ArticleThe Journal of physiology2014
Bidirectional regulation of synaptic plasticity in the basolateral amygdala induced by the D1-like family of dopamine receptors and group II metabotropic glutamate receptors.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
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- Blockade of Dopamine D3 Receptors in the Ventral Tegmental Area Mitigates Fear Memory Generalization.International journal of molecular sciences · 2025Article
- Regulator of G protein signalling 14 (RGS14) protein expression profile in the adult mouse brain.The European journal of neuroscience · 2024Article
- Neuronal excitation-inhibition imbalance in the basolateral amygdala is involved in propofol-mediated enhancement of fear memory.Communications biology · 2024Article
- Dopamine projections to the basolateral amygdala drive the encoding of identity-specific reward memories.Nature neuroscience · 2024Article
- Advances in translating mGluPharmacology, biochemistry, and behavior · 2022Review
- Metaplasticity at the addicted tetrapartite synapse: A common denominator of drug induced adaptations and potential treatment target for addiction.Neurobiology of learning and memory · 2018Review
- Metabotropic Glutamate Receptors in Alcohol Use Disorder: Physiology, Plasticity, and Promising Pharmacotherapies.ACS chemical neuroscience · 2018Article
- Effect of long-term treatment with classical neuroleptics on NPQ/spexin, kisspeptin and POMC mRNA expression in the male rat amygdala.Journal of neural transmission (Vienna, Austria : 1996) · 2018Article
- Closing the gap: long-term presynaptic plasticity in brain function and disease.Current opinion in neurobiology · 2017Review
- An intra-amygdala circuit specifically regulates social fear learning.Nature neuroscience · 2017Article
- Developmental disruption of amygdala transcriptome and socioemotional behavior in rats exposed to valproic acid prenatally.Molecular autism · 2017Article
- Stress-Induced Reinstatement of Nicotine Preference Requires Dynorphin/Kappa Opioid Activity in the Basolateral Amygdala.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Resolving Behavioral Output via Chemogenetic Designer Receptors Exclusively Activated by Designer Drugs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Review
- Combining Dopaminergic Facilitation with Robot-Assisted Upper Limb Therapy in Stroke Survivors: A Focused Review.American journal of physical medicine & rehabilitation · 2016Review
- Amygdala-prefrontal interactions in (mal)adaptive learning.Trends in neurosciences · 2015Review
- Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Competing mechanisms of long-term potentiation (LTP) and long-term depression (LTD) in principal neurons of the basolateral amygdala (BLA) are thought to underlie the acquisition and consolidation of fear memories, and their subsequent extinction. However, no study to date has examined the locus of action and/or the cellular mechanism(s) by which these processes interact. Here, we report that synaptic plasticity in the cortical pathway onto BLA principal neurons is frequency-dependent and shows a transition from LTD to LTP at stimulation frequencies of ∼10 Hz. At the crossover point from LTD to LTP induction we show that concurrent activation of D1 and group II metabotropic glutamate (mGluR2/3) receptors act to nullify any net change in synaptic strength. Significantly, blockade of either D1 or mGluR2/3 receptors unmasked 10 Hz stimulation-induced LTD and LTP, respectively. Significantly, prior activation of presynaptic D1 receptors caused a time-dependent attenuation of mGluR2/3-induced depotentiation of previously induced LTP. Furthermore, studies with cell type-specific postsynaptic transgene expression of designer receptors activated by designer drugs (DREADDs) suggest that the interaction results via bidirectional modulation of adenylate cyclase activity in presynaptic glutamatergic terminals. The results of our study raise the possibility that the temporal sequence of activation of either presynaptic D1 receptors or mGluR2/3 receptors may critically regulate the direction of synaptic plasticity in afferent pathways onto BLA principal neurons. Hence, the interaction of these two neurotransmitter systems may represent an important mechanism for bidirectional metaplasticity in BLA circuits and thus modulate the acquisition and extinction of fear memory.
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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.