ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
LMO4 is essential for paraventricular hypothalamic neuronal activity and calcium channel expression to prevent hyperphagia.
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 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
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- How "Neuronal" Are Human Skin Mast Cells?International journal of molecular sciences · 2022Review
- Differential regulation of alcohol consumption and reward by the transcriptional cofactor LMO4.Molecular psychiatry · 2021Article
- Neuronal protein-tyrosine phosphatase 1B hinders sensory-motor functional recovery and causes affective disorders in two different focal ischemic stroke models.Neural regeneration research · 2021Article
- Neuronal Protein Tyrosine Phosphatase 1B Hastens Amyloid β-Associated Alzheimer's Disease in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Electrophysiological properties of identified oxytocin and vasopressin neurones.Journal of neuroendocrinology · 2019Review
- Arcuate Nucleus Orexin-A Signaling Alleviates Cisplatin-Induced Nausea and Vomiting Through the Paraventricular Nucleus of the Hypothalamus in Rats.Frontiers in physiology · 2018Article
- A Selective Role for Lmo4 in Cue-Reward Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Cisplatin-induced apoptosis in auditory, renal, and neuronal cells is associated with nitration and downregulation of LMO4.Cell death discoveryArticle
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The dramatic increase in the prevalence of obesity reflects a lack of progress in combating one of the most serious health problems of this century. Recent studies have improved our understanding of the appetitive network by focusing on the paraventricular hypothalamus (PVH), a key region responsible for the homeostatic balance of food intake. Here we show that mice with PVH-specific ablation of LIM domain only 4 (Lmo4) become rapidly obese when fed regular chow due to hyperphagia rather than to reduced energy expenditure. Brain slice recording of LMO4-deficient PVH neurons showed reduced basal cellular excitability together with reduced voltage-activated Ca(2+) currents. Real-time PCR quantification revealed that LMO4 regulates the expression of Ca(2+) channels (Cacna1h, Cacna1e) that underlie neuronal excitability. By increasing neuronal activity using designer receptors exclusively activated by designer drugs technology, we could suppress food intake of PVH-specific LMO4-deficient mice. Together, these results demonstrate that reduced neural activity in LMO4-deficient PVH neurons accounts for hyperphagia. Thus, maintaining PVH activity is important to prevent hyperphagia-induced obesity.
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