ArticlePloS one2011
Synergistic activation of dopamine D1 and TrkB receptors mediate gain control of synaptic plasticity in the basolateral amygdala.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Exercise prescription to improve executive functioning in children and adolescents with attention deficit hyperactivity disorder: a network meta-analysis.Frontiers in psychiatry · 2026Pooled it
- Aberrant Fear: Biological Underpinnings Relevant to Psychosis, Antipsychotic Drugs, and Psychotherapeutic Treatments, a Translational Approach.International journal of molecular sciences · 2026Review
- Orexins and neuregulins as exemplars of peptide physiology in the brain: experimental challenges and implications for neuropathology.Frontiers in cellular neuroscience · 2026Article
- Parallel neuronal structural plasticity with memory trace formation in the orbitofrontal cortex.Nature communications · 2025Article
- Prenatal methadone exposure produces functional and molecular alterations in the basolateral amygdala and decreased voluntary ethanol intake in female, but not male offspring.Frontiers in behavioral neuroscience · 2025Article
- Dopamine D1-like receptors modulate synchronized oscillations in the hippocampal-prefrontal-amygdala circuit in contextual fear.Scientific reports · 2023Article
- Dopaminergic circuits underlying associative aversive learning.Frontiers in behavioral neuroscience · 2022Review
- Brain-Derived Neurotrophic Factor/Tropomyosin Receptor Kinase B Signaling Controls Excitability and Long-Term Depression in Oval Nucleus of the BNST.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- The physiology of regulated BDNF release.Cell and tissue research · 2020Review
- Neurotrophin signalling in amygdala-dependent cued fear learning.Cell and tissue research · 2020Review
- A VTA to Basal Amygdala Dopamine Projection Contributes to Signal Salient Somatosensory Events during Fear Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Kir6.1 Heterozygous Mice Exhibit Aberrant Amygdala-Dependent Cued Fear Memory.Molecular neurobiology · 2020Article
- Dopamine D1 and Glutamate Receptors Co-operate With Brain-Derived Neurotrophic Factor (BDNF) and TrkB to Modulate ERK Signaling in Adult Striatal Slices.Frontiers in cellular neuroscience · 2020Article
- Aberrant Amygdala-Dependent Cued Fear Memory in NaMolecular neurobiology · 2019Article
- PSD95 and nNOS interaction as a novel molecular target to modulate conditioned fear: relevance to PTSD.Translational psychiatry · 2018Article
- RDoC-based categorization of amygdala functions and its implications in autism.Neuroscience and biobehavioral reviews · 2018Review
- Repeated shock stress facilitates basolateral amygdala synaptic plasticity through decreased cAMP-specific phosphodiesterase type IV (PDE4) expression.Brain structure & function · 2018Article
- Serotonin gating of cortical and thalamic glutamate inputs onto principal neurons of the basolateral amygdala.Neuropharmacology · 2017Article
- Connections of the Mouse Orbitofrontal Cortex and Regulation of Goal-Directed Action Selection by Brain-Derived Neurotrophic Factor.Biological psychiatry · 2017Article
- Developmental disruption of amygdala transcriptome and socioemotional behavior in rats exposed to valproic acid prenatally.Molecular autism · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Fear memory formation is thought to require dopamine, brain-derived neurotrophic factor (BDNF) and zinc release in the basolateral amygdala (BLA), as well as the induction of long term potentiation (LTP) in BLA principal neurons. However, no study to date has shown any relationship between these processes in the BLA. Here, we have used in vitro whole-cell patch clamp recording from BLA principal neurons to investigate how dopamine, BDNF, and zinc release may interact to modulate the LTP induction in the BLA. LTP was induced by either theta burst stimulation (TBS) protocol or spaced 5 times high frequency stimulation (5xHFS). Significantly, both TBS and 5xHFS induced LTP was fully blocked by the dopamine D1 receptor antagonist, SCH23390. LTP induction was also blocked by the BDNF scavenger, TrkB-FC, the zinc chelator, DETC, as well as by an inhibitor of matrix metalloproteinases (MMPs), gallardin. Conversely, prior application of the dopamine reuptake inhibitor, GBR12783, or the D1 receptor agonist, SKF39393, induced robust and stable LTP in response to a sub-threshold HFS protocol (2xHFS), which does not normally induce LTP. Similarly, prior activation of TrkB receptors with either a TrkB receptor agonist, or BDNF, also reduced the threshold for LTP-induction, an effect that was blocked by the MEK inhibitor, but not by zinc chelation. Intriguingly, the TrkB receptor agonist-induced reduction of LTP threshold was fully blocked by prior application of SCH23390, and the reduction of LTP threshold induced by GBR12783 was blocked by prior application of TrkB-FC. Together, our results suggest a cellular mechanism whereby the threshold for LTP induction in BLA principal neurons is critically dependent on the level of dopamine in the extracellular milieu and the synergistic activation of postsynaptic D1 and TrkB receptors. Moreover, activation of TrkB receptors appears to be dependent on concurrent release of zinc and activation of MMPs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.