# Hebrew University: nitric oxide feedback loop sustains synaptic potentiation in octopus brain

- Published: 2026-11-06 03:40 UTC
- Section: Life & Health › Neurotechnology
- Tags: octopus memory, nitric oxide synthase, long-term potentiation, Octopus vulgaris, vertical lobe, molecular switch, synaptic plasticity, Hebrew University, Journal of Neuroscience
- URL: https://realtech.media/news/rt-e21bd2abb0bfd5e4230f54f4_hebrew_university_nitric/

**Experiments on the vertical lobe of Octopus vulgaris show nitric oxide maintains long-term potentiation through persistent NOS activation, reported in Journal of Neuroscience.**

![Hebrew University: nitric oxide feedback loop sustains synaptic potentiation in octopus brain](https://sgzwpqqelzmajkcubgkl.supabase.co/storage/v1/object/public/rt-media/2026/11/b24b83374452ba25.jpg)
*Diego Delso, Wikimedia Commons, CC BY-SA 4.0*

A team led by Ana Luiza Turchetti-Maia, Tal Shomrat and Binyamin Hochner from the Hebrew University of Jerusalem and Ruppin Academic Center has described a nitric oxide (NO)-dependent mechanism that maintains strengthened synaptic connections in the octopus brain. The experimental study on Octopus vulgaris was published in the Journal of Neuroscience. [1]

The work focused on the vertical lobe, a brain region on which the octopus's learning capability depends. Synaptic input into this lobe shows robust activity-dependent long-term potentiation (LTP), a process widely considered one of the fundamental cellular mechanisms of learning and memory. The molecular steps behind it were only partially understood. [1]

## Role of nitric oxide in LTP

The authors report that, contrary to the prevailing view, NO does not mediate LTP induction in the octopus vertical lobe. Tetanization-induced LTP occurred even in the presence of inhibitors of NO synthase (NOS), the enzyme that produces NO. [1]

However, NOS inhibitors blocked the long-term presynaptic expression of LTP, and high doses of an NO donor induced short-term synaptic potentiation. The authors interpret this as evidence that a persistent rise in NO concentration mediates LTP expression. [1]

## Molecular switch and maintenance

In a distinct group of synapses, NOS inhibitors also disrupted LTP maintenance. After the drug was washed out, high-frequency stimulation reinstated full LTP, which suggests that NO is involved in maintaining it. [1]

The authors propose a molecular-switch mechanism: a positive feedback loop in which NO-dependent reactivation of NOS sustains its persistent activation, thereby maintaining LTP. Retrograde diffusion of NO then facilitates presynaptic transmitter release, which drives LTP expression. [1]

According to the study's press release, this process can maintain LTP without the production of new proteins, unlike many well-studied forms of memory-related plasticity in vertebrates. The authors say the findings show how adaptation of molluscan molecular mechanisms contributed to the advanced cognitive abilities of octopuses. [1]

## Sources

1. [Journal of Neuroscience](https://doi.org/10.1523/JNEUROSCI.1676-25.2026)
2. [EurekAlert](https://www.eurekalert.org/news-releases/1150577)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-e21bd2abb0bfd5e4230f54f4_hebrew_university_nitric/