The neuropeptide enkephalin, made up of five amino acids, it is essential for the encounter with someone that we have not seen before remains archived in our memory. This is stated by a study led by the Institute of Neurosciences of Alicante (CSIC / UMH) and performed on mice, a social species like humans. The results are published in Molecular Psychiatry.
“This work provides a novel and hitherto unknown mechanism for memory storage, in which the action of local inhibitory neurons produces a long-lasting synaptic plasticity –indispensable for the formation of this social memory– through the release of enkephalin and its action on delta opioid receptors ”, he explains Felix leroy, scientist from the Valencian institution.
We want to see how the plasticity that we have demonstrated in this publication can be used to rescue the ability to form social memory in these animals.
The synaptic plasticity refers to the changes that occur in the intensity of communication between neurons, and is the main mechanism involved in memory and learning. Meanwhile, enkephalin acts as a depressant of neuronal communication and is released by VIP neurons.
The VIP neurons, so called because they produce a peptide that was initially isolated in the intestine called vasoactive intestinal peptide, they are found in a small area of the hippocampus called CA2, which is involved in the formation of social memory. These VIP cells act in this area of the brain as disinhibitory neurons, because they slow down the inhibitory neurons. In this way, excitatory neurons can be activated indirectly.
Thus, VIP neurons show greater activity during the encounter with an unknown individual than against another relative and also when faced with a new object. When the VIP interneurons in CA2 release enkephalin, a special type of plasticity is induced, called ITDP (Input-timing-dependent plasticity), which is fundamental for the formation of the social memory.
When the VIP interneurons in CA2 release enkephalin, a special type of plasticity is induced that is essential for the formation of social memory
“CA2 dysfunction has been linked to schizophrenia in humans and is believed to contribute to social memory deficits. A better understanding of how endogenous opioids regulate CA2 function will contribute to a better understanding of the mechanisms of the disease, ”adds Leroy.
“From the mouse models of schizophrenia we know that the CA2 zone is poorly regulated in this pathology, and that these mice cannot form social memory. What we are doing now is to see how the plasticity demonstrated in this publication can be used to rescue the ability to form said social memory in these animals ”, concludes the researcher.
Leroy, F., de Solis, CA, Boyle, LM et al. Enkephalin release from VIP interneurons in the hippocampal CA2 / 3a region mediates heterosynaptic plasticity and social memory. Mol Psychiatry (2021). DOI: 10.1038 / s41380-021-01124-y
Rights: Creative Commons.