ArticleJournal of neurophysiology2016
Brain stem as a target site for the metabolic side effects of olanzapine.
Article in Journal of neurophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Supraventricular Tachycardia in an Adolescent with Acute Psychotic Disorder Treated with Olanzapine: A Rare Event Managed with Aripiprazole.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026Article
- Olanzapine Administration Reduces Chemotherapy-Induced Nausea Behavior in Rats.Biological research for nursing · 2021Article
- Neuronal defects in a human cellular model of 22q11.2 deletion syndrome.Nature medicine · 2020Article
- N-acetylcysteine prevents olanzapine-induced oxidative stress in mHypoA-59 hypothalamic neurons.Scientific reports · 2020Article
- Universal Nature of Drug Treatment Responses in Drug-Tissue-Wide Model-Animal Experiments Using Tensor Decomposition-Based Unsupervised Feature Extraction.Frontiers in genetics · 2020Article
- Second-Generation Antipsychotics and Dysregulation of Glucose Metabolism: Beyond Weight Gain.Cells · 2019Review
- A case of sinus pause induced by swallowing in the setting of olanzapine and guanfacine overdose.Journal of the Intensive Care Society · 2019Article
- Molecular modeling studies of 1,2,4-triazine derivatives as novel h-DAAO inhibitors by 3D-QSAR, docking and dynamics simulations.RSC advances · 2018Article
- Lipid Processing in the Brain: A Key Regulator of Systemic Metabolism.Frontiers in endocrinology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Olanzapine, an atypical antipsychotic, is widely prescribed for the treatment of schizophrenia and bipolar disorder despite causing undesirable metabolic side effects. A variety of mechanisms and brain sites have been proposed as contributors to the side effects; however, the role of the dorsal motor nucleus of the vagus nerve (DMV), which plays a crucial role in the regulation of subdiaphragmatic organs and thus governs energy and glucose homeostasis, is largely unknown. Identifying the effect of olanzapine on the excitability of DMV neurons in both sexes is thus crucial to understanding possible underlying mechanisms. Whole cell patch-clamp electrophysiological recordings were conducted in stomach- and liver-related DMV neurons identified with retrograde viral tracers and in random DMV neurons. The effect of olanzapine on the neuronal excitability of DMV neurons both in male and female mice was established. Our data demonstrate that olanzapine hyperpolarizes the DMV neurons in both sexes and this effect is reversible. The hyperpolarization is associated with decreased firing rate and input resistance. Olanzapine also decreases the excitability of a subset of stomach- and liver-related DMV neurons. Our study demonstrates that olanzapine has a powerful effect on DMV neurons in both sexes, indicating its ability to reduce vagal output to the subdiaphragmatic organs, which likely contributes to the metabolic side effects observed in both humans and experimental models. These findings suggest that the metabolic side effects of olanzapine may partially originate in the DMV.
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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.