ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Nicotine enhances excitability of medial habenular neurons via facilitation of neurokinin signaling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- Nicotinic Receptors in the Medial Habenula to Interpeduncular Nucleus Pathway: Modulators of Reward, Aversion and Emotion.The European journal of neuroscience · 2025Review
- A medial habenula neural circuit controlling anxiety-like behaviors in response to acute stress.Molecular psychiatry · 2025Article
- Article
- Extracellular ATP Neurotransmission and Nicotine Sex-Specifically Modulate Habenular Neuronal Activity in Adolescence.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Understanding the habenula: A major node in circuits regulating emotion and motivation.Pharmacological research · 2023Review
- Epigenetic Mechanisms Mediate Nicotine-Induced Reward and Behaviour in Zebrafish.Current neuropharmacology · 2022Article
- Neurobiological Mechanisms of Nicotine Reward and Aversion.Pharmacological reviews · 2022Review
- Addiction-related neuroadaptations following chronic nicotine exposure.Journal of neurochemistry · 2021Review
- Chronic sleep fragmentation enhances habenula cholinergic neural activity.Molecular psychiatry · 2021Article
- Implications of Oligomeric Amyloid-Beta (oAβThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Nicotinic acetylcholine receptors and nicotine addiction: A brief introduction.Neuropharmacology · 2020Review
- Neurokinin receptors in drug and alcohol addiction.Brain research · 2020Review
- Acute and Chronic Nicotine Exposures Differentially Affect Central Serotonin 2A Receptor Function: Focus on the Lateral Habenula.International journal of molecular sciences · 2020Article
- The α5 Nicotinic Acetylcholine Receptor Subunit Differentially Modulates α4β2Frontiers in synaptic neuroscience · 2020Review
- From controlled to compulsive drug-taking: The role of the habenula in addiction.Neuroscience and biobehavioral reviews · 2019Review
- Chronic Nicotine Exposure Alters the Neurophysiology of Habenulo-Interpeduncular Circuitry.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- [The roles of habenula and related neural circuits in neuropsychiatric diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019Review
- Chrna5-Expressing Neurons in the Interpeduncular Nucleus Mediate Aversion Primed by Prior Stimulation or Nicotine Exposure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Neuropeptidomics of the Rat Habenular Nuclei.Journal of proteome research · 2018Article
- Differential regulation of neuronal excitability by nicotine and substance P in subdivisions of the medial habenula.Animal cells and systems · 2018Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The medial habenula (MHb) densely expresses nicotinic acetylcholine receptors (nAChRs) and participates in nicotine-related behaviors such as nicotine withdrawal and regulating nicotine intake. Although specific nAChR subunits are identified as being involved in withdrawal behavior, the cellular mechanisms through which nicotine acts to cause this aversive experience is unclear. Here, we demonstrate an interaction between the nicotinic and neurokinin signaling systems that may form the basis for some symptoms experienced during nicotine withdrawal. Using patch-clamp electrophysiology in mouse brain slices, we show that nicotine (1 μm) increases intrinsic excitability in MHb neurons. This nicotine-induced phenomenon requires α5-containing nAChRs and depends on intact neurokinin signaling. The effect is blocked by preincubation with neurokinin 1 (NK1; L-732138, 10 μm) and NK3 (SB222200, 2 μm) antagonists and mimicked by NK1 (substance P, 100 nm) and NK3 (neurokinin B [NKB], 100 nm) agonists. Microinjections (1 μl) of L-732138 (50 nm) and SB222200 (100 nm) into the MHb induces withdrawal behavior in chronic nicotine-treated (8.4 mg/kg/d, 2 weeks) mice. Conversely, withdrawal behavior is absent with analogous microinjections into the lateral habenula of nicotine-treated mice or in mice chronically treated with a vehicle solution. Further, chronic nicotine reduces nicotine's acute modulation of intrinsic excitability while sparing modulation by NKB. Our work elucidates the interplay between two neuromodulatory signaling systems in the brain through which nicotine acts to influence intrinsic excitability. More importantly, we document a neuroadaptation of this mechanism to chronic nicotine exposure and implicate these mechanisms collectively in the emergence of nicotine withdrawal behavior.
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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.