What is neuroplasticity?
The circumstances under which neuroplasticity may occur and its impact on cognitive functioning.
It was Santiago Ramón y Cajal’s great intuition to notice that the spines that appeared to be upon the neurons of cortical matter were not merely artefacts of the staining method but structural features of the neurons themselves. With this he considered their purpose and inferred that as they would greatly expand the available surface area of the neurons, these spines would thereby allow the capacity of a neuron to receive connections from other neurons to be extended (Yuste 2015).
In allowing the structure of the brain to alter in shape, these processes would allow intelligence to emerge as a consequence of the capacity to learn, Professor Johansen-Berg (CITE) quotes Cajal as saying “the acquisition of new abilities requires many years of mental and physical practice. In order to fully understand this complicated phenomenon, it is necessary to admit, in addition to the strengthening of pre-established organic pathways, the establishment of new ones, through ramification and progressive growth of dendritic arborizations and nervous terminals”.
The capacity of the brain’s structure to alter over time is the measure of that brain’s neuroplasticity.
Neuroplasticity refers to the fact that the brain reacts to the external environment and the internal processes of the brain and body, Cramer et al. (2011) have argued that “Neuroplasticity can be defined as the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections.” These responses happen over a variety of timescales, and these responses are a function of various processes that occur within the brain.
This variation along timescales is paralleled by the scale at which these responses impact upon the structure of the brain, at the smallest scales these structural changes (or responses to external/internal stimuli) can occur more quickly than the changes which are exhibited at the largest scales.
Following from Duclis et al.’s 2013 work which showed evidence that neurotransmitter expression altered at the synaptic level in response to stimuli, where the authors suggested that “Activity-dependent transmitter switching may serve [neuroplasticity] functions” Birren and Marder (2013) argued that “The mechanisms that change the profile of neurotransmitter release provide opportunities for plastic changes in circuit function, and consequently in organism behaviour”.
Many neurons release more than one neurotransmitter, often these will involve cotransmitters that will have very different structures and consequently very different effects. This allows many degrees of freedom in the chemical conversation between the axon and the dendrite. These differences can cause modulations in the activity of the target neuron over different time scales (Nusbaum et al. 2001). Should different mixes of neurotransmitters be released by the axon terminal into the synaptic cleft these mixes should provoke different responses and firing patterns in the target cell creating space for alteration, and thus neuroplasticity to occur.
The structure of the synapse has well defined neuroplastic elements. At the synaptic level neurotransmitters released across into the synaptic cleft bind with receptors on the post synaptic membrane of the target neuron. This binding allows sodium channels in the target cells membrane to open altering the electrical potential within the target cell and thus causing the target neuron to fire (if the firing threshold is breached). The target neuron’s likelihood to fire can be altered upwards (potentiation) or downwards (depression) through the creation or destruction of ion channels which can be triggered by the neurotransmitters of the axon terminal, if the number or type change this will alter the behaviour of the target neuron.
Even if there is no alteration in the structure of the post synaptic membrane, the axon terminal can self-regulate its activity, as Bender et al. (2010) have shown endogenously produced dopamine can cause axons certain cells to downregulate the flow of calcium ions through its cellular membrane causing the release of synaptic vesicles to slow down – depressing the activity at the synapse. Alternatively if there was a mechanism that could increase the number of calcium channels then this would increase the rate of release, thus inducing potentiation.
These synaptic changes form an important part of the brain’s neuroplastic activity.
Where potentiation or depression occurs across a synapse it can become a self-reinforcing, triggering the pruning of connections between neurons, or the sprouting of new axon terminals or dendric branches. Frequently firing connections are strengthened and reinforced while axons, and even entire cells, can atrophy for want of activity.
It is through these processes that grey matter alters structure within the brain, with increasingly densely connected regions requiring increasing volume. The high metabolic cost of brain tissue that requires that our body’s processes cull inactive cells (which causes the system to lose information) while the cost of losing important information opposes this, these contrasting forces create an environment what promotes the efficient maintenance of those connections which most important, or at least that is the assumption of Groussard et al (2014)
Finally Sampaio-Baptista et al. have shown evidence of white matter structures altering in response to skilled learning in rats which suggests the potential for even higher levels of neuroplastic activity across the brain.
Cramer, S. C., Sur, M., Dobkin, B. H., O’Brien, C., Sanger, T. D., Trojanowski, J. Q., … & Chen, W. G. (2011). Harnessing neuroplasticity for clinical applications. Brain, 134(6), 1591-1609.
Dulcis, D., Jamshidi, P., Leutgeb, S., & Spitzer, N. C. (2013). Neurotransmitter switching in the adult brain regulates behavior. Science,340(6131), 449-453.
Nusbaum, M. P., Blitz, D. M., Swensen, A. M., Wood, D., & Marder, E. (2001). The roles of co-transmission in neural network modulation. Trends in neurosciences, 24(3), 146-154.
Bender, K. J., Ford, C. P., & Trussell, L. O. (2010). Dopaminergic modulation of axon initial segment calcium channels regulates action potential initiation. Neuron, 68(3), 500-511.
Groussard, M., Viader, F., Landeau, B., Desgranges, B., Eustache, F., & Platel, H. (2014). The effects of musical practice on structural plasticity: the dynamics of grey matter changes. Brain and cognition, 90, 174-180.
Sampaio-Baptista, C., Khrapitchev, A. A., Foxley, S., Schlagheck, T., Scholz, J., Jbabdi, S., … & Kleim, J. (2013). Motor skill learning induces changes in white matter microstructure and myelination. The Journal of Neuroscience, 33(50), 19499-19503.
