Synapses may not be the basis of memory

Brain It 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 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 brain plasticity or neuroplasticity.

Until now, it has been assumed that this ability to modulate synapses plays a role in active in two activities as important for brain development as learning and the memory. I say so far, since there is a new alternative current to this explanatory scheme, according to which to understand how memory works, synapses are not that important as is normally believed.

The history of synapses

Thanks to Ramón y Cajal, we know that neurons They do not form a unified tissue, but are all separated by interneuronal spaces, microscopic places that Sherrington would later call "synapses." Decades later, the psychologist Donald Hebb would offer a theory according to which 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 postulating 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 complete opposite of the first, that is, a reduction in the transmission of information.

Memory and neuroscience, empirical evidence with controversy

The learning It is the process by which we associate things and events in life to acquire new knowledge. Memory is the activity of maintaining and retaining these 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 research, they saw that changes in synaptic conductivity were generated as a consequence of how the animal responds to the environment, showing that the synapse is involved in the process of learning and memorizing. But a more recent experiment with Aplysia by Chen et al. (2014) have found something that conflicts 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 whole process of memory.

Another case that supports this idea arises from 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 by directly and under a synapse inhibition by drugs, against all prognosis, they continued to mark the rhythm. Johansson concluded that their memory is not influenced by external mechanisms, and that they are the cells of Purkinje alone who control the mechanism individually, regardless of the influences of the synapse.

By last, a project performed by Ryan et al. (2015) served to demonstrate that the strength of the synapse is not a critical point in memory consolidation. According to their work, when injecting protein inhibitors into animals, a 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 (method known as optogenetics), yes that memory can be retained despite the chemical block induced.

Learning and memory, united or independent mechanisms?

In order to memorize something, we first have to learn about it. I do not know if it is for this reason, but the current neuroscientific literature tends to put these two terms together and the experiments on which they are based tend to have an ambiguous conclusion, which does not allow 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 learning center. The research base focused on the N-Methyl-D-Aspartate (NMDA) receptors, a protein that recognizes the neurotransmitter glutamate and that participates in the LTP signal. They showed that without long-term enhancement in hypothalamic cells, it is impossible to learn new knowledge. The experiment consisted of administering NMDA receptor blockers to rats, which are left in a drum of water 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 receives training prior to the administration of inhibitors, the rat "compensates" for the loss of LTP, that is, it has memory. The conclusion to be shown is that the LTP actively participates in learning, but it is not so clear that it does so in information retrieval.

The implication of brain plasticity

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

Instead, its 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 memory mechanism is within cells rather than synapses. But as the psychologist and neuroscientist Ralph Adolph points out, neuroscience will figure out how learning and memory work in the next fifty years, that is, only time clears everything up.

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. USES. 111, 14930-14934. doi: 10.1073 / pnas.1415371111.
• Kandel, E. R., and Siegelbaum, S. TO. (2013). "Cellular mechanisms of implicit memory storage and the biological basis of individuality," in Principles of Neural Science, 5th Edn., Eds E. R. Kandel, J. H. Schwartz, T. M. Jessell, S. TO. Siegelbaum, and A. J. 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 / hypo.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.