic of interest. With the field constantly changing, there is often a consensus on what the hottest topics of interest are. Some scientists may thrive of the energy that comes with a well-packed niche, however that may not necessarily work for everyone. She stressed the importance of knowing your topic, loving it and going after it. Researching what you love will never lead you to a juncture in which you are unsure of the next step to take. Also, the three word sentence to always remember was: Never. Stop. Working.

It was uplighting and encouraging, especially as I hold it in light of my future career plans and the trajectory that I would like to take.

I plan to look at a bunch of posters this afternoon and report back with a detailed synopsis of my favorite, similar to the last post.

Hold tight and don’t forget to drink your water.

P.S. the lines at the McCormick place Starbucks are unforgivable.

What had happened was… SfN poster delight Day 1!


I definitely had a delightful session this afternoon. Lots of noteworthy posters. I stopped at a couple, however, I will discuss my absolute favorite poster of the day.

Poster #1: Kv1.3 mediates cholinergic hyperexcitability in a mouse model of Parkinson’s disease

1Ifibio-Houssay-Conicet-University of Buenos Aires, Capital Federal, Argentina; 2Ininfa-Conicet-University of Buenos Aires, Capital Federal, Argentina; 3Departament of Physiology-School of Medicin-University of Buenos Aires, Capital Federal, Argentina

Cholinergic neurons which are known to exhibit a pause in response to dopamine neuron bursts in a reward context, lose their ability to pause in Parkinson’s disease. This pause is reflected as a slow AHP (after-hyperpolarization) that is not well understood in these neurons. During sustained firing in response to current injections, cholinergic neurons typically fire in response to depolarizing inputs, and are able to sustain their firing, without showing any accommodation… however, this is only in Juvenile mice. In adults, this is lost (they show accommodation). Interestingly, however, adult Parkinsonian mice (6 hydroxydopamine lesioned) show this same absence of accommodation as in normal juvenile mice. So the question then emerges, what ionic current mediates this difference in accommodation and how is that related to the pause that is often seen in cholinergic neurons in response to dopamine neuron bursts?

They used invitro electrophysiology in juvenile control and 6-OHDA lesioned mice to investigate the difference in the accommodation phenomenon.

First, they observed a larger ratio of non-accommodating cholinergic neurons in the juvenile mice, showing a developmental down regulation, compared to adult mice. They then pharmacologically attempted to isolate the ionic current that contributed to the accommodation. They tested frequency-intensity curves in the presence of Margotoxin ( MgTx – a Kv1.3 channel blocker) and alpha-Dendrotoxin (DTX – a Kv1.1, Kv1.2 and Kv1.6 channel blocker) and both significantly led to an increase in the firing rates of the neurons, and elimination of accommodation. They had suspected that Kv7 contributed to the accommodation, however that was not the case.

Next, they examined the currents underlying the differences in excitability by examining the ramp currents, and observed a nice reduction in the overall currents in response to to MgTX which correlated nicely with the timing of the last spike within the same neuron (the timing is a measure of the accommodation). Due to the promiscuous nature of DTX blocking two Kv currents, they carried out laser capture micro dissection (LCM) that allowed them to isolate specific cells and subsequently run a RT-PCR to examine the presence of the Kv channels… turns out only Kv1.1 and Kv1.3 are present in the cholinergic neurons.

So at this point, not only have they established that there is an accommodating phenotype that is present in adult cholinergic neurons, absent in Juvenile and Parkinsonian cholinergic neurons, but they show that Kv1.1 and Kv1.3 currents mediate that accommodation. The question that remains is this – is there a change in the Kv1.1 and Kv1.3 currents in the Parkinsonian Cholinergic neurons? They examined 6-OHDA mice and as opposed the control, there is a larger degree of non-accommodating cholinergic neurons, similar to what was observed among the Juvenile control cholinergic neurons. And – yes, you guessed it! There was a down-regulation of the Kv1.3 currents (MgTX3 sstv currents) in the 6-OHDA cholinergic neurons present in these neurons (6-OHDA – Cholinergic).

Lastly, they examined the “pause” that results in the cholingeric neurons in response to the dopamine neuron burst, by examining the slow AHP. What they find is that the MgTX sstv current, Kv1.3 current, does mediate the slow AHP.

In essence, what they observe is a neat mechanistic adjustment that occurs in the cholinergic neurons as a result of dopaminergic loss during Parkinson’s – the down regulation of Kv1.3 currents that would strongly silence the cholinergic neurons in response to dopamine neurons bursts had it still been present.

I thoroughly enjoyed this poster, mostly because it is right up my alley of ion channels being involved in disease mechanism. I would be interested in knowing at what stage this change occurs as the disease progresses, is this a homeostatic change due to the loss of the dopamine neurons, and what functional circuit reorganization occurs as a result of the change where the ability for the cholinergic neurons to pause is lost.

I also had other posters I really enjoyed, however, I am going to give a shout-out instead of a summary:

Univ. of Virginia, Charlottesville, VA

1Pharmacol. and Toxicology, Univ. of Texas Med. Br., Galveston, TX; 2Inst. of Human Physiology, Med. School, Univ. Cattolica, Rome, Italy

1Neurosci. Ctr., 2Dept. of Cell Biol. and Anat., 3Dept. of Cell Biol. and Anatomy, Neurosci. Ctr., 4Neurosci. Center, Dept. of Cell Biol. and Anat., Louisiana State Univ. Hlth. Sci. Ctr., New Orleans, LA

Getting through your First day of #SfN15 (A Random encouragement of sorts!)

  1. Do get caffeinated – keep it steady, no need crashing towards the end of the day… you still have the presidential lecture to attend and the socials of course.
  2. Do make your itinerary before stepping into Hall A …
  3. Do stay wear comfortable shoes and stay hydrated.
  4. Do network and be friendly – you never know who knows who.
  5. Do take sitting breaks.
  6. Do have a few posters that you plan to have in-depth conversations with the presenter.
  7. Do activate your dopamine neurons by rewarding yourself with some swigs of libations at the day.

You’ve been fore-armed.

Enjoy and come back later today for my take on the awesome posters I’ve observed 🙂

SfN 2015!

I will be blogging about this year’s Neuroscience meeting happening in Chicago from Oct 17-22. Stay tuned for updates! I will be posting on interesting posters related to Themes B and C – Neural Excitability and Disorders of the Nervous System. Prepare to have your synapses potentiated 🙂

Chicago here I come!!!

Okay, back to getting my poster ready!

Favorite Poster of Neuroscience 13 Day 2

In keeping in line with the neurons closest to my heart’s delight, my favorite poster of Day 2 was on substantia nigra compacta dopamine neurons, and on a role that K-ATP channels may play in these neurons.

Poster E8 – ATP-sensitive potassium (K-ATP) channels are coupled to voltage-gated calcium channels in dopamine substantia nigra neurons – Sylvie Kutterer / Jochen Roeper

This group had previously published a few papers on the role that K-ATP channels play in dopamine neurons. They had first shown that K-ATP channels were differentially expressed in dopamine neurons and could underlie the degeneration of dopamine neurons in Parkinson’s disease. These ion channels were initially found to be present in pancreatic beta cells, they open in response to mitochondrial complex I inhibition, an increase in oxidative stress (ROS) and depletion of ATP. Lastly, in a 2012 paper, this same group has shown that these channels mediate dopamine neuron bursting and exploratory behavior in mice.

This poster seemed to be a continuation of the K-ATP story, but more specifically to the last point in attempting to understand what ion channels mediate burst firing in dopamine neurons. The author started by verifying the presence of K-ATP currents using perforated patch clamp electrophysiology. These single channel openings could not be observed in the K-ATP full knockout mice or in the presence of glibenclamide – an established antidibetic drug that belongs to the class of sulfonyureas, which blocks K-ATP channels by binding to SUR1 which forms part of the K-ATP channel complex. Additionally, they used NN414 and Tolbutamide which are specific K-ATP channel blockers and agonists respectively to block and enhance the K-ATP channels and observe the effect on the cell’s firing. In the absence of K-ATP, there is an increase in cell firing frequency and precision, showing their involvement in firing regulation. They next examined if the K-ATP channels were electrically coupled with other voltage-gated ion channels, as it is well established that other ion channels are involved in the precision and frequency of the cell’s firing. In the presence of apamin and TTX, there was little to no enhancement in the open probability of the K-ATP channels. However, in the presence of the L-type calcium channel blocker – isipiridine, they observed a decrease in the K-ATP open channel probability. The same was observed with the T-type channel blocker – NNC 55-0396. Finally, an enhancement of L-type channel activity with Bay-K 8644 resulted in an increase in the K-ATP channel open probability.

Thus, the major conclusion from this body of work is the coupling of the voltage-gated calcium ion channels to the K-ATP channels. In the pathologic state, one can imagine that in response to oxidative stress, the K-ATP channels would have an increase in their open channel probability… which would subsequently affect firing, resulting in the cell bursting more frequently which is linked to the T-type calcium channels which mediate burst firing and L-type calcium channels.

While I look forward to the completion of this story, as it does seem to go in hand with other literature that implicate the susceptibility of these neurons to death in Parkinson’s due to calcium influx, I did have a couple of questions. The synergistic role of the K-ATP channels with the calcium channels seem to contradict the mechanism of action of glibenclamide on these channels – their block results in an influx of calcium and subsequent release of insulin. However, while one can argue that there could simply be synergistic coupling with the L- and T-type calcium channels and negative coupling with the N-type calcium channels, I would have liked to see the response of the K-ATP channels in the presence of omega-conotoxin. Lastly, I was not sure about the specificity of the T-type channel blocker, as this was my first time coming across this blocker. I would have liked to see the experiment repeated in more popularly known T-type channel blockers. It was also interesting that these channels were indirectly shown to mediate firing in these neurons, as L-type calcium channels are believed to be the main mediators of firing. Another source of evidence especially via either single cell RT-PCR or direct single channel recordings will add more robustness to this last claim.

Favorite Neuroscience13 poster of the Day 1

Dopamine neurons of the substantia nigra, notorious for degenerating in Parkinson’s disease, are constantly on the hot bench of basic studies. Aside from their marked death in the aforementioned disease, they are implicated in reward and motivation. As with all diseases, and the main focus of neuroscience – understanding the underlying mechanism of function of the nervous system, the challenge is to get at the underpinnings in the healthy system which may offer clues as to what might be occurring in the diseased state. Along those lines, understanding the developing brain and how the excitability of single neurons change over time may lead us to pinpoint critical stages for disease intervention. This was the subject of the following poster I enjoyed today –

“Electrophysiological and molecular development of rat substantia nigra compacta dopaminergic neurons” – Author Block: *M. DUFOUR1, A. WOODHOUSE2, J. AMENDOLA3, J.-M. GOAILLARD3; 1INSERM, Marseille, France; 2Univ. of Tasmania, Hobart, Australia; 3INSERM UMR1072, Marseille, France.

In examining the basic electrophysiological properties of the compacta dopamine neurons, they found that the P2 dopamine neurons fired with burst like activity and exhibited a pronounced AHP. This firing mode changed in as little as 3 days, with the firing regularity increasing significantly by P5 and by above P12 or so, the neurons exhibited regular pacemaking activity which is a firing characteristic of these neurons. The coefficient of variation of the interspike interval was also markedly reduced over time as the rats advanced in age.
Along the lines the change in their electrical properties, they also observed an decrease in the input resistance (which was in the thousands of megaOhms at P2!) and the extent of spike adaptation (consistent with a shift in their burst-like pattern of firing to a tonic firing pattern).
The same pattern of change was also observed with the sag amplitude in response to hyperpolarization (indicative of H-current). They saw an increase in sag amplitude as the rats got older.
Finally, taking 8 different electrophysiological membrane properties – interspike interval, input resistance, AHP amplitude amongst others, they performed both an augmentive and PCA clustering analysis to determine the classification that would emerge from all the neurons recorded regardless of age. True to their experimental observations, three classes emerged – P0-P2/3, P5-7 and older which displayed distinct firing patterns.

I appreciated the work they did, especially as there are few papers out there that attempt to chronicle the change in the electrophysiological properties of compacta dopamine neurons. It also raises a valid concern on the age of rodents being routinely used for electrophysiological slice recordings especially when these questions have nothing to do with development. Additionally, the change in distinct electrophysiological hallmark features of the dopamine neurons over time raise the obvious question of the complement of ion channels in these neurons as they age, and their key modulators. Are these same ion channels that develop with time also affected in parkinson’s? What key modulators control the complement of ion channels that shape their changing excitability over time? Could these modulators that affect their development also be used later in life to enhance neighboring compacta neurons and probably enhance neuroprotection to prevent their future neurodegeneration (that is in the event of of early disease onset)?

More to come from @noviceneuroscientist in Sunny San Diego #neuroscience13 #sfn13

#SfN12: Day 1 through the spectacles of a seasoned Novice Neuroscientist – Favorite Poster of the day.

***Disclaimer: None of the science here is mine and credit is given where due. These summaries are my understanding of what I listened to.

I made dense plans yesterday – visit all the posters in my sub-theme of interest: Basal Ganglia physiology, attend the Presidential lecture and a networking session. I would say that I thought having a more organized itinerary compared to last year would leave me less exhausted. I couldn’t have been more wrong. I was not overwhelmed which was a big progress from last year, however, after almost 2.5 hours of talking science and listening to science, I think I had reached my standing-absorption ceiling (your limit to absorb new material while standing – yes, I just invented a term and gave it a definition).  Overall, I would say it was a great first day – brilliant science, motivated scientists and schmoozing networkers. I loved it.

My favorite poster of the day had to be:

Excitatory input onto midbrain dopaminergic neurons: nucleus-specific influence on long-term synaptic change.

J.L. Bland, C.A. Paladini; Department of Biology, UTSA, San Antonio, Texas, U.S.A.

The author investigated the influence of excitatory inputs on the dopaminergic neurons of the substantia nigra compacta by using both traditional electrical stimulation and optogenetic stimulation. The two major nuclei that give excitatory inputs into the Compacta are the subthalamic nucleus (STN) and the Pedunclopontine nucleus (PPN). Being that they both provide excitatory input, it is expected that their stimulation would elicit burst firing either individually or together. Interestingly, she found that using either of the methods, stimulation either via the STN or PPN alone, did not elicit burst firing in the compacta neurons, but dual stimulation did. Using an LTP protocol, she found that the AMPA currents from the PPN were consistently low compared to the NMDA currents, which was not the case in the STN. There were large AMPA currents (calcium-permeable) from the stimulation of the STN, and these were GluR2 lacking. She proved this by the use of a blocker and a voltage step I-V curve that showed an inward rectification of the current. In addition to that, synaptic facilitation was observed from the STN, whereas depression was observed from the PPN. From this work so far, she has shown that despite the co-stimulation of these two structures causing burst firing in the compacta neurons, there are different mechanisms that underlie their of action.

In sum, I saw this work through the lenses of “different means lead to the same end”. On the one hand, while stimulation of either set of afferents doesn’t led to bursting in the compacta, co-stimulation does. One would think that they would use the same mechanistic method to elicit the end result. The novelty of her work is that this isn’t the case.

It was my favorite because I had to give her props for the finding, not only is it novel and unexpected, but it involves the PPN, a structure with which there is a slight relative deficit in knowledge of it’s excitability properties compared to say the compacta and reticulata neurons of the substantia nigra. In addition to that, in my opinion, I think that the large influx of calcium into the compacta that occurs via the STN sheds more light on the possible routes of mechanistic failure that can occur leading up to the death of compacta neurons in Parkinson’s disease. A large influx of calcium is believed to be the culprit in this case. While L-type gated calcium channels are implicated in the just mentioned case, it is possible other sources of calcium could contribute just as well.

Overall, I definitely got some synapses potentiated. Great presentation skills from the author too!

And now I am off to schmooze some more with fellow neuroscientists and attend the best mini-symposium ever –  🙂

Come back later for Day 2’s favorite of the day!

Navigating your way through Neuroscience 2012

After almost a year of much deafening silence on this blog, I thought to myself, what better way of bringing sound back than channeling neuroscience 2012 on here? And hence, this piece!

This is my second year in attendance and as a “veteran” (meant to be sarcastic), looking back I thought I would write down some helpful tips on navigating the conference. In my imaginary world, I would like to think someone out there in the globe who is headed to Neuroscience for the first time, would stumble upon this on the world wide web and use it as their treasure map (let me dream!)

  1. Attend the Presidential lectures. Doesn’t matter if it’s your subject area or not, just attend these talks. It gives you a broad spectrum across the field especially if you are a newly minted freshie in the field. I made the mistake of not attending a single one last year, followed by being stupefied that there were a bunch of lectures I was ignorant about… And not to mention being bewildered as my cohort mates had conversations amongst themselves about the “facts and new questions” they learnt. I felt left out, which was my fault – improper planning on my part. Thankfully, I have this year to redeem myself!
  2. Don’t wait till the last minute to make an itinerary. Maybe you are just planning yours now, that’s okay. Don’t stand in the halls of the convention center to make one – too confusing and overwhelming. Trust me, I’ve tried it. Some very convenient links this year: Neuroscience 2012 Oasis Planner, Hubbian and of course, the-life-saving-and-can’t-do-without-uber-convenient Neuroscience 2012 app (We can now truly say there really is an app for everything with the arrival of this one :D) And of course, if you still love the feel of processed trees through your fingers, there are daily program books to be picked up everyday in the convention center… usually at the entrance.
  3. Pick a sub-theme or two of poster sessions and follow them throughout. Please, please and please, don’t attempt to follow a whole theme or even think of wandering through Hall F-J and think you can just shotgun your way to posters. You end up drained and sad and sitting on the floor staring at people with a dazed wonder in your eyes. I was that person last year 😦
  4. Pick out some networking events to attend. You may attend your institution’s or sneak into another’s and feign to be an interested graduate school applicant or even an postdoc looking for a job (not that I imposed as any of these by the way). The point is that you may or may not know anyone there, however, the key goal should be met – network, network and network. Alcohol and neuroscience have a way of making dense connectomes that span the widespread waters of the globe. With that said, put yourself out there.
  5. Enjoy the city. Grab a few new scientist friends and explore the streets you might not get to revisit. Walk the streets of New Orleans with thousands of fellow brainpower enthusiasts. Enjoy the plethora of jumbled overheard words most frequently seen and heard of in your sleep and in class and in lab (don’t deny that you’ve dreamt of your Purves and Kandel textbooks – I know you have).
  6. Above all, enjoy the science. Ask, question and be ignited. After all, the unifying theme that has brought us to New Orleans is our deep and insatiable curiosity on the marvelous workings of the beloved nervous system (and to self-promote our science too of course!)

More to follow from the desk of the budding novice neuroscientist.

Have yourself a wonderful day of synaptic potentiation!!!

I will return with summaries of events I attended, and pictures of the city of course.

Neurodenegenerative disorders… Ion Channels… or both?


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Interestingly, I never got to update on the Neuroscience 2011 posters that caught my attention. A combination of the lack of energy from my return, and having  my comprehensive exams come up were the penultimate time takers. Speaking of comprehensive exams – utterly brutal process that makes you sick to the stomach and conjure the evilest of imaginations of failure. Whoever invented that knew it would be an effective torturous ‘welcome to graduate school’ gift. Needless to say, I survived. I passed provisionally – I have to rewrite two questions, one from each of my exams. At the end of the day, I realized that psychology played a big part in how my cohort mates and I prepared for this exam. We were so gripped with trepidation that we learnt needless details – who needs to know the names of the three middle ear ossicles for a systems neuroscience exam? In the grand scheme of things, it should be about the medial geniculate nucleus and upwards in the auditory pathway. Remind me of that in my reincarnated life. Trailing off from that, I wonder if I will still be a graduate student in a reincarnated life. Regardless of if you think it possible or not, would you take the same path you have been through/are on if you had a second chance? Anyways, I digress. Comprehensive Exams. Right. That. Is. Over. With. Thank God.

Moving on. Back to #sfn11.

Apart from the occasional confusion at how enormous SFN was, and my continual overworked body during the whole conference, I thoroughly enjoyed it. Lovely parties I tell you. And even more, great science. And a grand epiphany!

I met with two P.Is in D.C. They are both stationed at the government lab location where I will be moving to upon the completion of my classes in May. Here is the catch: they both work in the area of biophysics of ion channels! If you’ll recall my first lab rotation, I’d written about how I rotated in a lab that focused on parkinson’s. And although I am yet to elaborate on this blog, I have an interest in neurodegenerative diseases that led to my whole spill in my personal statement to graduate schools on why I want to study neuroscience. However I am learning slowly that indeed it is of the utmost importance to truly keep an open mind upon entering graduate school. I came in thinking I was dead-set on studying either parkinson’s, alzheimer’s or huntington’s. And of a truth, it isn’t because I have a background of laboratory research in those areas. Maybe it ties down to my pre-med nature want to be close to the area of diseases (oh, I used to be a pre-med, yup, I’m one of those – I should really write my undergraduate life story on here shouldn’t I?). Time and time again during graduate school interviews I was told by many faculty to keep an open mind as my interests could and would change. And I’ve been told by older graduate students, no one is going to check my personal statement and ask why I’m not in a neurodegenerative lab. To compound to my somewhat dilemma, my molecular Neuroscience class, the paper I presented in that class and the lab I’m currently rotating in have violently swayed my interests toward ion channels and electrophysiology.

So back to my epiphany. At SFN, I found myself galavanting between posters on neurodegenerative disorders and ion channels and they both fascinated me… An outside observer would then say: “Why not just work in a lab that interfaces the two?” I am not widely read in both fields and only know of the implication of a possible role of calcium ion channels in parkinson’s. I relayed to both P.Is my personal statements and my intention to interface molecular techniques and electrophysiology. For the purposes of onward conversations let us call each of the P.Is: P.I.#1 and P.I.#2. I instantly liked P.I.#1, I felt very comfortable with him. He is a brand new faculty, just setting up his lab, energetic and willing to take on a graduate student. He is interested in the modulation of ion channels and will be willing to take me on to rotate. I thought: “Awesome!” But then he asked if I was interested in biophysics. And I cringed? What does that really mean? It created worry in me. And I felt confused and not sure that I would find a project that I am wholly passionate and devoted to if I venture into studying ion channels. I can’t imagine working on a project for the next four odd something years if i’m not passionately inlove with it (not to sound like a zealot, but I’m sure you know what I mean). I therefore left feeling impressed with him, and comfortable, however a bit intimidated as to how a project would go (mentally), although he was encouraging in that I could easily learn the techniques etc. P.I.#2, I liked as well, although I can’t say I liked him as much as P.I.#1. He is up for tenure. He is more seasoned, a smallish lab and has graduated a graduate student. And he talked about how his lab is transitioning into projects that would involve recordings from ion channels in alzheimer’s mice models  … That excited me – it seems like the perfect interface between my two interests… but then comes another confounder – what if I rotate, and end up being more comfortable in P.I.#1’s lab and like P.I.#2’s projects better? I’ve been told by all to pick environment over project – always? What do you think dear reader?

In a nutshell, that is a summary of my epiphany – that I want to have a thesis project where I can study ion channels in a neurodegenerative disease… I can’t seem to think of something else that excites me more. And I’ve prepared myself that worst case scenario, I can do an ion channel project for my thesis and work in a neurodegenerative disorder lab for a postdoc, that is a fad these days anyhow – people hardly stay in the same field for both Ph.D and postdoc, in neuroscience as I know of. I will conclusively know whose lab environment I will like better and whose lab projects would be worth losing sleep over in my mind of course.

In other news, Happy Holidays: Merry Christmas, Happy Hannukah, Happy Sallah etc in arrears and Happy New Year in advance. I will be enjoying the next few days as I prepare for a month of neuroanatomy and right after spring semester classes 😐

And keep an eye out on this space for reviews of scientific articles, soon to be posted!

And by way of a shamless plug, don’t be shy to show the novice a wave of hand by following me on twitter: @noviceneurosci. Much appreciated!