Introduction & Summary

This video was broadcasted on Youtube by the University of California TV in the context of a series of videos about Alzheimer’s Disease (AD). In this video, Roberto Makinov is interviewed about his research on role of synapses in memory creation and loss. Roberto Makinov is a professor of neuroscience and neurobiology, his language is quite technical but the purpose of this video is to spread the knowledge that research has allowed to accumulate on the subject, then it really can make sense for anyone.

R. Makinov first gives a global definition of synapses. He explains synapses are the connection between a giving nerve cell, that releases neurotransmitters when is electrically excited, and a receiving nerve cell on which neurotransmitters bind themselves. When receptors of the receiving cell are stimulated, they open ion channels and allow thus the electrical signal to continue its way. The second point that R. Makinov exposes is that when we learn something, synapses can be modified (change on quantity of neurotransmitters, increased or decreased sensibility of receptors, etc.). He presents how Scandinavian searchers (Bliss & Lomo, 1973), in the early 1970’s, discovered that if a synapse is stimulated at a really high frequency, this synapse end to be strengthened and to stay this way for decades. This phenomenon is called Long Term Potentiation (LTP). Conversely, a very low frequency stimulation can weaken the synapse : it is the Long Term Depression (LTD).

Then, R. Makinov presents his own study : he created associative memory among rats by highly stimulating nerve cells an giving an electrical choc at the same time. This high frequency stimulation leads to LTP between the stimulated nerve cells and the fear center, to the extent that rats freeze when those nerve cells are stimulated, even when there are no electrical choc anymore. Through LTP, R. Makinov created a stable, and yet irrelevant, knowledge in rats memory. He extended the experiment further by making this memory disappear through LTD. Finally, the extraordinary last try he made was to make the memory re-appear with another LTP of those nerve cells, and it worked ; rats started again to freeze when the target nerve cells were stimulated!

Analysis

At the end of the video, R. Makinov and the interviewer are cautiously suggesting that those findings could open the way to further research in the context of AD therapy. I think it’s a good thing that they remain careful in their conclusion because people could easily get too enthusiastic and imagine that LTP could restore patients with AD’s memory. Yet, LTP has been precisely shown to be impaired in AD (Chen, Kagan, Hirakura & Xie, 2000). Plus, research proving that LTP can restore memories have solely been conducted on rats or mice whereas human memory is known to be particularly complex with semantic knowledge interacting with episodic memory. In conclusion, this video made me discover how incredible the neuronal plasticity could be, but it also puzzled me because it seems to me that such a complex pathology as AD shouldn’t be dealt under the unique and quiet reductive perspective of neurobiology.

Written by Canelle GARNIER, M2 PPCECC

Words I have learned :

– ion channels = canaux ioniques

– to be strengthened/weakened = être renforcé/affaibli

– conversely = inversement

– Long Term Potentiation/Depression = potentialisation/dépression à long terme

– it puzzled me = ça m’a laissée perplexe

Bibliography:

Chen, Q. S., Kagan, B. L., Hirakura, Y., & Xie, C. W. (2000). Impairment of hippocampal long term potentiation by Alzheimer amyloid β‐peptides. Journal of neuroscience research, 60(1), 65-72.

Bliss, T. V. P. & Lomo, T. (1973). Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. The Journal of Physiology, 232(2),‎ 331–356.

Link to the video : https://www.youtube.com/watch?v=VYNh3-21HmA

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