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Writing blogs on mobile devices, yay or nay?
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Sex differences in memory after stress exposure
Its well know that chronic stress impairs declarative memory, whereas acute stress brings improvement. Chronic Unpredictable Stress Battery (chronic stress), Predator Scent Stress (acute stress), and control group were evaluated in male and female rats. The results showed that males and females sense the stress differentially. Whereas chronic stress affects more intense in females acute stress disrupts more in males.
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Why theory matters?
In the first post on this blog, I want to discuss my motivations for writing about Theory in Neuroscience. My honest motivation is so that I can learn more about the role of theory in neuroscience (the best way to learn is by doing?). But why should I or we care?
We should care because, collectively, we all want to understand the brain. By understanding, what I am referring to is be able to describe mechanisms for the function or phenomenon of interest. This would require that the multiple datapoints pertaining to the system can eventually build a cohesive and consistent picture. For me, this naturally invokes the need to have a “theoretical” model in mind, which would enable explicitly stating the assumptions built into our understanding, and to identify the relevant variables. This model built from available data can guide us into the unknown, helping us define the gaps and how they can be addressed most effectively.
In addition, there are a few external factors that suggest that this exploration would be a learning exercise worth carrying out. One of them is the series of interviews of theorists and experimentalists conducted at COSYNE 16 which confirms that the theory-experiment interplay is yet to be properly understood and developed. The interview participants agree that this interplay is fundamentally necessary to building a useful scientific understanding of the brain. Another is several articles in recent years suggesting the need to think about theoretical motivations of our experiments (whether at the circuit level, or at the level of behaviour), so that we can make sense of all the data we are collecting in neuroscience. I am fairly new in the field to fully grasp how big the big data explosion is, still, these articles feel cautionary. From what I hear, they reflect a sentiment that is certainly not new, but perhaps far more relevant now with our access to a multitude of new and fancy tools to map and dissect and reconstruct nervous systems.
Another factor that has been pointed out in the Theory Matter series mentioned above, and in an excellent perspective piece on the role of theory in neuroscience by Larry Abbott is that gathering every possible datapoint may not be as helpful in building understanding. Both of these highlight the idea that the map is not the territory, and thus establishing generalizable rules and models require a theoretical, model-driven approach. To determine what matters, and what doesn’t matter is almost more important than characterizing systems fully. This sentiment seems to echo from students of neuroscience even at very early stages of their careers. I was at an undergraduate student breakfast recently, and one of the students asked the visiting speaker – “how do we know what do we need to know”? The number of unknowns seem so high, and it’s not clear what manipulations are necessary and sufficient. And I find this line of thinking exciting, and something we don’t spend too much time pondering on in our daily research lives.
To end for now, I will list here a few questions and thoughts that I gathered from the COSYNE series that highlight the broad questions on this topic. Beyond that, though, my core interest in the topic is to understand the process adopted by scientists who work at this interface (or students who want to). How do theorist-experimentalist collaborations begin and foster? And how do young scientists (students) learn to think and work at this interface from the get-go?
Notes from Theory Matters at COSYNE 16 (videos available here)
- What is the role of theory in neuroscience?
- What kinds of theories would benefit from experimentation?
- Did theory have an impact on neuroscience?
- Why do we need to promote theory in neuroscience?
- What computational tools made a significant impact in neuroscience?
- What do we need to (do) bring theorists and experimentalists together?
- How is it like to be in an experimental lab and theory lab at the same time? (Be willing to ask dumb questions)
- Did theories help your experiments?
- There is a strong need for models and theories to capture the heterogeneity of cell-types and neural responses (Anne Churchland)
- In terms of an experimentalist who moved into theory it’s trying to understand the basic phenomenon, the underlying principle of the experimental question of interest (Bradley Voytek)
- Experiments can establish “necessary” conditions for phenomenon, but experimental neuroscience cannot, but theory can, establish “sufficient” conditions. Together, these can work out the necessary and sufficient conditions, which is exactly what we want to understand to understand how nature works. (Eugene Izhikevich)
- We rely on theory mostly to explain our data and characterize it better, but we really want theory to do is to make predictions to drive experiments (Benjamin Scholl)
One of the interviewees said that for experimentalists and theorists working together, they should “be willing to ask dumb questions” – I hope to do exactly that to people who work at this interface.
(Here’s a link to an open access version for the blog post if you’d like to share with anyone in the wider community - https://www.evernote.com/l/AT6Jm_3v26lG45BNcJ97qAHg1kcvlo58Hw4/)
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What Advice Do You Have For Dissertation Writing?
I’ve done it! I have finally written the first few sentences of my dissertation! I started this blog a year ago thinking I would be done by now. But I have finally started writing. I have a few paragraphs out of order written. They probably will be edited ten times over, but for now, I have words on a page. Hooray!
With that being said, does anyone out there have advice on writing a dissertation? What kind of things did you wish you knew before you started? A preference for EndNote or Mendeley or another program? Great advice someone else gave you? I’m all ears.
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The next "misnomer" about spinal neurons
It costed me an entire case of Stella Artois…
…I was sure I had this bet when I opened my mouth and set the bet, afterall I consider myself a spinal cord physiologist…
The bet was on the question, whether there has been any published evidence on the cholinergic neurons with somas near the central canal to be sending axons out of the cord into the sympathetic chain ganglia. In other words, is there evidence that these cholinergic neurons - that are not located in the intermedio-lateral cell column, are in fact sympathetic neurons.
I knew they were hypothesized to be part of sympathetic nerveous system, but the fact that they have exiting axons much like the classical IML cells - was something I did not see evidence for (until a student brought it to me, with my sincere thanks…)
From now on, I will have to tone down my statements that I often make about sympathetic neurons to students during the Autonomic lectures - as I often would way - all of those neurons are in the lateral cell columns - which is not entirely true… thanks to good, thorough anatomist (from AU, I believe). - 3
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(Replace this first paragraph with a brief description of your new category. This guidance will appear in the category selection area, so try to keep it below 200 characters.)
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(Selection below from A McRae, GK. Davis, N Baboolal and JA. Morren (2008). Alzheimer’s Disease in the Middle-Aged. Chapter 12 Biomarkers in Alzheimer’s Disease . Editors: Hyun Sil Jeong. ISBN: 978-1-60456-480-8).
One of the earliest documented views of the immune function of microglia was that of Franz Nissl in 1899 (1) who used the term stabchenzellen or rod cells to describe microglia. He emphasized that rod cells appeared to be reactive glia cells and that their major attributes were that of migration, phagocytosis and proliferation. Nissl stated,
“It is highly likely that glia cells in addition to producing an intercellular substance have a second task which is approximately the same as the one leukocytes have in other tissues”
Interestingly microglia has been a cardinal feature of the hallmark lesions of AD pathology ever since its initial descriptions by Alois Alzheimer in 1906 (2). The formation of a microglia coffin around cortical pyramidal neurons was probably one of the first observations (3). Though about eighty years too early it was Oskar Fischer (4,5) who noted that plaque formation was an extra-cellular event, which provoked inflammation followed by regeneration. Morphological tools at the time did not allow him to observe an immune response around the plaques and he was also unable to observe complement.
Thus from the very beginning of the description of AD pathology microglia as well as astrocytes have been considered to participate in hallmark lesions in particular plaque formation (3, 6-8). It was even hypothesized that the formation of primitive plaques began around a central microglia cell (9).
While microglia was morphologically recognized in association with plaques one of the longest running debates in the history of neuroscience was ongoing about the origin of the ramified microglia or the form, which resides in the brain. Based on beliefs four schools of thought were formed concerning the derivation of microglia: i) invasion of mesodermal pial elements, ii) neuroectodermal matrix cells together with the macroglia, iii) from pericytes and iv) invasion of monocytes in early development. (for review see 10) How did this debate actually begin?
Rio Hortega (11) was the first to demonstrate ramified microglia. He was persuaded that these cells originated from the invasion of mesodermal pial elements. He postulated that pial elements invade the brain tissue to become the globose (rounded and amoeboid microgliocytes (young microglia) and subsequently develop into ramified microglia. He described the migratory and phagocytic properties of microglia (12). His method to reveal microglia, a sliver stain almost abolished the concept of a ramified microglia. However Mori and Leblond (13) adapted a weaker staining procedure, which allowed an electron microscopic analysis of ramified microglia in the brain. The accepted concept about the origin of ramified microglia that being from monocytes was proposed by Santha and Jiba (14). They noted that the arrival of ramified microglia coincided with the vascularization of the brain and considered that ramified microglia was derived from the circulating monocytes. Elegant studies conducted by Ling and his co-workers (15,16) established that ramified microglia are true entities of the brain.
It is be noted that amoeboid microglia in early postnatal development are reactive macrophages phagocytosing degenerating cells and processes (for review see 10). With the closure of the blood brain barrier these cells gradually take on a ramified shape or enter into a resting mode. In response to neuronal damage these cells change their morphology, immunophenotype and proliferate to become activated microglia or full-blown brain macrophages
The injection of carbon particles into the periphery in 5- day old postnatal rats revealed that amoeboid microglia were derived from circulating monocytes (15,16). During early postnatal development these amoeboid microglia are active or proliferate. In this respect one would expect that the number of amoeboid microglia would increase in the brain. However surprisingly there is a constant decrease in these cells and eventually by postnatal day 15 they disappeared. About thirty percent of amoeboid microglia transform into ramified microglia (15). The carbon labeling studies identified that both amoeboid microglia and ramified ones were laden with carbon. Thus this added significant support for a monocyte origin for ramified microglia (15,16). The transformation of amoeboid microglial cells into ramified microglia results from a regressive phenomenon (17).
With the origin of the ramified microglia fairly well established the next stages in the history of microglia saw it evolve from a scavenger cell to the immune cell. With the advent of immunocytochemistry and antibodies it was possible to reveal the immunophenotype of microglia (18-22). Even more important was the ability to associate antigen expression with morphological change. As the result of an injury immediate microglia morphological changes occur (18-22). In the first instant slender microglia processes begin look swollen. About a week later microglia begin to withdraw their process and take on a more rounded or activated form. By the time they are full blown macrophages the cells are rounded with no processes. Each of different stage of morphological changes is denoted by the expression of different antigens. In first proliferating stages microglia express complement- 3 (CR3) receptors in the next stages there is enhanced expression of major histocompatibilty complex (MHC) antigens with MHC I expressed by activated microglia and MHC II by the full-blown macrophages (18-22). The expression of these antigens conferred antigen- presenting capacity to microglia. Thus, by the late 1980s microglia had moved up the ranks as the accepted immune cell of the brain (18).
The long journey, which witnessed the progression of microglia from a scavenger cell to that of the immune cell of the brain was completed. Microglia was now to embark on another journey, which would place them as early participants in a cascade of events leading to the pathogenesis of AD. Interesting features in this cascade are the combination of innate immune responses and chronic inflammation.- Nissl, F., Ueber einige Beziehungen zwischen Nervenzellenerkrankungen und gliosen Erscheinungen bei verschiedenen Psychosen, Arch. Psychiatry, 1899 32 1-21.
- Alzheimer, A. “Uber eine eigenartige Erkrankung der Hirnrinde.”. Allg. Z. Psychiat. Psych.-Gerichtl. Med 1907. 64 (1-2): 146–148.
- Alzheimer A. Uber Eigenartige Krankheitsfalle des spateren Alters. Zeitschr f d Ges Neurol Psychiatr 1911 ;4: 356–485.
- Fischer O (1907) Miliare Nekrosen mit drusigen Wucherungen der Neurofibrillen, eine regelm€aassige Ver€aanderung der Hirnrinde bei seni- ler Demenz. Monatsch Psychiat u Neurol 1907 22: 361–372
- Fischer O (1910) Die presbyophrene Demenz, deren anatomische Grundlage und klinische Abgrenzung. Z Ges Neurol u Psychiat 1910 3: 371–471
- Simchowicz T Histologische student uber die senile demenz Histol Histopathol Arb 1911 4 267-444
- Wisniewski HN and Terry AD Reexamination of the pathogenesis of the senile plaque Prog Neuropathology 1973 2 1-26
- Kozlowski, P., Wisniewski, R.M., Moretz, R.C. and Lossinsky, A.S., Evidence of induction of localized amyloid deposits in neuritic plaques by an infectious agent, Ann. Neurol., 1981 10 517-523.
- Probst A Brunnschweiler H Lautenschlager C Ulrich J A special type of senile plaque possibly an initial stage Acta Neuropathol 198774 133-141
- Ling, E.A. and Wong, WC. The origin and nature of ramified and ameoboid microglia: A historical review and current concepts. Glia 1993 7: 9-18.
- Rio-Hortega, P. del. (1932) Microglia. In: Cytology and Cellular Pathologv of the Nervous System, Vol. 2. Penfield, W (ed) Paul B. Hoeber, New York, pp. 481-584.
- Rio-Hortega P. del and Penfield, W ( Cerebral cicatrix: the reaction of neuroglial and microglia to brain wounds. Johns Hopkins Hosp. Bull. 1927 41: 278-313.
- Mori S and Leblond CP Identification of microglia in light and electron microscopy J Comp Neurology 135 57-80 1969
- Santha K and Juba A Arch Psychiat Nervenkr 1933 98: 598-613
- Ling EA Transformation of monocytes into amoeboid microglia in the corpus callosum of postnatal rats as shown by labeling monocytes with carbon particles J Anat 1979 128 847-858
- Ling, E.A., Penney, D. and Leblond, C.P. Use of carbon labeling to demonstrate the role of blood monocytes as the precursors of the ameboid cells" in the corpus callosum of postnatal rats. J.Comp Neurol 1980 193:631~57.
- Kaur C , Ling EA and Wong WC Transformation of amoeboid microglial cells into microglia in the corpus callosum of the postnatal rat brain An electron microscopic study Arch Histol Jpn 1985 48 17-25
- Guilian, D., Ameboid microglia as effectors of inflammation in the central nervous system, J. Neurosci. Res., 18 (1987) 155-171.
- Streit, W.J., Graeber, M.B. and Kreutzbcrg, G. W. Functional plasticity of microglia: A review. Glia 1988 I: 301-307.
- Ling, E.A., Kaur, C., Vide, T. and Wong, WC. Immunocytochemical loca1izationof CR3 complement receptors with OX 42 in amoeboid microglia in postnatal rats. Anat. Embryol. 1990 182: 481-486.
- Ling, E.A., Kaur, C. and Wong, WC. Expression of major histocompatibility complex antigens and CR3 complement receptors in activated microglia following an injection of ricin into the sciatic nerve in rats. Histol. Histopathol. 1992 7: 93-100.
- Streit WJ, Walter SA, Pennell NA Reactive microgliosis Progressive in Neurobiology 1999 57 563-581
Blog 3 will look at the role of microglia in the pathophysiology of neurodegenerative disorders in particular Alzheimer’s disease
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New research from London!
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Trained to quit?
It’s a long time since I thought of sharing my views on post PhD careers in Academia. I am sure my view is a little different from what we have been listening to for most of the time on non-academic career options or finding alternate careers, I rather not hate the later if I ended up with a PhD Degree by chance.
During PhD training, a student acquires the skills to identify and critically view scientific issues and ask relevant questions to address it by designing and performing feasible experiments. During the process a student not only learns in depth about a particular scientific problem that he/she is engaged on, but develops special skills on how to approach and solve scientific issues in general using, most importantly, intellectual, technical and social skills.
Moving on, life is beautiful when you meet your passion in your job. A PhD graduate, if graduated not by chance (I repeat) would definitely want to, and capable of, be in research jobs. A quick landing point is a post-PhD research job in academics. Many of us conveniently call this, a postdoctoral training. I would rather strictly call this an academic research job because the core components of the ‘so called’ post-doctoral training (grant writing, teaching, mentoring, supervision of trainees and technicians) is unfortunately not offered in most of the labs. Needless to say, the supervisor and the whole lab utilize the intellectual, technical and managerial capacity of this research personnel and use it towards the progress of ongoing research projects in the lab. Fair enough, but please call it a job and of course many universities officially started recognizing postdoctoral position as an employment. However, the tenure of the employment is still restricted to a definite period, mostly five years or below, regardless of how efficient you perform. Needless to say, the lucrative features that attract supervisors towards the postdoctoral species - access to external fellowships and compromised salary structure- also end after this fixed tenure.
What happens after the five year tenure. Now this is the time everyone around shoots at you with the same question; why don’t you become an assistant professor? Why don’t you work as a research scientist in the industry? Obviously, the limited number of tenure-track positions and industrial jobs do not match with the number of PhD graduates out and it totally makes sense why most of the PhD graduates fail to find a position in those two places. As the next right fit, you apply for research positions in other labs, and now you hear the funniest thing- YOU ARE OVERQAULIFIED TO ACCOMMODATE. Whaaaaaaaat? Overqualified to do research?..then what was all the training for…… Now the conversation brings to the same point of becoming an assistant professor and being independent.
Now let me ask a question. Do all the engineering graduates start their own company to find a job? Do all the physicians start their own hospital so that they could practice. If they could be hired as engineers and physicians, why research graduates are considered overqualified when comes to hiring them as research scientists in academia. I am wondering who do the grant funding agencies expect to run their million dollar projects. Do they expect Masters students, PhD trainees and technicians to shoulder their million dollar projects? (Of course the Principal Investigator (PI) can’t run behind all the intellectual and technical aspects of the projects). I am afraid they lose many relevant observations, interventions and protocol improvements by doing so. My next humble question to the funding agencies is, are you offering fellowships to PhD trainees and postdoctoral fellows to let them quit academic research, if not ended up an assistant professor? When private companies hire well-qualified PhD graduates, not to risk their projects, and being successful, why grant funding agencies are not recommending hiring such qualified individuals to run their grants. Is this the main reason why academic research always lags behind industrial research? My intention does not support filling the whole lab with post-PhD employees and blocking the opportunities of incoming trainees, rather I think it is quite reasonable to permanently employ at the least one PhD graduate in each academic lab to manage ongoing projects (few universities in united states has already started employing PhD graduates as staff scientists). I underscore ‘permanent position’ because job stability matters a lot on how you function and how focused you are.
I think it is high time to alert funding agencies on the importance of a trained PhD individual, at the level of a staff scientist, to be a part of each approved grant. If you agree with me, please discuss with your postdoctoral association what they think and do to secure your right to be in academic research.
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Scientists transfer sea slug memories with RNA
Hi all,
It’s been an busy time of the year for me (end of semester after teaching my own class + trying to find a post-doc while finishing up my PhD/defending soon…plus planning a wedding, finding a house, and other ‘small’ life things like that
), BUT I wanted to share an awesome new study 
hot off-the-press at none other than SfN’s own open-access journal eNeuro:"RNA from Trained Aplysia Can Induce an Epigenetic Engram for Long-Term Sensitization in Untrained Aplysia" by Alexis Bédécarrats et al. from the lab of David Glazman @ UCLA.
The study has been picked-up by a massive amount of outlets around the web so I won’t belabor the study more than the pro’s that get paid to do it. But the short n’ sweet is that if you transfer brain RNA from slugs that get zapped (shocked) repeatedly for a day and transfer it to naive slugs, they respond to shocks as if they’d experienced them before (longer defensive withdrawal response)!
There’s a great deal more in the paper, and many medical and sci-fi-esque implications. but regardless of how realistic they are, it’s remarkable study that I’m sure will be an instant-classic.
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The Neuroscience of the Arts
The blog will discuss new research and commentary in the field of neuroscience and music as well as the neuroscience underlying other art forms.
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Non-academic Career Options and Transition
This is a space to discuss non-academic career options, thoughts and even just a place to vent. Creating a CV or resume for a non-academic position is entirely different than what you may be used to. And then when you get hired…being in an office is definitely a culture shock to say the least. This area will be a place to help you discuss options, where to look for opportunities, the good, the bad and the ugly. There are many pros and cons to a non-academic position and having a network of people to help guide whatever direction you may go can be the key to a successful and happy transition.
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The Biohybrid Brain
This blog intends to be a platform linking scientific and technological progression of the Neural Engineering field, including Artificial Intelligence applied to the Neurosciences, and the ethical and psycho-social concerns raised by the concept of man-machine hybridization; its scope is to raise awareness and understanding and to address the misconceptions and fears of biohybrid biomedical interventions to cure the brain.
Why should people use this category?
This category lies at the border among science, technology and ethics. It may be used to start any topic relating to neurotechnology, biological-to-artificial (biohybrid) interfaces, neuropsychology and cognitive neuroscience relative to the concepts of restoration of brain function and augmentation of it, both for therapeutic purposes and for enhancing human brain performance.This category intends to be a cross-disciplinary platform expanding beyond the research, where people can actively engage in constructive debates about S&T progression relative to man-machine hybridization along with the ethics and policy concerns deriving from it.
What should topics in this category generally contain?
Topics in this category should go well beyond the world of Neuroscience alone, including Philosophy of Science and History of Philosophy in a unique conceptual framework, drawing from the different topics around the forum.- Read more...
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Neuroinflammation and Brain Disorders
Neuroinflammation and neurodegenerative & psychiatric disorders
- This category would help highlight recent updates about the relation between brain disorders and the immune system. This category would also highlight the use of recent techniques to understand the interdependence of the same.
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