ArticleFrontiers in integrative neuroscience2014
Acute morphine alters GABAergic transmission in the central amygdala during naloxone-precipitated morphine withdrawal: role of cyclic AMP.
Article in Frontiers in integrative neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Association between aperiodic activity and impulsivity in individuals with methamphetamine use disorder.Psychopharmacology · 2026Article
- Parabrachial CGRP Neurons Regulate Opioid Reinforcement.bioRxiv : the preprint server for biology · 2026Article
- Crosstalk Between Glycinergic and N-Methyl-D-Aspartate Receptor-Mediated Glutamatergic Transmission in Behaviours Associated with Opioid Use Disorder.International journal of molecular sciences · 2025Review
- Calcium imaging of central amygdala activity after escalation of fentanyl self-administration.Neuropharmacology · 2025Article
- YTHDF1 in periaqueductal gray inhibitory neurons contributes to morphine withdrawal responses in mice.BMC medicine · 2024Article
- Opioid withdrawal: role in addiction and neural mechanisms.Psychopharmacology · 2023Review
- Repeated ketamine anesthesia during neurodevelopment upregulates hippocampal activity and enhances drug reward in male mice.Communications biology · 2022Article
- Similarities in alcohol and opioid withdrawal syndromes suggest common negative reinforcement mechanisms involving the interoceptive antireward pathway.Neuroscience and biobehavioral reviews · 2021Review
- Self-Administration of Entactogen Psychostimulants Dysregulates Gamma-Aminobutyric Acid (GABA) and Kappa Opioid Receptor Signaling in the Central Nucleus of the Amygdala of Female Wistar Rats.Frontiers in behavioral neuroscience · 2021Article
- Silver nanoparticles (Ag-NPs) in the central amygdala protect the rat conditioned by morphine from withdrawal attack due to naloxone via high-level nitric oxide.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- The amygdalar opioid system.Handbook of behavioral neuroscience · 2020Article
- Fentanyl Inhibits Air Puff-Evoked Sensory Information Processing in Mouse Cerebellar Neurons RecordedFrontiers in systems neuroscience · 2020Article
- Differential effects of novel kappa opioid receptor antagonists on dopamine neurons using acute brain slice electrophysiology.PloS one · 2020Article
- Mu opioid receptor regulation of glutamate efflux in the central amygdala in response to predator odor.Neurobiology of stress · 2019Article
- Estimating Mental Health Conditions of Patients with Opioid Use Disorder.Journal of addiction · 2019Article
- Inhibition of GABAergic Neurotransmission by HIV-1 Tat and Opioid Treatment in the Striatum Involves μ-Opioid Receptors.Frontiers in neuroscience · 2016Article
- The addicted brain: understanding the neurophysiological mechanisms of addictive disorders.Frontiers in integrative neuroscience · 2015Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
The central amygdala (CeA) plays an important role in opioid addiction. Therefore, we examined the effects of naloxone-precipitated morphine withdrawal (WD) on GABAergic transmission in rat CeA neurons using whole-cell recordings with naloxone in the bath. The basal frequency of miniature inhibitory postsynaptic currents (mIPSCs) increased in CeA neurons from WD compared to placebo rats. Acute morphine (10 μ M) had mixed effects (≥20% change from baseline) on mIPSCs in placebo and WD rats. In most CeA neurons (64%) from placebo rats, morphine significantly decreased mIPSC frequency and amplitude. In 32% of placebo neurons, morphine significantly increased mIPSC amplitudes but had no effect on mIPSC frequency. In WD rats, acute morphine significantly increased mIPSC frequency but had no effect on mIPSC amplitude in 41% of CeA neurons. In 45% of cells, acute morphine significantly decreased mIPSC frequency and amplitude. Pre-treatment with the cyclic AMP inhibitor (R)-adenosine, cyclic 3',5'-(hydrogenphosphorothioate) triethylammonium (RP), prevented acute morphine-induced potentiation of mIPSCs. Pre-treatment of slices with the Gi/o G-protein subunit inhibitor pertussis toxin (PTX) did not prevent the acute morphine-induced enhancement or inhibition of mIPSCs. PTX and RP decreased basal mIPSC frequencies and amplitudes only in WD rats. The results suggest that inhibition of GABAergic transmission in the CeA by acute morphine is mediated by PTX-insensitive mechanisms, although PTX-sensitive mechanisms cannot be ruled out for non-morphine responsive cells; by contrast, potentiation of GABAergic transmission is mediated by activated cAMP signaling that also mediates the increased basal GABAergic transmission in WD rats. Our data indicate that during the acute phase of WD, the CeA opioid and GABAergic systems undergo neuroadaptative changes conditioned by a previous chronic morphine exposure and dependence.
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