ArticleJournal of neuroscience research2022
Amino acid systems in the interpeduncular nucleus are altered in a sex-dependent manner during nicotine withdrawal.
Article in Journal of neuroscience research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Ionotropic Glutamate Receptor Function in Interpeduncular Nucleus Is Modulated by Nicotine Exposure.eNeuro · 2025Article
- Nicotinic Receptors in the Medial Habenula to Interpeduncular Nucleus Pathway: Modulators of Reward, Aversion and Emotion.The European journal of neuroscience · 2025Review
- Shentong Zhuyu Decoction Alleviates Neuropathic Pain in Mice by Inhibiting the NMDAR-2B Receptor-Mediated CaMKII/CREB Signaling Pathway in GABAergic Neurons of the Interpeduncular Nucleus.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The influence of ovarian hormones on the putative mechanisms that promote female nicotine use.Current opinion in neurobiology · 2024Review
- Article
- Nicotine addiction: More than just dopamine.Current opinion in neurobiology · 2023Review
- Chronic exposure to cigarette smoke extract increases nicotine withdrawal symptoms in adult and adolescent male rats.Advances in drug and alcohol research · 2023Article
- Highlighting the contributions of Minority Serving Institutions to neuroscience.Journal of neuroscience research · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Prior work in male rodents established that the medial habenula-interpeduncular nucleus (MHb-IPN) pathway modulates nicotine withdrawal. Specifically, withdrawal severity has been closely associated with inhibitory tone in the IPN via interneurons that release γ-aminobutyric acid (GABA). Inhibitory tone in the IPN is regulated by projections from the MHb that co-release glutamate and acetylcholine. Within the IPN, inhibitory tone is also regulated via corticotropin-releasing factor type 1 (CRF1) receptors that control GABA release from local interneurons. This study extends previous work by comparing sex differences in GABA, glutamate, as well serotonin levels in the IPN during precipitated nicotine withdrawal. Sex differences in withdrawal-induced neurochemical effects were also compared following systemic administration of a CRF1 receptor antagonist. The results revealed that there were no group differences in serotonin levels in the IPN. A major finding was that females displayed a larger withdrawal-induced increases in GABA levels in the IPN than males. Also, withdrawal increased IPN glutamate levels in a similar manner in females and males. Blockade of CRF1 receptors produced a larger suppression of the withdrawal-induced increases in GABA levels in the IPN of females versus males, an effect that was likely related to the robust increase in glutamate following administration of the CRF1 receptor antagonist in females. These data suggest that amino acid systems in the IPN modulate sex differences in the behavioral effects of nicotine withdrawal. Furthermore, our data imply that medications that target stress-induced activation of the IPN may reduce withdrawal severity, particularly in females.
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