The brain contains thousands and thousands of interconnections between its neurons, which are separated by a small space known as a synapse. It is here that the transmission of information passes from neuron to neuron .

It has been seen for some time now that synapse activity is not static, i.e. it is not always the same. It can be enhanced or diminished as a consequence of external stimuli, such as things we experience. This quality of being able to modulate the synapse is known as cerebral plasticity or neuroplasticity.

Until now, it has been assumed that this ability to modulate synapses actively participates in two activities as important for the development of the brain as learning and memory. I say until now, since there is a new alternative current to this explanatory scheme, according to which to understand the functioning of memory synapses are not as important as is normally believed.

The history of synapses

Thanks to Ramón y Cajal, we know that neurons do not form a unified tissue, but that they are all separated by interneuronal spaces, microscopic places that Sherrington would later call “synapses”. Decades later, psychologist Donald Hebb offered a theory according to which synapses are not always the same over time and can be modulated, that is, he spoke of what we know as neuroplasticity: two or more neurons can cause the relationship between them to consolidate or degrade , making certain communication pathways more frequent than others. As a curiosity, fifty years before postulating this theory, Ramón y Cajal left evidence of the existence of this modulation in his writings.

Today we know of two mechanisms that are used in the process of brain plasticity: long-term potentiation (LTP), which is an intensification of the synapse between two neurons; and long-term depression (LTD), which is the opposite of the first, i.e. a reduction in the transmission of information.

Memory and neuroscience, empirical evidence with controversy

Learning is the process by which we associate things and events in life to acquire new knowledge. Memory is the activity of maintaining and retaining this learned knowledge over time. Throughout history, hundreds of experiments have been conducted in search of how the brain performs these two activities.

A classic in this research is the work of Kandel and Siegelbaum (2013) with a small invertebrate, the sea snail known as Aplysia. In this research, they saw that changes in synaptic conductivity were generated as a consequence of how the animal responds to the environment , demonstrating that synapses are involved in the process of learning and memorizing. But a more recent experiment with Aplysia by Chen et al. (2014) has found something that clashes with the conclusions reached earlier. The study reveals that long-term memory persists in the animal in motor functions after the synapse has been inhibited by drugs, calling into question the idea that the synapse is involved in the whole memory process.

Another case that supports this idea arises from the experiment proposed by Johansson et al. On this occasion, Purkinje cells from the cerebellum were studied. These cells have among their functions that of controlling the rhythm of movements, and being stimulated directly and under a synapse inhibition by drugs, against all odds, they continued to set the pace. Johansson concluded that their memory is not influenced by external mechanisms, and that it is the Purkinje cells themselves that control the mechanism individually, regardless of synapse influences.

Finally, a project carried out by Ryan et al. (2015) served to demonstrate that the strength of synapses is not a critical point in the consolidation of memory. According to their work, injecting protein inhibitors into animals produces retrograde amnesia, that is, they cannot retain new knowledge. But if, in this same situation, we apply small flashes of light that stimulate the production of certain proteins (a method known as optogenetics), memory can be retained despite the chemical blockage induced.

Learning and memory, linked or independent mechanisms?

In order to memorize something, we first have to learn about it . I don’t know if it is because of this, but the current neuroscientific literature tends to put these two terms together and the experiments on which they are based usually have an ambiguous conclusion, which does not allow us to distinguish between learning and memory processes, making it difficult to understand whether they use a common mechanism or not.

A good example is the work of Martin and Morris (2002) in the study of the hippocampus as a centre of learning. The basis of the research was focused on N-Methyl-D-Aspartate (NMDA) receptors, a protein that recognizes the neurotransmitter glutamate and is involved in the LTP signal. They demonstrated that without long-lasting potentiation in hypothalamus cells, it is impossible to learn new knowledge. The experiment consisted of administering NMDA receptor blockers in rats, which are left in a water tank with a raft, being unable to learn the location of the raft by repeating the test, unlike rats without inhibitors.

Further studies reveal that if the rat is trained prior to administering the inhibitors, the rat “compensates” for the loss of LTP, i.e. it has a memory. The conclusion we want to show is that the LTP participates actively in learning, but it is not so clear that it does so in the recovery of information .

The implication of brain plasticity

There are many experiments that show that neuroplasticity actively participates in the acquisition of new knowledge , for example the case mentioned above or in the creation of transgenic mice in which the gene for glutamate production is eliminated, which severely hinders the animal’s learning.

Instead, its role in memory is beginning to be more questioned, as you have been able to read with a few examples cited. A theory has begun to emerge that the mechanism of memory is within cells rather than at synapses. But as psychologist and neuroscientist Ralph Adolph points out, neuroscience will solve how learning and memory work over the next fifty years , that is, only time will tell.

Bibliographic references:

  • Chen, S., Cai, D., Pearce, K., Sun, P. Y.-W., Roberts, A. C., and Glanzman, D. L. (2014). Reinstatement of long-term memory following erasure of its behavioral and synaptic expression in Aplysia. eLife 3:e03896. doi: 10.7554/eLife.03896.
  • Johansson, F., Jirenhed, D.-A., Rasmussen, A., Zucca, R., y Hesslow, G. (2014). Rastreo de memoria y mecanismo de tiempo localizado en las células cerebelosas de Purkinje. Proc. Natl. Acad. Sci. U.S.A. 111, 14930-14934. doi: 10.1073/pnas.1415371111.
  • Kandel, E. R., y Siegelbaum, S. A. (2013). “Cellular mechanisms of implicit memory storage and the biological basis of individuality”, en Principles of Neural Science, 5th Edn., eds E. R. Kandel, J. H. Schwartz, T. M. Jessell, S. A. Siegelbaum, y A. J. Hudspeth (New York, NY: McGraw-Hill), 1461-1486.
  • Martin, S. J., y Morris, R. G. M. (2002). Nueva vida en una vieja idea: la plasticidad sináptica y la hipótesis de la memoria revisitada. Hipocampo 12, 609-636. doi: 10.1002/hipo.10107.
  • Ryan, T. J., Roy, D. S., Pignatelli, M., Arons, A., y Tonegawa, S. (2015). Las células engramadas retienen la memoria bajo amnesia retrógrada. Science 348, 1007-1013. doi: 10.1126/science.aaa5542.