ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2009
PKG and PKA signaling in LTP at GABAergic synapses.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- BDNF restores impaired long-term potentiation of GABAergic synapses induced by chronic ethanol exposure in the VTA and attenuates reward-seeking behavior.Molecular psychiatry · 2026Article
- Kappa Opioid Receptors Control a Stress-Sensitive Brain Circuit and Drive Cocaine Seeking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Protein Kinase A-Dependent Plasticity of Local Inhibitory Synapses from Hilar Somatostatin-Expressing Neurons.eNeuro · 2023Article
- Ethanol blocks a novel form of iLTD, but not iLTP of inhibitory inputs to VTA GABA neurons.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Sex differences in VTA GABA transmission and plasticity during opioid withdrawal.Scientific reports · 2023Article
- Advances in the Electrophysiological Recordings of Long-Term Potentiation.International journal of molecular sciences · 2023Review
- Prkg2 regulates alveolar type 2-mediated re-alveolarization.Stem cell research & therapy · 2022Article
- Nitric Oxide Signaling Pathway in Ventral Tegmental Area is Involved in Regulation of 7,8-Dihydroxyflavone on Alcohol Consumption in Rats.Molecular neurobiology · 2022Article
- Brain is modulated by neuronal plasticity during postnatal development.The journal of physiological sciences : JPS · 2021Review
- Opioid-Induced Molecular and Cellular Plasticity of Ventral Tegmental Area Dopamine Neurons.Cold Spring Harbor perspectives in medicine · 2021Review
- CB1 cannabinoid receptor-mediated plasticity of GABAergic synapses in the mouse insular cortex.Scientific reports · 2020Article
- PKG1α oxidation negatively regulates food seeking behaviour and reward.Redox biology · 2019Article
- Inhibitory Plasticity of Mesocorticolimbic Circuits in Addiction and Mental Illness.Trends in neurosciences · 2018Review
- Role of spinal GABA receptors in the acute antinociceptive response of mice to hyperbaric oxygen.Brain research · 2018Article
- Synaptic function and plasticity in identified inhibitory inputs onto VTA dopamine neurons.The European journal of neuroscience · 2018Article
- Overexpression of Thioredoxin-1 Blocks Morphine-Induced Conditioned Place Preference Through Regulating the Interaction of γ-Aminobutyric Acid and Dopamine Systems.Frontiers in neurology · 2018Article
- Differential expression of long-term potentiation among identified inhibitory inputs to dopamine neurons.Journal of neurophysiology · 2017Article
- Control of neuronal excitability by Group I metabotropic glutamate receptors.Biophysical reviews · 2017Review
- Opiates and Plasticity in the Ventral Tegmental Area.ACS chemical neuroscience · 2017Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Drugs of abuse usurp the mechanisms underlying synaptic plasticity in areas of the brain, a process that may contribute to the development of addiction. We previously reported that GABAergic synapses onto dopaminergic neurons in the ventral tegmental area (VTA) exhibit long-term potentiation (LTP(GABA)) blocked by in vivo exposure to morphine. The presynaptically maintained LTP requires the retrogradely released nitric oxide (NO) to activate a presynaptic cGMP signaling cascade. Previous work reported that inhibitory GABA(A) receptor synapses in the VTA are also potentiated by cAMP. Here, we explored the interactions between cGMP-dependent (PKG) and cAMP-dependent (PKA) protein kinases in the regulation of these GABAergic synapses and LTP(GABA). Activation of PKG was required for NO-cGMP signaling and was also essential for the induction of synaptically elicited LTP(GABA), but not for its maintenance. Synapses containing GABA(A) receptors were potentiated by NO-cGMP signaling, whereas synapses containing GABA(B) receptors on the same cells were not potentiated. Moreover, although the cAMP-PKA system potentiated GABA(A) synapses, synaptically induced LTP(GABA) was independent of PKA activation. Surprisingly, however, raising cGMP levels saturated potentiation of these synapses, precluding further potentiation by cAMP and suggesting a convergent end point for both signaling pathways in the regulation of GABAergic release. We further found that persistent GABAergic synaptic modifications observed with in vivo morphine did not involve the presynaptic cAMP-PKA cascade. Taken together, our data suggest a synapse-specific role for NO-cGMP-PKG signaling pathway in opioid-induced plasticity of VTA GABA(A) synapses.
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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.