ArticleMolecular psychiatry2023
Activation of Kv7 channels normalizes hyperactivity of the VTA-NAcLat circuit and attenuates methamphetamine-induced conditioned place preference and sensitization in mice.
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Methamphetamine induces long-lasting dysbiosis of the gut microbiota.Molecular psychiatry · 2026Article
- Activation of Kv7.3 channels in mPFC engram neurons suppresses methamphetamine memory retrieval by reducing excitability and glutamate release in the mPFC-NAc circuit.Cellular and molecular life sciences : CMLS · 2026Article
- MicroRNA-132/212 negatively modulates opioid reward by targeting dopamine transporter in the ventral tegmental area.Translational psychiatry · 2026Article
- KAddiction biology · 2024Article
- Different Doses of Methamphetamine Are Needed to Produce Locomotor or Blood Pressure Sensitization in Mice.Life (Basel, Switzerland) · 2024Article
- Identification of the circRNA-miRNA-mRNA network for treating methamphetamine-induced relapse and behavioral sensitization with cannabidiol.CNS neuroscience & therapeutics · 2024Article
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
Abstract
The brain circuit projecting from the ventral tegmental area (VTA) to the nucleus accumbens lateral shell (NAcLat) has a key role in methamphetamine (MA) addiction. As different dopamine (DA) neuron subpopulations in the VTA participate in different neuronal circuits, it is a challenge to isolate these DA neuron subtypes. Using retrograde tracing and Patch-seq, we isolated DA neurons in the VTA-NAcLat circuit in MA-treated mice and performed gene expression profiling. Among the differentially expressed genes, KCNQ genes were dramatically downregulated. KCNQ genes encode Kv7 channel proteins, which modulate neuronal excitability. Injection of both the Kv7.2/3 agonist ICA069673 and the Kv7.4 agonist fasudil into the VTA attenuated MA-induced conditioned place preference and locomotor sensitization and decreased neuronal excitability. Increasing Kv7.2/3 activity decreased neural oscillations, synaptic plasticity and DA release in the VTA-NacLat circuit in MA-treated mice. Furthermore, overexpression of only Kv7.3 channels in the VTA-NacLat circuit was sufficient to attenuate MA-induced reward behavior and decrease VTA neuron excitability. Activation of Kv7 channels in the VTA may become a novel treatment strategy for MA abuse.
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