Neuroplasticity is also referred to as brain plasticity, cortical plasticity or cortical re-mapping. Neuroplasticity refers to change in the organisation of the neural circuits, by adding new nerve cells, strengthen the synaptic connections, or forming new synaptic connections or by cortical re-mapping, in the adult central nervous system. The idea as first proposed in 1892 by Santiago Ramon ‘Y Cajal, the proposer of the neuron doctrine, though the idea was largely neglected for the next fifty years. Neuroplasticity challenges the old idea that the brain circuits are fixed and will not change in life.
n mammals, neurons in the brain, which process vision, actually develop after birth based on signals from the eyes. A landmark experiment by David H. Hubel and Torsten Wiesel (1963) showed that cats which had one eye sewn shut from birth to three months of age (monocular deprivation) only fully developed vision in the open eye. They showed that columns in the primary visual cortex receiving inputs from the other eye took over the areas that would normally receive input from the deprived eye. In general electrophysiological analyses of axons and neurons in the lateral geniculate nucleus showed that the visual receptive field properties was comparable to adult cats; however, the layers of cortex that were deprived had less activity and fewer responses were able to be isolated. The kittens had abnormally small ocular dominance columns (part of the brain that processes sight) connected to the closed eye, and abnormally large columns connected to the open eye. Because the critical period time had elapsed, it would be impossible for the kittens to alter and develop vision in the closed eye. This did not happen to adult cats even when one eye was sewn shut for a year because they had fully developed their vision during their critical period. Later experiments in monkeys found similar results
Good question!
I think all depends on radial glial cells (RGCs) status. RGCs are extremely active during earlier development and decline their activity in aging, but still conserve the ability to help regenerating brain. In case that you described (Hubel&Wiesel), who did not know much about multiple function of RGCs, (neither Ramon-y-Cajal who made discovering and drawings of them), the cells (RGCs) did not get probably stimulating inputs (from traumatic eye) and that is why the neuronal structure was not developed in time. So, let say, a "brain hardware" was dramatically declined. On the other hand, in adult traumatic cats their matured brain have the base structure developed long time ago, and , thus, when trauma has happened in adult, the visual cortex was fully developed and the cortex was recruited to relearn de novo information and to process information from non-traumatic side (from non-traumatic eye). Therefore, there is a limit for regeneration (if RGCs were not well developed in earlier stage) and there is no conflict between neuroplasticity (which clearly exist in adult) and development hypothesis (which is also true).
Since, RGCs are the universal precursors of both: glia and neurons, this broke the dogma that neurons and glia have separate lineages (Malatesta et al., 2000, Development, 127(24): 5253-5263); also, there is an evidance that adult human brain is regenerating (Eriksson, Perfilieva et al., 1998, Nature Medicine, 4: 1313-1317) as well as in adult rodents (Kaplan, 1981, J.Comp.Neuropl., 195(2):323-338).
Still regeneration in adult brain is present (Eriksson et al., 1999), the limit for regeneration is early development (Kreigstein&Alvarez-Buylla, 2009, Ann. Rev. Neurosci., 32: 149-184; Pilz et al., 2013, Nature Communication, 4: 2125; Betezeau et al., 2013, Neuron, 80(2):442-457).
Very cordially, Serguei.
Now the things are clearer ! Then this is giving rise to two more doubts:
1. In developmental stage, does critical periods take center stage which will determine neuroplasticty ( for e.g., in intellectual disability, there is ample chance that they might have missed critical periods and hence it needs more number of trials for learning and display a strong resistance towards unlearning and relearning)
2. what about systematic pruning in the developmental stage? does this also determine critical periods (in the view of glial cells)
Dear S.R. Joshi,
answering first question we automatically could know an answer to second question:
a critical time for irreversible damage is probably few minutes in adult and ten minutes in newborn known as a result of hypoxic ischemic encephalopathy (HIE).
Once blood supply from mother body stopped, the baby is in danger; not because glial cells died, but neurons. Metabolism of glial cells does not require much oxygen (they rely on Glycolis, Krebs cycle) while neurons can not live without the oxygen and energy fuel. An apoptotic death of neurons is irreversible. Still junior brain resist dramatic birth trauma, while adult not.
The problem is that THIS critical time (minutes) are an enigma of survival: glial cells became rapidly reactive and will rather release proteases to kill severely damaged neurons (which show no functionality) than will try helping them. That is a pity and a problem of searching for new methods of brain recovery. Intriguingly, this recovery occur. Simple example--after a stroke and in a year of the training many paralyzed persons give very good recovery . That is a regenerating of connections in CNS that have been lost during stroke by glial cell scar and by de novo neuronal birth by RGCs.
Even gllial cells are capable to give de novo birth of new neurons, they do not much help the nearly-dead one. Look, all PNS traumas are practically irreversible in adult human and even in children (example,-nerve cut).
If we compare moderately reversibility in newborn with nearly completely reversible cases in some amphibian and in some fish, we should be critically thinking on "What is a reason of such difference?". So, scientists now are trying to understand why fish can regenerate in adulthood, while mammals not. Big difference is due to growing: fish grows all life, mammals not.
However, recently, new method came from Dr. Yuriy Danilov lab, Wisconsin University, who clearly demonstrated recovery in many cases of pathology and disabilities. The technique is based on stimulating by electrical impulses that have been brought to the CNS via brainstem, while the signal delivery is on tangue. Dr. Danilov group recorded even an increase in brain mass after training for MS patients. I think that oligodendrocytes grow in response to Danilov's stumualtion and can better isolate axons in MS, pls neuronal regeneration.In addition, I think they stimulate RGCs.
Sorry, not much I can tell now. Who can?
Very cordially, Serguei.
Dr. Skatchkov,
Thank you for pointing out Dr. Danilov's research on rehabilitation using neuroplasticity--I found it very interesting. Links to two of the articles from Dr. Danilov's group:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2970617/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4017705/
Dear S. R.,
In brief, the answer is no, it is not a contradiction. It is more a matter of degree. The brain has to solve two problems: first, to correctly interpret the outside world, and second, to be able to learn new things. Some plasticity can still exist in adults under certain circumstances. It is just not the same extent as the plasticity that exists during critical periods, when the system has be correctly wired up during development. Once the wiring is in place, the plasticity is actively downregulated by many mechanisms. Under what conditions this limitation can be overcome is a very active area of research, since it has implications for the repair of the damaged CNS.
I am sure this is not the only review about this subject, but you may want to start your reading here:
Bavelier D, Levi DM, Li RW, Dan Y, Hensch TK. Removing brakes on adult brain plasticity: from molecular to behavioral interventions. J Neurosci. 2010 Nov 10;30(45):14964-71. doi: 10.1523/JNEUROSCI.4812-10.2010.
Best,
Jill
Yes, I completely agree with Jill and thanks to Rosi.
Indeed, there is no contradiction between plasticity (existing in deep age) and "critical periods" (which are always present. Any inflammation gives a chance to regeneration; to de novo building proteins and even cells).
New wiring is what is scientists have tried to achieve and to understand. However, even without implanting stem cells the old brain is capable to make new wiring. New technology allows now treating recovering from multiple sclerosis, from the damaged functions of MS and scientists have seen the ability of the brain to change. So, the old brain is fixing itself. Please, look on the potentials which Dr. Danilov group is suggesting (attached article from American Way).
Very cordially, Serguei.
Thank you Jill and Rosi for the explanation and wonderful articles shared.
So there are certain periods in life where plasticity is high and potential for wiring. In fact critical periods are not contradictory but complimentary for plasticity.
So are these critical periods determined by the environment or they simply bloom with age. In understanding 'Walking in infants' Linda Smith and Ester Thelen say that the locomotive systems evolve from creeping to crawling and to walking. However, the ultimate output is 'walking' there is no program in brain for crawling. Then this tells us two things: first, for walking the infant has to cross 'a determined' period in time; and because other systems take time to support bipedal the infant resolves the problem by crawling. If this is critical period it is already determined (we see many children adapted to akward walking even though their other systems did not qualify for walking), which means critical periods are determined by time of onset (cascade of events). other example is the status of RGCs, which is again completely deterministic. According to Bavelier, Adult brain plasticity, although possible, remains more restricted in scope than during development. Second, how did the infant resolve the problem of locomotion is just because of environmental demands (exploratory activity and affordances, by JJGibson).
are critical periods experience-dependent or experience-independent ? or there are some which can be divided into two of these experiences? can they be assessed
"critical periods are determined by time of onset (cascade of events). other example is the status of RGCs, which is again completely deterministic."
I don't think anything in biology is actually determined. In fact I think the word determine should be banned from biology, as it causes endless confusion and rancour. How, for example, can anything be incompletely deterministic? It is either deterministic, or it is not. If anyone knows an example of a deterministic gene, could they please enter it on my RG question on Determinism?
I totally agree with you Sir. Determinism here means something which no alternative out come, except for one.
http://synapse.princeton.edu/~sam/knudsen_critical_periods_jcn_2004.pdf
Dear S.R.,
A good textbook that may answer your questions is "Development of the Nervous System, 2nd. edition" Dan H. Sanes, Thomas A. Reh, and William Harris, ed. 2006. San Diego, CA: Elsevier Academic Press. However, I will try to briefly answer your main question about neuronal activity and critical periods.
The formation of the correct wiring patterns during the developmental critical period are dependent on neuronal activity for all of the sensory-motor systems that I am aware of EXCEPT for the wiring of the barrel cortex. (However, I have not kept up on the research in barrel cortex, so please check a current review for that particular system). That is why developmental neuroscientists coined the phrase "The neurons that fire together, wire together". So, whatever causes the neurons to fire in a particular way that leads to the strengthening of appropriate synaptic connections or the elimination of inappropriate synaptic connections is most important during the critical period, or the circuits will not be correctly patterned in the adult animal. The Knudsen review that you cite above has an explanation of this.
There are two types of neuronal activity. The first is spontaneous activity, which is the intrinsic firing pattern of the neuron. The second is driven activity, which depends on what input the neuron receives that causes it to fire. I study the visual system, so that is the system with which I am most familiar. In the visual system, the retinal ganglion cells are spontaneously active, but there is also correlated activity that appears during development. Waves of retinal ganglion cell activity sweep across the retina, and this is dependent on other retinal neurons (this is a field of active research, so please read a current review). This correlated activity is what sets up the "nearest neighbor" RGCs that "fire together". This strengthens appropriate connections in the brain through a Hebbian mechanism, so that they "wire together" in the target. This is what creates the correct wiring for the topographic "map" of visual space, a process has been studied mostly in the connections of the RGCs with their targets in the optic tectum (anamniotes and chicks) or the superior colliculus (rodents), where the retinotopic map is easy to understand and to visualize. To correctly wire the visual responses of the visual cortex takes longer, since this depends on two circuits--the RGCs correctly wiring to the neurons of the lateral geniculate nucleus (LGN), and the LGN correctly wiring to the neurons in visual cortex.
I do not study locomotion, but plasticity of this system is also an active area of research in order to design rehabilitation after traumatic spinal cord injury (Activity-dependent plasticity in spinal cord injury. Lynskey JV(1), Belanger A, Jung R. J Rehabil Res Dev. 2008;45(2):229-40.) However, a similar sort of spontanous bursting activity takes place in the developing spinal cord, and this influences how the spinal motor neurons link up with the muscles (Spontaneous rhythmic activity in early chick spinal cord influences distinct motor axon pathfinding decisions. Hanson MG(1), Milner LD, Landmesser LT. Brain Res Rev. 2008 Jan;57(1):77-85.). Locomotion is dependent on this correct initial wiring, but is a much more complex behavior that depends on coordinated activity of a larger number of circuits. Thus, there is a longer developmental time frame needed to achieve the correct output. The introduction of this paper may be helpful: From spontaneous motor activity to coordinated behaviour: a developmental model. Marques HG(1), Bharadwaj A(1), Iida F(1). PLoS Comput Biol. 2014 Jul 24;10(7):e1003653. doi:10.1371/journal.pcbi.1003653.
Happy Reading!
Regards,
Jill
Dear S.R.,
Not to inundate you with reading, but a very interesting new paper has been published in Neuron about restoration of "critical period" levels of plasticity in adult visual cortex:
Melissa F. Davis, Dario X. Figueroa Velez, Roblen P. Guevarra, Michael C. Yang, Mariyam Habeeb, Mathew C. Carathedathu, Sunil P. Gandhi. Inhibitory Neuron Transplantation into Adult Visual Cortex Creates a New Critical Period that Rescues Impaired Vision. Neuron, Volume 86, Issue 4, 20 May 2015, Pages 1055-1066, ISSN 0896-6273, http://dx.doi.org/10.1016/j.neuron.2015.03.062.
(http://www.sciencedirect.com/science/article/pii/S089662731500286X)
Good Morning Jill,
Thank you for the papers shared. I shall study the papers you have sent me and get back to the discussion.
while studying, I found this :
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3574806/pdf/cer-11-12.pdf
Dear S.R.,
The article you linked, from a publication by the Dana Foundation, is a really good overview of some of the current work in plasticity.
Dear Miotke ! Thank you for the comment. Here is another article on the risk of prolonged cortical plasticity lead to destabilization of cortical circuits in young adults.
http://www.alamaya.net/wp-content/uploads/2015/04/Morishita_Biol.Psy_._2015_Epub.pdf
- Badges
- Science topic
- Similar topics
- Psychology
- Developmental Psychology