Fear erasure in mice requires synergy between antidepressant drugs and extinction training
Open accessAbstract
Long-term loss of fearful memories can be achieved through a combination of antidepressant drugs and exposure therapy.
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Results from animal and human subjects suggest enhancement of neuronal plasticity as a result of elevated 5-HT levels after treatment with SSRIs.
“Moreover, results from animal (Karpova et al., 2011;Piubelli et al., 2011;Vetencourt et al., 2008;Vetencourt et al., 2011) and human subjects (Boldrini et al., 2013;Kraus et al., 2014;Nitsche et al., 2009;Serra-Millas et al., 2011) suggest enhancement of neuronal plasticity as a result of elevated 5-HT levels after treatment with SSRIs.”
From Serotonin and neuroplasticity – Links between molecular, functional and structural pathophysiology in depression (2017) · cites this paper as Karpova et al., 2011
The Abstract reports that fluoxetine increased synaptic plasticity in mice, and the passage on lateral-amygdala recordings reports greater potentiation after treatment. The paper does not show that elevated 5-HT levels caused that increase; it identifies local BDNF as part of the observed mechanism. This citation appears in the animal-subject group, so it is not being asked to support the sentence's human-subject component. (LLM, conf=0.86)
Experimental — accuracy not yet measuredTypical antidepressants, with chronic treatment, produce a slow increase in neurotrophic factor expression and enhance synaptic plasticity.
“In contrast to the effects of stress and depression, typical antidepressants, with chronic treatment, produce a slow increase in neurotrophic factor expression and enhance synaptic plasticity.”
From Synaptic Dysfunction in Depression: Potential Therapeutic Targets (2012) · cites this paper as [42]
The paper reports that chronic fluoxetine increased BDNF expression and enhanced synaptic plasticity in mice (passages labeled Abstract, page unavailable). It does not establish that the increase was slow or that these effects apply to typical antidepressants as a class. (LLM, conf=0.85)
Experimental — accuracy not yet measuredOwing to animal experiments and optogenetics, the molecular and cellular mechanisms of fear conditioning in the amygdala are increasingly understood.
“Owing to the availability of elegant animal experiments (Karpova et al., 2011) and experimental techniques such as optogenetics, the molecular and cellular mechanisms of fear conditioning in the amygdala, are increasingly understood (Johansen et al., 2011;Rodrigues et al., 2004).”
From Serotonin and neuroplasticity – Links between molecular, functional and structural pathophysiology in depression (2017) · cites this paper as Karpova et al., 2011
The effects of the traditional antidepressant fluoxetine on synaptic plasticity and fear extinction are dependent on BDNF.
“the effects of the traditional antidepressant fluoxetine on synaptic plasticity and fear extinction have been shown to be dependent on BDNF (141, 142)”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [141]
Antidepressants reactivate early-life plasticity also in mood-relevant circuitry.
“Importantly, antidepressants reactivate early-life plasticity also in mood-relevant circuitry (Autry et al., 2011;Karpova et al., 2011;Duman, 2018)”
From Psychedelics and Neural Plasticity: Therapeutic Implications (2022) · cites this paper as Karpova et al., 2011
Reopening of critical periods in adulthood has been shown for several pharmacological manipulations, including fluoxetine, ketamine, R,R-HNK, and MDMA.
“An example of this is the reopening of critical periods in adulthood which has been shown for a number of pharmacological manipulations, including fluoxetine (Maya Vetencourt et al., 2008;Karpova et al., 2011), ketamine (Grieco et al., 2020;Casarotto et al., 2021), R,R-HNK (Cannarozzo et al., 2022), and MDMA (Nardou et al., 2019).”
From Psychedelics and Neural Plasticity: Therapeutic Implications (2022) · cites this paper as Karpova et al., 2011
Fluoxetine's effects on fear extinction depend on BDNF signaling.
“the effects of fluoxetine on fear extinction were also dependent on BDNF signaling”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [143]
Chronic oral fluoxetine induces markers of juvenile-like plasticity and promotes LTP in the amygdala.
“Chronic peroral fluoxetine exposure induces markers of critical period-like plasticity and promotes LTP in the amygdala”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [143]
Fluoxetine's effects on fear extinction appear only when fluoxetine treatment is combined with extinction training.
“were apparent only when fluoxetine treatment was combined with rehabilitation, in this case extinction training143.”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [143]
When fluoxetine treatment is combined with extinction training, it reactivates the ability to suppress fearful memories.
“These effects also reactivate the ability to suppress fearful memories when fluoxetine treatment is combined with extinction training143.”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [143]
iPlasticity may provide a neurobiological basis for the finding that combining antidepressant treatment with psychotherapy works better than either alone.
“iPlasticity may constitute a neurobiological basis for the observation that the combination of antidepressant treatment and psychotherapy works better than either treatment alone143.”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [143]
Pre-clinical rodent studies have shown that venlafaxine (an SNRI) and fluoxetine (an SSRI) can facilitate between-session extinction of conditioned fear.
“Pre-clinical rodent studies have shown that monoaminergic specific antidepressants such as venlafaxine (serotonin–norepinephrine reuptake inhibitor; SNRI) and fluoxetine (serotonin specific reuptake inhibitor; SSRI) can facilitate between-session extinction (79, 80) and prevent reinstatement of conditioned fear (80, 81).”
From Conditioned fear associated phenotypes as robust, translational indices of trauma-, stressor-, and anxiety-related behaviors (2014) · cites this paper as [79]
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“Furthermore, an important molecular mechanism through which fluoxetine produces extinction-associated reductions in fearmay be the transformation of adult plasticity mechanisms to a juvenile state (Karpova et al., 2011).”
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“…of critical periods in adulthood which has been shown for a number of pharmacological manipulations, including fluoxetine (Maya Vetencourt et al., 2008; Karpova et al., 2011), ketamine (Grieco et al., 2020; Casarotto et al., 2021), R,R -HNK (Cannarozzo et al., 2022), and MDMA (Nardou et al., 2019).”
Self-citationiPlasticity: Induced juvenile‐like plasticity in the adult brain as a mechanism of antidepressants
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- Authors
- Karpova, N. N., Pickenhagen, A., Lindholm, J., Tiraboschi, E., Kulesskaya, N., Ágústsdóttir, A., Antila, H., Popova, D., Akamine, Y., Sullivan, R., Hen, R., Drew, L. J., & Castrén, E.
- Affiliations
- University of Helsinki (FI)
- NYU Langone Health (US)
- Sigrid Jusélius Laboratory, Neuroscience Center, University of Helsinki, 00014 Helsinki, Finland.
- Columbia University (US)
- ORCID
- Venue
- Science
- Published
- 2011-12-23
- Volume
- 334
- Issue
- 6063
- Pages
- 1731-1734
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3929964
- OpenAlex
- W2036499082
- Cited by
- 382
- References
- 40
- Citations by year
- 2026: 14 · 2025: 14 · 2024: 21 · 2023: 20 · 2022: 25 · 2021: 34 · 2020: 20 · 2019: 26 · 2018: 26 · 2017: 34 · 2016: 26 · 2015: 21 · 2014: 33 · 2013: 39 · 2012: 27
- FWCI
- 16.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institute on Deafness and Other Communication Disorders (DC-009910, DC-003906, R01DC009910, R01DC003906)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- fear extinction, fear memory, fluoxetine, antidepressants, extinction training, synaptic plasticity, brain-derived neurotrophic factor, mood disorders
- MeSH terms
- Amygdala, Animals, Anxiety Disorders, Behavior Therapy, Combined Modality Therapy, Conditioning, Classical, Extinction, Psychological, Fear, Fluoxetine, Interneurons, Male, Memory, Mice, Inbred C57BL, Nerve Net, Synaptic Transmission, Neuronal Plasticity, Neurons, Antidepressive Agents, Second-Generation, Brain-Derived Neurotrophic Factor, Excitatory Postsynaptic Potentials, Mice
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.
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