ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013
NPY Y1 receptors differentially modulate GABAA and NMDA receptors via divergent signal-transduction pathways to reduce excitability of amygdala neurons.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Chemical multiplexing in the nervous system: molecular architecture, functional stratification, and pathophysiological plasticity of neuropeptide-classical neurotransmitter cotransmission.Frontiers in molecular neuroscience · 2026Review
- Nanoparticle-encapsulated neuropeptide Y provides robust seizure protection in SCN1A-derived epilepsy.Epilepsia · 2026Article
- Hippocampal dipeptidyl peptidase 9 bidirectionally regulates memory associated with synaptic plasticity.Journal of advanced research · 2025Article
- Modulation of temporoammonic-CA1 synapses by neuropeptide Y is through Y1 receptors in mice.Neuropeptides · 2025Article
- NPY-mediated synaptic plasticity in the extended amygdala prioritizes feeding during starvation.Nature communications · 2024Article
- Basolateral amygdala neuropeptide Y system modulates binge ethanol consumption.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- The plasticity of neuropeptide Y-Y1 receptor system onTheranostics · 2024Article
- Endocannabinoid Hydrolase Inhibitors: Potential Novel Anxiolytic Drugs.Drug design, development and therapy · 2024Review
- Convergent Energy State-Dependent Antagonistic Signaling by Cocaine- and Amphetamine-Regulated Transcript (CART) and Neuropeptide Y (NPY) Modulates the Plasticity of Forebrain Neurons to Regulate Feeding in Zebrafish.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Hunting for Genes Underlying Emotionality in the Laboratory Rat: Maps, Tools and Traps.Current neuropharmacology · 2023Review
- Neuropeptide Y modulates excitatory synaptic transmission and promotes social behavior in the mouse nucleus accumbens.Neuropharmacology · 2022Article
- GABAergic circuits of the basolateral amygdala and generation of anxiety after traumatic brain injury.Amino acids · 2022Review
- Avian Neuropeptide Y: Beyond Feed Intake Regulation.Veterinary sciences · 2022Review
- Neuropeptide System Regulation of Prefrontal Cortex Circuitry: Implications for Neuropsychiatric Disorders.Frontiers in neural circuits · 2022Review
- Neuropeptide Y Reduces Nasal Epithelial T2R Bitter Taste Receptor-Stimulated Nitric Oxide Production.Nutrients · 2021Article
- Contribution of NPY YThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Panic results in unique molecular and network changes in the amygdala that facilitate fear responses.Molecular psychiatry · 2020Article
- Electro-Acupuncture Attenuates Chronic Stress ResponsesFrontiers in neuroscience · 2020Article
- Moderate maternal separation mitigates the altered synaptic transmission and neuronal activation in amygdala by chronic stress in adult mice.Molecular brain · 2019Article
- NPYThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Neuropeptide Y (NPY) administration into the basolateral amygdala (BLA) decreases anxiety-like behavior, mediated in part through the Y1 receptor (Y1R) isoform. Activation of Y1Rs results in G-protein-mediated reduction of cAMP levels, which results in reduced excitability of amygdala projection neurons. Understanding the mechanisms linking decreased cAMP levels to reduced excitability in amygdala neurons is important for identifying novel anxiolytic targets. We studied the intracellular mechanisms of activation of Y1Rs on synaptic transmission in the BLA. Activating Y1Rs by [Leu(31),Pro(34)]-NPY (L-P NPY) reduced the amplitude of evoked NMDA-mediated excitatory postsynaptic currents (eEPSCs), without affecting AMPA-mediated eEPSCs, but conversely increased the amplitude of GABAA-mediated evoked inhibitory postsynaptic currents (eIPSCs). Both effects were abolished by the Y1R antagonist, PD160170. Intracellular GDP-β-S, or pre-treatment with either forskolin or 8Br-cAMP, eliminated the effects of L-P NPY on both NMDA- and GABAA-mediated currents. Thus, both the NMDA and GABAA effects of Y1R activation in the BLA are G-protein-mediated and cAMP-dependent. Pipette inclusion of protein kinase A (PKA) catalytic subunit blocked the effect of L-P NPY on GABAA-mediated eIPSCs, but not on NMDA-mediated eEPSCs. Conversely, activating the exchange protein activated by cAMP (Epac) with 8CPT-2Me-cAMP blocked the effect of L-P NPY on NMDA-mediated eEPSCs, but not on GABAA-mediated eIPSCs. Thus, NPY regulates amygdala excitability via two signal-transduction events, with reduced PKA activity enhancing GABAA-mediated eIPSCs and Epac deactivation reducing NMDA-mediated eEPSCs. This multipathway regulation of NMDA- and GABAA-mediated currents may be important for NPY plasticity and stress resilience in the amygdala.
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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.