Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities

Brain-derived neurotrophic factor (BDNF) has trophic effects on serotonergic (5-HT) neurons in the central nervous system. However, the role of endogenous BDNF in the development and function of these neurons has not been established in vivo because of the early postnatal lethality of BDNF null mice...

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Päätekijät: Lyons, W. Ernest, Mamounas, Laura A., Ricaurte, George A., Coppola, Vincenzo, Reid, Susan W., Bora, Susan H., Wihler, Cornelia, Koliatsos, Vassilis E., Tessarollo, Lino
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Julkaistu: The National Academy of Sciences 1999
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Biological Sciences
Linkit:https://ncbi.nlm.nih.gov/pmc/articles/PMC24804/
https://ncbi.nlm.nih.gov/pubmed/10611369
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spelling pubmed-248042001-03-09 Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities Lyons, W. Ernest Mamounas, Laura A. Ricaurte, George A. Coppola, Vincenzo Reid, Susan W. Bora, Susan H. Wihler, Cornelia Koliatsos, Vassilis E. Tessarollo, Lino Proc Natl Acad Sci U S A Biological Sciences Brain-derived neurotrophic factor (BDNF) has trophic effects on serotonergic (5-HT) neurons in the central nervous system. However, the role of endogenous BDNF in the development and function of these neurons has not been established in vivo because of the early postnatal lethality of BDNF null mice. In the present study, we use heterozygous BDNF(+/−) mice that have a normal life span and show that these animals develop enhanced intermale aggressiveness and hyperphagia accompanied by significant weight gain in early adulthood; these behavioral abnormalities are known to correlate with 5-HT dysfunction. Forebrain 5-HT levels and fiber density in BDNF(+/−) mice are normal at an early age but undergo premature age-associated decrements. However, young adult BDNF(+/−) mice show a blunted c-fos induction by the specific serotonin releaser-uptake inhibitor dexfenfluramine and alterations in the expression of several 5-HT receptors in the cortex, hippocampus, and hypothalamus. The heightened aggressiveness can be ameliorated by the selective serotonin reuptake inhibitor fluoxetine. Our results indicate that endogenous BDNF is critical for the normal development and function of central 5-HT neurons and for the elaboration of behaviors that depend on these nerve cells. Therefore, BDNF(+/−) mice may provide a useful model to study human psychiatric disorders attributed to dysfunction of serotonergic neurons. The National Academy of Sciences 1999-12-21 /pmc/articles/PMC24804/ /pubmed/10611369 Text en Copyright © 1999, The National Academy of Sciences
institution US National Library of Medicine
collection PubMed Central
language en
format Article
topic Biological Sciences
spellingShingle Biological Sciences
Lyons, W. Ernest
Mamounas, Laura A.
Ricaurte, George A.
Coppola, Vincenzo
Reid, Susan W.
Bora, Susan H.
Wihler, Cornelia
Koliatsos, Vassilis E.
Tessarollo, Lino
Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities
description Brain-derived neurotrophic factor (BDNF) has trophic effects on serotonergic (5-HT) neurons in the central nervous system. However, the role of endogenous BDNF in the development and function of these neurons has not been established in vivo because of the early postnatal lethality of BDNF null mice. In the present study, we use heterozygous BDNF(+/−) mice that have a normal life span and show that these animals develop enhanced intermale aggressiveness and hyperphagia accompanied by significant weight gain in early adulthood; these behavioral abnormalities are known to correlate with 5-HT dysfunction. Forebrain 5-HT levels and fiber density in BDNF(+/−) mice are normal at an early age but undergo premature age-associated decrements. However, young adult BDNF(+/−) mice show a blunted c-fos induction by the specific serotonin releaser-uptake inhibitor dexfenfluramine and alterations in the expression of several 5-HT receptors in the cortex, hippocampus, and hypothalamus. The heightened aggressiveness can be ameliorated by the selective serotonin reuptake inhibitor fluoxetine. Our results indicate that endogenous BDNF is critical for the normal development and function of central 5-HT neurons and for the elaboration of behaviors that depend on these nerve cells. Therefore, BDNF(+/−) mice may provide a useful model to study human psychiatric disorders attributed to dysfunction of serotonergic neurons.
author Lyons, W. Ernest
Mamounas, Laura A.
Ricaurte, George A.
Coppola, Vincenzo
Reid, Susan W.
Bora, Susan H.
Wihler, Cornelia
Koliatsos, Vassilis E.
Tessarollo, Lino
author_facet Lyons, W. Ernest
Mamounas, Laura A.
Ricaurte, George A.
Coppola, Vincenzo
Reid, Susan W.
Bora, Susan H.
Wihler, Cornelia
Koliatsos, Vassilis E.
Tessarollo, Lino
author_sort Lyons, W. Ernest
title Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities
title_short Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities
title_full Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities
title_fullStr Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities
title_full_unstemmed Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities
title_sort brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities
publisher The National Academy of Sciences
publisher_facet The National Academy of Sciences
publishDate 1999
url https://ncbi.nlm.nih.gov/pmc/articles/PMC24804/
https://ncbi.nlm.nih.gov/pubmed/10611369
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