A great question. It was Ramon y' Cahal who defined what a Neuron is using the Golgi staining. This was at the beginning of the 20th century. Everyone simply accepted his definition without any question because of who he was. We can call it the "Einstein Effect". My neurology mentor Dr. Hyman Donnenfeld questioned this definition. He is not alive today, but he used to tell us that the Immune System is a "Floating Brain". He was sure that one day, it will be found that the Nervous System and the Immune System will be found to be two parts of One Organ/System. Certainly the immune cells do not look like neurons. thanks.

Hi,

Glial cells are different from neurons, one major difference is the fact that they do not possess chemical synapses or a role in chemical transmission of impulses. This is the solely done by neurons.

I hope that was helpfu!

You may go to any textbook for definition of neuron and the differences with glia.

What is a neuron and what is not a neuron is easily objectivable by means of simple assays.

It is true that you have in your brain hundreds of different neuronal types;

Had this been so simple and direct, I would never have asked this question in the first place. What are the properties that set neurons apart?; is a tough question. Excitability is there in other cells also, length is not a parameter as many neurons are short also. Localization is not also a parameter as glia are almost as rampant as neurons.

I agree with Sebastian.

Also I think that the central nervous system is not "simple" but to distinguish a neuron from another cell, it is easy. In other words there are hundred of questions related to CNS and I work on CNS-related research to try to answer some of them.

You may want to take a look at single cell RNA-Seq results. There you´ll find the molecular fingerprint of a neuron if you´d average genes expressed by neuronal cells vs astrocytes/oligos/NSCs and such.

But function of neurons vs glia already let´s you distinguish between them quite easily, I´d say.

Best

FB

Functionally, neurons synthesize neurotransmitters and are conduced by anterograde axonal transport towards synaptic cleff, being packaged into pre-synaptic vesicles, before, they are released to drive the action potential. Only in neurons when the membrane potential reaches a threshold it generates a spike to its axon. Axonal sprouting mediated by neurotrophins is other characteristic of neuron. On the other hand, glial cells uptake neurotransmitters, exhibit nutritional functions and stabilize neurons synapses (maintaining ionic milieu and providing scaffold). The major distinction is that glia does not participate in synaptic interactions and electrical signaling.

Another explanation may be embryological. Neural stem cells (NSCs) give rise to neurons, astrocytes and oligodendrocytes in the brain. NSCs of the lateral ventricles wall undergo changes in morphology and produce different progeny as brain development proceeds. Thus, transcription factors play pivotal roles on fate determination of neurons and glia cells. For example, Olig2 regulates oligodendrocyte differentiation and He's 1 induce astrocyte formation. Immature neurons migrate to cerebral cortex and become mature neurons, after that, NSCs finally differentiate into glia cells for neuronal maintenance and support.

Regards,

I agree that it is a profound question; that takes us to the core of what is neuroscience.

To say for example that what charaterizes neuros is the property of initiating action potentials, is to ignore the neurons of the intrinsic circuit of vertebrate retinas, in which, bipolar, horizontal and most amacrine cells do not have action potentials.

First we have to cnsider the historical development of CNS histology, tightly coupled to technical development in dyes and optics of microscopes.

Finnally the functional role of each population, still in discussion. Although there is no question about the input/output role of neurons, the role of the glial network is still in debate.

This is not a profound, nor subtle, nor difficult question... the very CLEAR and CORRECT answer was given by Diego Noé Rodríguez Sánchez above.

(BTW, glia do not lack electrical excitability and/or signalling. They do in fact have distinct resting potentials that differ in pathological or activation states. And astrocytes can signal each other via calcium waves.)

A great question. It was Ramon y' Cahal who defined what a Neuron is using the Golgi staining. This was at the beginning of the 20th century. Everyone simply accepted his definition without any question because of who he was. We can call it the "Einstein Effect". My neurology mentor Dr. Hyman Donnenfeld questioned this definition. He is not alive today, but he used to tell us that the Immune System is a "Floating Brain". He was sure that one day, it will be found that the Nervous System and the Immune System will be found to be two parts of One Organ/System. Certainly the immune cells do not look like neurons. thanks.

This cells are able to process the various stimulus it gets and give appropriate feedback to it

The notion that neurons simply transmit information electrically as spike codes that convert into chemical transmissionsv interneuronally seems a forced dogma on which a century of research is based. I am glad to see it now questioned:

Article Thinking about the nerve impulse: A critical analysis of the...

as metabolic activity is deemed relevant. This raises all sorts of interesting questions about glia-neuron interaction with a lot more happening in the local microenvironments than once thought. For too long the March of Science was paced to the drumbeat of the funding gate keepers' notions, making young researchers Jesuits of the old popes dominating neuroscience funding. This imprisons the future in the past, rarely retested for confirmation, fortified by simplistic computer models. Invariably-- but oh so slowly-- the drip of confounding discoveries corodes past dogmas causing them to collapses in confusion once untenible. Current work on glia-neuron interaction-- as a unit-- is worth our attention. We must cast wide nets and reap what we sow!!!!

Hi Daniel

I agree withmost of what you write abd glia-neuron as a unit may be likely but glia and neurons are different and easily identifiable as glia or neuron.

The original question was: why glia aren't neurons?

Thinking of glia and neurons as easily differentiated seems to be more of a belief without evidence rather than science. I would request you to kindly explain your statement with jusifications and evidence from published literature and coherent logic. That will help the lesser mortals like me to understand my question better. As far as I understand, I find it always intriguing and complex when we work with definitions. The explanation that I get a fell of a neuron when I see and neuron and I get a feel of glia when I see a glial cell works for me, but that is not science.

Hi Muneeeb when you see a nose is a nose and when you see an eye is an eye. Same with neurons and glia.

To be sure, a horse is not a cow because we define them in such a way as to distinguish them. And, a baby is certainly not an adult, nor an old man. But the real question is what do neurons do in that crazy quilt called the brain? If you know, how do you make undergrads understand it enough to want to know more, because unless they wonder, there won't be enough brains devoted to find out. Do we have all our ducks in a row the way Endocrinologists like our brilliant colleague, Prof. Hayden might have? How much do we know about the special housekeeping functions of neurons and glia as opposed to their systemic function. In neurosurgery, where once you open the dura chances are that that alone will kill your patient, we often find ourselves declaring a patient "BRAIN DEAD." I memorized the LEGAL definition, yet I also know tow outliers on opposite extremes: at one end a number of long brain dead reawaken completely and to the best of our ability FORGOT NOTHING pre-coma. At the other is the 100% prognosis who just slips away. We morphologically and behaviorally identify Alzheimer's but no one yet can explain its pathology. For almost six decades I have been trying to understand what a neuron does, so obsessively that my house is sinking from thousands of papers marked up with colored highlighters, lines and comments. And yet, I have often taken refuge in the beauty and excitement of endocrine, hepatic and renal tissues just to escape the frustration of neuroscience. Half those years I watched, pardon the term, "Mickey Mouse" psychiatrists diagnose in all sorts of ways but treating almost the same every time. Thanks to the conservatism of muscles I had found solace in the physiology of sensorimotor neurology. While most excited by our own challenge to Sherrington through section of spinal roots and watching recovery, I must say that Bizzi had really confounded the orderly notions we all lived by building on the myotatic reflex, his notions of "spinal synergies" may not make sense to an electrician wiring your house but imply amazing notions that have been critical to both motor physiology and medicine. The gamma neuron that Granit and Mathews, just to name two, so enriched the reAFFERENT and reEFFERENT norions that make possible the amazing basal ganglia work of today, that we find ourselves drowning in premptive take-it-or-leave-it MOST BEAUTIFUL computer models that invaded the physiology literature, more because these don't anger PETA, but in dealing with patient pain and motor disorders don't help much. In the end, Grillner's tutorials on the evolution of the vertebrate basal ganglia has propelled us far past the brainstem, cerebellum and thalamus. While we all attributed totem qualities to the cerebral cortex as a columnar ultimate evolution, the entire telencephalon of birds, with it seems more neurons than chimps and as many as us in some cases leaves us in a state of duhhh!

Neurophysiologists seem to divide in "CONDUCTORS" (electricians) and "TRANSMITTERS" (chemists), leaving us to wonder still as much as ever: how do neurons link up to make a mind? How many "neuron" have to die before the brain "dies" and we can rape the body for organ transplant harvests? Plasticity and down and back up activity of the neuron is still utterly hypothetical, settling for satisfaction if it fits the statistics. Yet mass conducting dendrites summating in the perykarion and, upon reaching a threshold in the axon hillock, conducts non-decrimentally, only to interact with Ca++ currents to release chemicals into the synapse,cannot help but make one wonder: what the hell is information anyway and how the hell does it translate into consciousness...I wouldn't dare mention mental will! Unpredictability seems to indicate thinking and the solving of problems that stump grad students intelligence. But how Neuron A in assoiation with Glias X,Y, and Z, still stumps us as we note a sense of INTENT in otherwise annoyingly simple organisms on second look, so much so that now the Mushroom Body of an amazingly clever bee, solving problems and teaching its solution to others, has led to calling it the bee's basal ganglia!

In conclusion, for almost 60 years I have been doing a split between psychology and neurophysiology and understand why so many avoid the lab and just use blunt electrodes on wake patients in the OR: because the end of tremor, pain or other abnormality, since you don't widely retract the dura, leads to patients who think you a god and you never have to tel them what the hell you did and why. However, Dr. Benabid's brilliant use of light instead of electricity (that cooks brain tissue eventually) to treat Parkinsonian symptoms and then switching from the blue wave spectrum to the red-infrared to save the mitochondria of neurons has been much celebrated, reminding us how amazingly complex is the neuron in its relationship to the glia that, yes, are distinguishable once differentiated, but just as few appreciate the wonders sone by the obscure woman behind the celebrated man, we are in no position to bee to declarative lest we invoke a distinction without a difference; for as they say about love and marriage, YOU CAN'T HAVE ONE WITHOUT THE OTHER-- you can in a petri dish, but it's ohhhh so lonely and does none of the wonders that make us glad to be alive.

Daniel, you have a very primitive view about this question. It is central about how the brain works. of course one can answer in several ways, for example saying that glial cells are the interface between brain and body and neurons input and output. This simplification forgets that all input and output is axon/glia too.

In sensory processing, motor control what is the role of each network? We do not know.

The interface among endothelium and microglia is made through the macroglial network, the dynamics of theese interactins in my view are the key to understand autoimmune responses and their psychological expressions.

Macroglia and neurons will take any shape depending of the locus they are inserted.

You must forgive me as old age has ravaged how my fingers, effectively making them very defiant, protesting with pain, hence it may have been hard to make my point. I always assumed that glia and neurons are of one piece. As to the immune category of glia, I must demure as I feel that we really don't know too much about that. My concern was more with metabolic support. The "primitive" view I put across was not mine, but one expressed by a French researcher who used light in the red-infrared spectrum and found that 6-hydroxydopamine poisoned neurons in SNc did not degenerate. Thus, he argued, though 70% of such neurons are gone by the time we clinical Dx Parkinson's, he is looking for alerting indicants appearing long before that.

My interest was in his discussion of mitochondrial disappearance as an indicant of catastrophic prognosis for the SNc dopaminergic neurons. And, can the glia be exploited in some way to compensate. Now, autoimmune or residual immune effects is a most interesting microglial issue and certainly quite relevant to numerous disorders. But I don't think we are very clear, or rather clear enough, so as to say what makes progenitors into glia vs neurons and exactly what that difference means. But my approach is from the view that what we deem "neuronal information" is full of suppositions. I do not feel comfortable distinguishing the role of glia in brain language, messaging and info storage. But I recall older work suggesting info load is a shared function of neurons and glia. Also, glia seem to play an important role in regeneration after rhizotomy. So, my question was not glia-specific. I am very much aware and was thus very intent to read some very interesting reviews on the role of glia (types to be sure, not any and all) in regeneration, so called deaffernetation pain and how regenerated libers do and don't impede feedback free motoneuronal activity. I leave wide open subclassification of glia as it is a subject of ongoing study; rather, I had hoped others might update me on more specific advances of glial ontogeny and fuctionality. How well can we separate the glial contribution form the neuronal? And, how well do we understand how they work together in CNS nuclei? All in all, they too are affected, beyond microglial immune activity, in the neuronal circuits of the CNS, n'est pas?

I kind of was hoping that your response would go on to elaborate on how the glial millieu contributes to plasticity and how it interferes with it. Assuming that scaring is part of immunodefence, how well do we understand the trophic and supportive glial functions as opposed to defensive in the eventually dramatic plasticity we see? Does our CNS lesioning restrict damage. Does the swift as opposed to regressive adaptation to the same surgical proceedures on different conspecific subjects relate to neuronal, glial, vascular, scar and/or plasticity phenomena we see? Are glia the same reserves recruitted into different functional morphoses depending on local conditions? Indeed there are cogent embryological discussions of glial function. But, what changes as neuronal nets are set down. Is the pedagogical distinction between macro and micro-glia solid? I don't even think we hve completely settled whether committed glia and reverse and become something else or at least we can't come up with a mechanism. So fascinating in vitro work, how much does it say about the in vivo setting. And, how has glia function evolved with brain evolution? All these questions are subjects of study for me as I seek some sort of reassurance that plasticity does not mean that removal of orderly sensory input results in a disordered trophic activity. Along this line, various "glia" have been blamed for the good, the bad and the ugly and I don't think, or so it seems to me, that we are in a position to decide on the basis of known glial research what tampering with the CNS does to brain function. That is basically what I was asking. Also, as I search for understanding in the field of glial activity, I don't feel too comfortable being less than primitive. If the field has much evolved since then, I can only say HURRAH, please direct me, I am ready to be a follower as over the last 50 years I have seen a lot of "hard" neuroscience fall as "too simple" given new data.

There are many ways to differentiate between neurons and glia, or for that matter any cell(s) in a tissue. They are different in their transcriptional makeup which results in neuronal/glial specific structural and functional outcomes. To simplify neurons and glia are as a result of a neural stem cell taking two different fates, and can be identified by differential transcriptional signatures. Both neurons/glia are differentiated cells as they cannot generate cells of other types, although glial cells generate more glia, but not same case with neurons. In layman language, as put by Dr. Rafael Franco "when you see a nose is a nose and when you see an eye is an eye. Same with neurons and glia".

I fear that the old saying: PHYLOGENY RECAPITULATES ONTOLOGY, or visa-versa, leaves with clear descriptive distinctions if the categorical distinctions we make are based on evo-devo morphological unities and distinctions that clue us to function. Glial cells were long separated from neurons on an assumed form/function basis, leading to an assumed theory of functional distinction between glia types. And so, if we attribute to neurons "mind-components" functions and to glia, "liver parenchima-immuno-inflammatory like" functions as some kind of support or protective tissues, we follow in perplexity the development of glia into neurons. In a sense, this is not so strange when one considers the undifferentiated early cells of the embryo. But, on the assumption of endpoint "maturity," glia and neurons are alleged to perform different functions. And so, Dr. Franco's nose and eye distinction is very acceptable. However, when one contemplates what role neurons play in "brain function" as opposed to glia, recent data suggests-- as they used to say about love-and-marriage in the 1950s-- you can't have one without the other when it comes to memory and cognition. My supposedly "primitive" view of glia is muddled by the seeming dual role of BOTH glia and neurons in memory and cognition. Thus, the end-state of cellular differentiation is not as much at issue as the way both serve information storage and processing, beyond the "service" role assigned to glia traditionally. That is the conundrum that I was referring to in my original statement and any information in that area would be greatly appreciated. Glial response to DM2, for example, and to other neuronal mitochondrial failure, interest me tremendously. But is there more to the relationship with neurons involving actual memory processing and storage?