BLA to vHPC inputs modulate anxiety-related behaviors
Open accessAbstract
The basolateral amygdala (BLA) and ventral hippocampus (vHPC) have both been implicated in mediating anxiety-related behaviors, but the functional contribution of BLA inputs to the vHPC has never been directly investigated. Here we show that activation of BLA-vHPC synapses acutely and robustly increased anxiety-related behaviors, while inhibition of BLA-vHPC synapses decreased anxiety-related behaviors. We combined optogenetic approaches with in vivo pharmacological manipulations and ex vivo whole-cell patch-clamp recordings to dissect the local circuit mechanisms, demonstrating that activation of BLA terminals in the vHPC provided monosynaptic, glutamatergic inputs to vHPC pyramidal neurons. Furthermore, BLA inputs exerted polysynaptic, inhibitory effects mediated by local interneurons in the vHPC that may serve to balance the circuit locally. These data establish a role for BLA-vHPC synapses in bidirectionally controlling anxiety-related behaviors in an immediate, yet reversible, manner and a model for the local circuit mechanism of BLA inputs in the vHPC.
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Optogenetic or pharmacological stimulation of the vHIP increases anxiety-like behavior.
“while optogenetic or pharmacological stimulation of the region has the opposite effect (16–18).”
From Perineuronal nets, inhibitory interneurons and anxiety-related ventral hippocampal neuronal oscillations are altered by early life adversity (2019) · cites this paper as [17]
BLA projection neurons innervating the nucleus accumbens and ventral hippocampus primarily encode information with positive and negative valence, respectively.
“This work has, for instance, proposed that BLA PNs innervating the NAc and vHPC primarily encode information with positive and negative valence, respectively (17,20,22,23).”
From Chronic Stress Remodels Synapses in an Amygdala Circuit-Specific Manner (2019) · cites this paper as [22]
Photostimulating BLA PNs targeting the vHPC increases anxiety-like behavior and reduces social interaction.
“Recent optogenetic studies have shown that photostimulating BLA PNs targeting the vHPC increases anxiety-like behavior and reduces social interaction, whereas photosilencing this pathway has the opposite effects, and, conversely, stimulating NAc-targeting BLA PNs promotes reward-seeking (20,22,23,39).”
From Chronic Stress Remodels Synapses in an Amygdala Circuit-Specific Manner (2019) · cites this paper as [22]
Photosilencing the BLA→vHPC pathway has effects opposite to photostimulation.
“Recent optogenetic studies have shown that photostimulating BLA PNs targeting the vHPC increases anxiety-like behavior and reduces social interaction, whereas photosilencing this pathway has the opposite effects, and, conversely, stimulating NAc-targeting BLA PNs promotes reward-seeking (20,22,23,39).”
From Chronic Stress Remodels Synapses in an Amygdala Circuit-Specific Manner (2019) · cites this paper as [22]
Stimulating NAc-targeting BLA PNs promotes reward-seeking.
“Recent optogenetic studies have shown that photostimulating BLA PNs targeting the vHPC increases anxiety-like behavior and reduces social interaction, whereas photosilencing this pathway has the opposite effects, and, conversely, stimulating NAc-targeting BLA PNs promotes reward-seeking (20,22,23,39).”
From Chronic Stress Remodels Synapses in an Amygdala Circuit-Specific Manner (2019) · cites this paper as [22]
Principal neurons and interneurons in the BLA receive monosynaptic input from the mPFC and vHPC, and send reciprocal projections to both of these regions.
“principal neurons and interneurons in the BLA have been shown to receive monosynaptic input from mPFC and vHPC, and send reciprocal projections to both of these regions66-68.”
From Resolving the neural circuits of anxiety (2015) · cites this paper as [66]
Glutamatergic terminals of BLA fibers onto pyramidal neurons in the CA1 region of the vHPC bidirectionally control innate anxiety-related behaviors in the EPM and OFT, such that increased activity in this projection enhances anxiety-like behavior and inactivation reduces anxiety-like behavior.
“Furthermore, glutamatergic terminals of BLA fibers onto pyramidal neurons in the CA1 region of the vHPC bidirectionally control innate anxiety-related behaviors in the EPM and OFT66, such that increased activity in this projection enhances anxiety-like behavior and inactivation of this pathway reduces anxiety-like behavior27,66.”
From Resolving the neural circuits of anxiety (2015) · cites this paper as [66]
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- Authors
- Felix-Ortiz, A. C., Beyeler, A., Seo, C., Leppla, C. A., Wildes, C. P., & Tye, K. M.
- Affiliations
- Massachusetts Institute of Technology (US)
- Corresponding author
- Tye, Kay M.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2013-08
- Volume
- 79
- Issue
- 4
- Pages
- 658-664
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC4205569
- OpenAlex
- W1997982013
- Cited by
- 592
- References
- 28
- Citations by year
- 2026: 45 · 2025: 38 · 2024: 55 · 2023: 64 · 2022: 52 · 2021: 63 · 2020: 47 · 2019: 48 · 2018: 46 · 2017: 34 · 2016: 31 · 2015: 37 · 2014: 30 · 2013: 2
- FWCI
- 18.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-sa)
- Funders
- Howard Hughes Medical Institute
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (143586)
- National Institute of Mental Health (R01MH102441)
- National Institute of Diabetes and Digestive and Kidney Diseases (DP2DK102256)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- basolateral amygdala, ventral hippocampus, anxiety-like behavior, glutamatergic input, pyramidal neurons, local interneurons, polysynaptic inhibition, monosynaptic excitation, optogenetics, whole-cell patch clamp
- MeSH terms
- Channelrhodopsins, Amygdala, Animals, Anxiety, Bacterial Proteins, Disease Models, Animal, Exploratory Behavior, Hippocampus, Luminescent Proteins, Male, Membrane Potentials, Mice, Inbred C57BL, Mice, Transgenic, Neural Pathways, Neurons, Synapses, Tetrodotoxin, Valine, Excitatory Amino Acid Antagonists, 6-Cyano-7-nitroquinoxaline-2,3-dione, Maze Learning, Halorhodopsins, Sodium Channel Blockers, Mice, Calcium-Calmodulin-Dependent Protein Kinase Type 2, In Vitro Techniques
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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