Summary: The brain communicates through more than just lightning-fast electrical pulses; it also relies on a slow, diffuse “chemical atmosphere” to regulate our moods. A study has identified SNAP-47 as the key protein responsible for the slow release of oxytocin within the brain. While serotonin is often called the “happiness molecule,” this discovery shows that oxytocin acts as the brain’s “social thermostat,” maintaining a basal tone that primes us for connection.
Unlike the oxytocin released into the bloodstream, this internal version is released from the neuron’s center, effectively setting the stage for how we react to every person we meet. The research explains how subtle changes in this protein can dictate whether we feel socially anxious or ready to bond.
Key Facts
- The Social Thermostat: SNAP-47 acts as a background system that lowers social anxiety and boosts motivation before a social stimulus even appears.
- Beyond Serotonin: While serotonin manages general mood, SNAP-47-driven oxytocin specifically “primes” the brain for high-quality social interactions.
- The “Slow-Release” Secret: The SNAP-47 protein is uniquely designed for slow, sustained release, matching the steady “social tone” required for deep emotional bonding.
- Quality Matters: Reducing this protein doesn’t stop mice from being social, but it makes their interactions shorter and less meaningful.
- Neuropsychiatric Target: This discovery offers a new way to look at social anxiety and bonding disorders by focusing on the brain’s “basal tone” rather than just quick chemical spikes.
Source: UMH
The brain does not only communicate through fast electrical impulses; it also relies on slower, more diffuse chemical signals that modulate our emotional and social states over time.
A study led by the Institute for Neurosciences (IN), a joint center of the Spanish National Research Council (CSIC) and the Miguel Hernández University of Elche (UMH), has identified a key molecular mechanism that regulates the release of oxytocin within the brain.
Published in the journal Communications Biology, the work sheds light on how this hormone maintains a “social tone” and how its release contributes to the quality of social interactions.
Oxytocin is a hormone widely recognized for its role in emotional bonding, sociability, and emotional regulation. Unlike classical neurotransmitters such as glutamate or GABA, which are released quickly and locally from neuronal axons, oxytocin belongs to the group of neuropeptides and can also be released from the cell body (soma) and dendrites.
This slower, more diffuse type of release affects broad regions of the brain, yet its underlying molecular mechanisms have remained largely unknown—until now.
“We knew that oxytocin is released within the brain from compartments other than the axon, but we had limited understanding of how this process is regulated”, explains researcher Sandra Jurado, who leads the Synaptic Neuromodulation Laboratory at the IN CSIC-UMH and headed the study.
“Our work focuses precisely on understanding the mechanisms that enable this slow and sustained release, which likely prepares the brain for social interaction”, she adds.
A Key Protein for Unconventional Release
In this study, the team identified the protein SNAP-47 as an essential component of the machinery that enables the transport and release of oxytocin from the soma and dendrites of hypothalamic neurons—the brain region where this hormone is produced. SNAP-47 belongs to the SNARE family of proteins, which are involved in vesicle fusion and the release of chemical signals, but it displays distinctive properties.
“While other proteins in this family mediate fast and highly efficient release, SNAP-47 operates more slowly”, explains Beatriz Aznar, first author of the study. “This fits well with the type of release we observe for oxytocin within the brain, which does not occur in rapid pulses but rather in a more sustained manner”, she adds.
This difference is key to understanding oxytocin’s function in the central nervous system. Oxytocinergic neurons in the hypothalamus send their axons outside the brain to release the hormone into the bloodstream. However, within the brain, the oxytocin that modulates social behavior is largely released from the soma and dendrites of these neurons through a mechanism that is independent of axonal release.
Experiments in Cell Culture and Animal Models
To unravel this process, the team combined experiments in neuronal cultures with studies in mice. In an initial phase, they examined how reducing SNAP-47 affected vesicular trafficking and oxytocin release in cultured cells. They then extended these findings to animal models using genetic manipulations specifically targeted to oxytocin-producing neurons.
The results showed that reducing SNAP-47 expression disrupts oxytocin release from the soma and dendrites, without affecting the classical mechanism of axonal release. This alteration had functional consequences for the animals’ social behavior: although the mice still displayed sociability, their interactions were shorter and less robust.
“The effects are subtle, but highly revealing”, explains Jurado. “This is not a complete loss of sociability, but rather a fine-tuning of the quality of interactions. This suggests that this release pathway maintains a basal level of oxytocin that primes the brain to respond appropriately to social stimuli”.
The authors suggest that this mechanism may function as a background system that regulates the brain’s social state, maintaining a steady flow of oxytocin that modulates processes such as social anxiety, motivation, and the propensity to interact.
“It represents a basal tone that does not trigger strong responses on its own, but that shapes how we react when a relevant social stimulus appears”, Aznar explains.
This finding broadens our understanding of how hormonal signaling is regulated in the brain and opens new avenues of research into how subtle alterations in these mechanisms could contribute to neuropsychiatric disorders in which oxytocin plays a significant role.
“The next step will be to identify the remaining components of this molecular machinery and understand how the different modes of oxytocin release are coordinated to produce a coherent response”, Jurado concludes.
Funding: This study was made possible thanks to funding from the Spanish State Research Agency–Ministry of Science, Innovation and Universities, the Prometeo Programme of the Valencian Regional Government (Generalitat Valenciana), and the Severo Ochoa Programme for Centres of Excellence.
Key Questions Answered:
A: Not quite. Serotonin is like the “power grid” for your mood, but the SNAP-47/Oxytocin system is the “Wi-Fi signal” for your social life. You need both for a high-quality connection. This protein ensures your “social signal” stays strong even when you aren’t actively talking to someone.
A: We’re getting closer. By identifying SNAP-47 as the “thermostat” for our social vibe, scientists can now look for ways to adjust that setting. If your brain isn’t maintaining a healthy “basal tone,” social situations feel exhausting or scary rather than rewarding.
A: It’s a biological clue. Some brains may be naturally better at maintaining a high social tone through more efficient SNAP-47 activity, meaning they stay “primed” for connection while others might need more effort to get into that same state.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this oxytocin and social neuroscience research news
Author: Angeles Gallar
Source: UMH
Contact: Angeles Gallar – UMH
Image: The image is credited to Neuroscience News
Original Research: Open access.
“SNAP-47 mediates somatic oxytocin dynamics in hypothalamic neurons” by Beatriz Aznar-Escolano, Maria Royo, Maria Pilar Madrigal, Adrián Portalés Montes, José Villanueva, Luis Miguel Gutiérrez & Sandra Jurado. Communications Biology
DOI:10.1038/s42003-025-09442-5
Abstract
SNAP-47 mediates somatic oxytocin dynamics in hypothalamic neurons
The neuropeptide oxytocin (OT) plays a crucial role in regulating homeostatic responses and complex behaviors, including social interaction. OT can be released from somatodendritic regions, enabling communication through retrograde, autocrine, and volume transmission.
However, the mechanisms governing somatodendritic OT dynamics and their impact on neuronal function and behavior are not yet fully understood.
Our study identifies SNAP-47, a member of the SNAP-25 protein family highly expressed in the soma of peptidergic neurons in the mouse hypothalamus, where it exhibits a close interaction with OT-containing compartments localized at the plasma membrane.
Knocking down SNAP-47 diminishes the recruitment of OT to the plasma membrane in the cell body under both basal conditions and following neuronal stimulation.
Reducing endogenous SNAP-47 expression in vivo results in altered spontaneous synaptic transmission in oxytocinergic neurons of the paraventricular nucleus (PVN) and decreases sociability, likely due to disrupted somatic trafficking.
These findings provide new insights into the molecular mechanisms governing somatic OT dynamics, its influence on hypothalamic neuromodulation, and its role in OT-dependent behaviors such as social interaction.
