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

For some time now it has been seen that the activity of the synapse is not static, that is, it is not always the same. It can be enhanced or diminished as a consequence of external stimuli, such as things that we live. 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 the synapses participates actively in two activities as important for brain development 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 the synapses are not so important as it is normally believed.

The history of synapses

Thanks to Ramón y Cajal, we know that neurons do not form a unified tissue, but all of them are separated by interneuronal spaces, microscopic places that later Sherrington would call "synapses". Decades later, the psychologist Donald Hebb would offer a theory according to which the synapses are not always equal in 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 channels more frequent than others. As a curious fact, fifty years before applying this theory, Ramón y Cajal left evidence of the existence of this modulation in his writings.

Today we know 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, that is, 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 knowledge learned 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 marine snail known as Aplysia. In this investigation, they saw that changes in synaptic conductivity were generated as a consequence of how the animal responds to the environment , demonstrating that the synapse is 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 previously. The study reveals that long-term memory persists in the animal in motor functions after the synapse has been inhibited by drugs, casting doubt on the idea that the synapse participates in the entire memory process.

Another case that supports this idea arises from the experiment proposed by Johansson et al. (2014). On this occasion the Purkinje cells of the cerebellum were studied. These cells have among their functions to control the rhythm of movements, and being stimulated directly and under an inhibition of synapses by drugs, against all prognosis, they continued to set the pace. Johansson concluded that his memory is not influenced by external mechanisms, and that it is the Purkinje cells themselves that control the mechanism individually, independently of the influences of the synapses.

Finally, a project by Ryan et al. (2015) served to demonstrate that the strength of the synapse is not a critical point in the consolidation of memory. According to his work, when injecting protein inhibitors in animals a retrograde amnesia is produced, that is, they can not 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), we can retain the memory despite the induced chemical blockade.

Learning and memory, united or independent mechanisms?

In order to memorize something, we must first learn about it . I do not 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 to distinguish between the learning process and memory, making it difficult to understand if 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 learning center. The research base focused on the receptors of N-Methyl-D-Aspartate (NMDA), a protein that recognizes the neurotransmitter glutamate and participates in the LTP signal. They demonstrated that without a long-lasting potentiation in cells of the hypothalamus, it is impossible to learn new knowledge. The experiment consisted of administering NMDA receptor blockers in rats, which are left in a water drum with a raft, being unable to learn the location of the raft by repeating the test, unlike rats without inhibitors.

Subsequent studies reveal that if the rat receives training prior to the administration of the inhibitors, the rat "compensates" for the loss of the LTP, that is, it has memory. The conclusion that we want to show is that the LTP participates actively in learning, but it is not so clear that it does so in information retrieval .

The implication of cerebral plasticity

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

Instead, your role in memory begins to be more in doubt, as you have read with a few examples cited. A theory has begun to emerge that the mechanism of memory is inside cells rather than at synapses. But as the psychologist and neuroscientist Ralph Adolph indicates, neuroscience will solve how learning and memory works in the next fifty years , that is, only time clarifies everything.

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., and Hesslow, G. (2014). Memory trace and timing mechanism localized to cerebellar Purkinje cells. Proc. Natl. Acad. Sci. U.S.A. 111, 14930-14934. doi: 10.1073 / pnas.1415371111.
• Kandel, E. R., and Siegelbaum, S. A. (2013). "Cellular mechanisms of implicit memory storage and the biological basis of individuality," in Principles of Neural Science, 5th Edn., Eds ER Kandel, JH Schwartz, TM Jessell, Siegelbaum SA, and AJ Hudspeth (New York, NY: McGraw-Hill ), 1461-1486.
• Martin, S. J., and Morris, R. G. M. (2002). New life in an old idea: the synaptic plasticity and memory hypothesis revisited. Hippocampus 12, 609-636. doi: 10.1002 / hipo.10107.
• Ryan, T. J., Roy, D. S., Pignatelli, M., Arons, A., and Tonegawa, S. (2015). Engram cells retain memory under retrograde amnesia. Science 348, 1007-1013. doi: 10.1126 / science.aaa5542.

The Nervous System, Part 3 - Synapses!: Crash Course A&P #10 (March 2024).