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12. Ceruloplasmin Deficiency Results in an Anxiety Phenotype Involving Deficits in Hippocampal Iron, Serotonin and BDNF

Author

Texel, Sarah J., Camandola, Simonetta, Ladenheim, Bruce, Rothman, Sarah M., Mughal, Mohamed R., Unger, Erica L., Cadet, Jean Lud, and Mattson, Mark P.

Subjects
Male, Serotonin, Transcription, Genetic, Anxiety, Motor Activity, Real-Time Polymerase Chain Reaction, Hippocampus, Article, Mice, Memory, Animals, Learning, Maze Learning, Postural Balance, Brain Chemistry, Mice, Knockout, Brain-Derived Neurotrophic Factor, Ceruloplasmin, Recognition, Psychology, Fear, Iron Deficiencies, Mice, Inbred C57BL, nervous system, Hindlimb Suspension, Corticosterone, Psychomotor Performance
Abstract

Ceruloplasmin (Cp) is a ferroxidase involved in iron metabolism by converting Fe2+ to Fe3+, and by regulating cellular iron efflux. In the ceruloplasmin knockout (CpKO) mouse, the deregulation of iron metabolism results in moderate liver and spleen hemosiderosis, but the impact of Cp deficiency on brain neurochemistry and behavior in this animal model is unknown. We found that in contrast to peripheral tissues, iron levels in the hippocampus are significantly reduced in CpKO mice. Although it does not cause any discernable deficits in motor function or learning and memory, Cp deficiency results in heightened anxiety-like behavior in the open field and elevated plus maze tests. This anxiety phenotype is associated with elevated levels of plasma corticosterone. Previous studies provided evidence that anxiety disorders and long-standing stress are associated with reductions in levels of serotonin and brain-derived neurotrophic factor (BDNF) in the hippocampus. We found that levels of serotonin and norepinephrine, and the expression of BDNF and its receptor trkB, are significantly reduced in the hippocampus of CpKO mice. Thus, Cp deficiency causes an anxiety phenotype by a mechanism that involves decreased levels of iron, serotonin, norepinephrine and BDNF in the hippocampus.

Published
2011

18. Attenuated response to methamphetamine sensitization and deficits in motor learning and memory after selective deletion of β-catenin in dopamine neurons

Author

Diaz-Ruiz, Oscar, primary, Zhang, YaJun, additional, Shan, Lufei, additional, Malik, Nasir, additional, Hoffman, Alexander F., additional, Ladenheim, Bruce, additional, Cadet, Jean Lud, additional, Lupica, Carl R., additional, Tagliaferro, Adriana, additional, Brusco, Alicia, additional, and Bäckman, Cristina M., additional

Published
2012
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29. Growth Factor Signals in Neural Cells

Author

Martin, Bronwen, primary, Brenneman, Randall, additional, Golden, Erin, additional, Walent, Tom, additional, Becker, Kevin G., additional, Prabhu, Vinayakumar V., additional, Wood, William, additional, Ladenheim, Bruce, additional, Cadet, Jean-Lud, additional, and Maudsley, Stuart, additional

Published
2009
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33. (±)-3,4-Methylenedioxymethamphefamine and Metabolite Disposition in Plasma and Striatum of Wild-Type and Multidrug Resistance Protein 1a Knock-Out Mice.

Author

Scheidweiler, Karl B., Ladenheim, Bruce, Barnes, Allan J., Cadet, Jean Lud, and Huestis, Marilyn A.

Subjects
*ECSTASY (Drug), *PHARMACOKINETICS, *MULTIDRUG resistance, *NEUROTOXICOLOGY, *LABORATORY mice, *ANIMAL models in research, *GAS chromatography, *MASS spectrometry
Abstract

The article presents a study that characterizes methylenedioxymethamphetamine (MDMA) pharmacokinetics in murine plasma and bran to determine whether mdr1a alters MDMA distribution. It notes that mice having inadequate multidrug resistance protein mdr1a has been protected from MDMA-induced neurotoxicity, highlighting a mechanism. Moreover, plasma and brain specimens from knock-out mice have been collected after MDMA to quantify the distribution through gas chromatography-mass spectrometry.

Published
2011
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34. Monoamine Oxidases Regulate Telencephalic Neural Progenitors in Late Embryonic and Early Postnatal Development.

Author

Aiwu Cheng, Scott, Anna L., Ladenheim, Bruce, Chen, Kevin, Xin Ouyang, Lathia, Justin D., Mughal, Mohamed, Cadet, Jean Lud, Mattson, Mark P., and Shih, Jean C.

Subjects
NEUROTRANSMITTERS, BRAIN, NEURAL stem cells, TELENCEPHALON, MITOSIS, SEROTONIN
Abstract

Monoamine neurotransmitters play major roles in regulating a range of brain functions in adults and increasing evidence suggests roles for monoamines in brain development. Here we show that mice lacking the monoamine metabolic enzymes MAO A and MAO B (MAO AB-deficient mice) exhibit diminished proliferation of neural stem cells (NSC) in the developing telencephalon beginning in late gestation [embryonic day (E) 17.5], a deficit that persists in neonatal and adult mice. These mice showed significantly increased monoamine levels and anxiety-like behaviors as adults. Assessments of markers of intermediate progenitor cells (IPC) and mitosis showed that NSC in the subventricular zone (SVZ), but not in the ventricular zone, are reduced in MAO AB-deficient mice. A developmental time course of monoamines in frontal cortical tissues revealed increased serotonin levels as early as E14.5, and a further large increase was found between E17.5 and postnatal day 2. Administration of an inhibitor of serotonin synthesis (parachlorophenylalanine) between E14.5 and E19.5 restored the IPC numbers and SVZ thickness, suggesting the role of serotonin in the suppression of IPC proliferation. Studies of neurosphere cultures prepared from the telencephalon at different embryonic and postnatal ages showed that serotonin stimulates proliferation in wild-type, but not in MAO AB-deficient, NSC. Together, these results suggest that a MAO-dependent long-lasting alteration in the proliferation capacity of NSC occurs late in embryonic development and is mediated by serotonin. Our findings reveal novel roles for MAOs and serotonin in the regulation of IPC proliferation in the developing brain. [ABSTRACT FROM AUTHOR]

Published
2010
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35. Methamphetamine Preconditioning Causes Differential Changes in Striatal Transcriptional Responses to Large Doses of the Drug.

Author

Cadet, Jean Lud, Brannock, Christie, Ladenheim, Bruce, McCoy, Michael T., Beauvais, Genevieve, Hodges, Amber B., Lehrmann, Elin, Wood, William H., Becker, Kevin G., and Krasnova, Irina N.

Subjects
*METHAMPHETAMINE, *DRUG toxicity, *DRUG abuse, *POLYMERASE chain reaction, *HEAT shock proteins, *GENETIC transcription, *GENE expression, *LABORATORY rats
Abstract

Methamphetamine (METH) is a toxic drug of abuse, which can cause significant decreases in the levels of monoamines in various brain regions. However, animals treated with progressively increasing doses of METH over several weeks are protected against the toxic effects of the drug. In the present study, we tested the possibility that this pattern of METH injections might be associated with transcriptional changes in the rat striatum, an area of the brain which is known to be very sensitive to METH toxicity and which is protected by METH preconditioning. We found that the presence and absence of preconditioning followed by injection of large doses of METH caused differential expression in different sets of striatal genes. Quantitative PCR confirmed METH-induced changes in some genes of interest. These include small heat shock 27 kD proteins 1 and 2 (HspB1 and HspB2), brain derived neurotrophic factor (BDNF), and heme oxygenase-1 (Hmox-1). Our observations are consistent with previous studies which have reported that ischemic or pharmacological preconditioning can cause reprogramming of gene expression after lethal ischemic insults. These studies add to the growing literature on the effects of preconditioning on the brain transcriptome. [ABSTRACT FROM AUTHOR]

Published
2011
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