Vasopressin and Oxytocin Excite Distinct Neuronal Populations in the Central Amygdala
Abstract
Vasopressin and oxytocin strongly modulate autonomic fear responses, through mechanisms that are still unclear. We describe how these neuropeptides excite distinct neuronal populations in the central amygdala, which provides the major output of the amygdaloid complex to the autonomic nervous system. We identified these two neuronal populations as part of an inhibitory network, through which vasopressin and oxytocin modulate the integration of excitatory information from the basolateral amygdala and cerebral cortex in opposite manners. Through this network, the expression and endogenous activation of vasopressin and oxytocin receptors may regulate the autonomic expression of fear.
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In the central amygdala, the medial part relates to fear and the lateral part to anxiety, and only the lateral part has abundant oxytocin receptors.
“The medial CeA (mCeA) and lateral CeA (lCeA) are involved in fear and anxiety,5 respectively, but only the lCeA is rich in OT receptors.6”
From Oxytocin increases anxiety to unpredictable threat (2013) · cites this paper as [6]
Within the rodent central amygdala, oxytocin receptor density differs across subdivisions.
“OT receptor density varies by subdivision within the central nucleus of the rodent amygdala (CeA)4,6”
From Oxytocin increases anxiety to unpredictable threat (2013) · cites this paper as [6]
OT is a neuromodulator with both excitatory and inhibitory effects in neurons of the central amygdala, suggesting that the behavioral effect of OT can go both ways.
“the finding that, at the cellular level, OT is a neuromodulator with both excitatory and inhibitory effects in neurons of the central amygdala (Huber et al., 2005) suggests that the behavioral effect of OT can go both ways.”
From The effect of oxytocin on cooperation in a prisoner's dilemma depends on the social context and a person's social value orientation (2014) · cites this paper as Huber et al., 2005
OXT can inhibit neurons in the centromedial amygdala through excitatory effects on GABAergic projections from the lateral and capsular central nucleus, disrupting integration of information and inhibiting amygdala output to fear-responding areas.
“Although the mechanisms of these effects are unclear, it has been shown that OXT can inhibit neurons in the centromedial amygdala through its excitatory effects on g-aminobutyric acid (GABA) inhibitory (GABAergic) projections that originate from the lateral and capsular part of the central nucleus of the amygdala, which disrupts integration of information and inhibits amygdala output to areas of”
From Oxytocin modulation of amygdala functional connectivity to fearful faces in generalized social anxiety disorder (2015) · cites this paper as Huber et al, 2005
OXT promotes GABAergic inhibition in the amygdala, making the amygdala a good candidate target for OXT's effects.
“The amygdala is a good candidate target for OXT's effects given that, like other anxiolytic pharmacotherapies, OXT promotes GABAergic inhibition in the amygdala (Huber et al, 2005).”
From Oxytocin modulation of amygdala functional connectivity to fearful faces in generalized social anxiety disorder (2015) · cites this paper as Huber et al, 2005
Distinct neuronal populations in sub-regions of the amygdala control specific behavioral responses to fear.
“Distinct neuronal populations in sub-regions of the amygdala have indeed been shown to control specific behavioral responses to fear [104, 108]”
From Oxytocin Signaling in the Central Amygdala Modulates Emotion Discrimination in Mice (2019) · cites this paper as [108]
Previous studies have shown that oxytocin receptors in the amygdala potentiate GABAergic inhibition.
“Previous studies have shown that OXT receptors in the amygdala potentiate GABAergic inhibition (ie, Huber et al, 2005;Viviani et al, 2011).”
From Modulation of Resting-State Amygdala-Frontal Functional Connectivity by Oxytocin in Generalized Social Anxiety Disorder (2014) · cites this paper as Huber et al, 2005
OT injection in lateral part of central amygdala stimulates GABAergic interneurons, leading to increased rate of inhibitory postsynaptic activity in central medial amygdala.
“OT injection in the lateral part of central amygdala stimulates GABAergic interneurons, leading to an increase in the rate of inhibitory postsynaptic activity in the central medial amygdala (Huber et al. 2005).”
From A precision medicine approach to oxytocin trials (2017) · cites this paper as Huber et al. 2005
In rats, oxytocinergic neurons regulate autonomic fear responses through a specialized circuit via the central amygdala.
“For mediating fear-related responses, it has been verified in rats that oxytocinergic neurons regulate autonomic fear responses through a specialized circuit via the central amygdala (Huber, 2005; Viviani et al., 2011).”
From Oxytocin and social cognition in rhesus macaques: Implications for understanding and treating human psychopathology (2014) · cites this paper as Huber, 2005
In preclinical studies, oxytocin has been shown to facilitate extinction and generally inhibit anxiety and fear-related responses and behaviours in rodents.
“In preclinical studies, oxytocin has been shown to facilitate extinction and generally inhibit anxietyand fear-related responses and behaviours in rodents (Calcagnoli et al., 2015;Huber et al., 2005;Neumann and Slattery, 2016;Viviani et al., 2011).”
From Meta-analytic review of the effects of a single dose of intranasal oxytocin on threat processing in humans (2018) · cites this paper as Huber et al., 2005
OT may have anxiolytic properties, possibly by inhibiting fear-associated output of the central amygdala to the brainstem and hypothalamus.
“Our findings extend accumulating evidence that OT may have anxiolytic properties, possibly by inhibiting fear-associated output of the central amygdala to the brainstem and hypothalamus (Huber et al, 2005).”
From Intranasal oxytocin administration dampens amygdala reactivity towards emotional faces in male and female PTSD patients (2016) · cites this paper as Huber et al, 2005
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- Authors
- Huber, D., Veinante, P., & Stoop, R.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Stoop, Ron
- Venue
- Science
- Published
- 2005-04-08
- Volume
- 308
- Issue
- 5719
- Pages
- 245-248
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W1998872047
- Cited by
- 804
- References
- 28
- Citations by year
- 2026: 15 · 2025: 19 · 2024: 25 · 2023: 18 · 2022: 32 · 2021: 43 · 2020: 56 · 2019: 30 · 2018: 47 · 2017: 50 · 2016: 38 · 2015: 60 · 2014: 45 · 2013: 47 · 2012: 52
- FWCI
- 44.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Topics
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- vasopressin, oxytocin, central amygdala, neuropeptide receptors, basolateral amygdala, cerebral cortex, fear expression
- MeSH terms
- Amygdala, Animals, Autoradiography, Fear, gamma-Aminobutyric Acid, Neurons, Oxytocin, Tetrodotoxin, Vasopressins, Rats, Sprague-Dawley, Receptors, Vasopressin, Receptors, Oxytocin, Patch-Clamp Techniques, Rats, Antidiuretic Hormone Receptor Antagonists, In Vitro Techniques
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