Alterations in the hippocampal and striatal catecholaminergic fiber densities of heterozygous reeler mice

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Alterations in the hippocampal and striatal catecholaminergic fiber densities of heterozygous reeler mice. / Nullmeier, S; Panther, P; Frotscher, M; Zhao, S; Schwegler, H.

in: NEUROSCIENCE, Jahrgang 275, 05.09.2014, S. 404-19.

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@article{3c133613ad224a27822ed2a883b0b400,
title = "Alterations in the hippocampal and striatal catecholaminergic fiber densities of heterozygous reeler mice",
abstract = "The heterozygous reeler mouse (HRM), haploinsufficient for reelin, shares several neurochemical and behavioral similarities with patients suffering from schizophrenia. It has been shown that defective reelin signaling influences the mesolimbic dopaminergic pathways in a specific manner. However, there is only little information about the impact of reelin haploinsufficiency on the monoaminergic innervation of different brain areas, known to be involved in the pathophysiology of schizophrenia. In the present study using immunocytochemical procedures, we investigated HRM and wild-type mice (WT) for differences in the densities of tyrosine hydroxylase (TH)-immunoreactive (IR) and serotonin (5-HT)-IR fibers in prefrontal cortex, ventral and dorsal hippocampal formation, amygdala and ventral and dorsal striatum. We found that HRM, compared to WT, shows a significant increase in TH-IR fiber densities in dorsal hippocampal CA1, CA3 and ventral CA1. In contrast, HRM exhibits a significant decrease of TH-IR in the shell of the nucleus accumbens (AcbShell), but no differences in the other brain areas investigated. Overall, no genotype differences were found in the 5-HT-IR fiber densities. In conclusion, these results support the view that reelin haploinsufficiency differentially influences the catecholaminergic (esp. dopaminergic) systems in brain areas associated with schizophrenia. The reelin haploinsufficient mouse may provide a useful model for studying the role of reelin in hippocampal dysfunction and its effect on the dopaminergic system as related to schizophrenia.",
author = "S Nullmeier and P Panther and M Frotscher and S Zhao and H Schwegler",
note = "Copyright {\textcopyright} 2014 IBRO. Published by Elsevier Ltd. All rights reserved.",
year = "2014",
month = sep,
day = "5",
doi = "10.1016/j.neuroscience.2014.06.027",
language = "English",
volume = "275",
pages = "404--19",
journal = "NEUROSCIENCE",
issn = "0306-4522",
publisher = "Elsevier Limited",

}

RIS

TY - JOUR

T1 - Alterations in the hippocampal and striatal catecholaminergic fiber densities of heterozygous reeler mice

AU - Nullmeier, S

AU - Panther, P

AU - Frotscher, M

AU - Zhao, S

AU - Schwegler, H

N1 - Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

PY - 2014/9/5

Y1 - 2014/9/5

N2 - The heterozygous reeler mouse (HRM), haploinsufficient for reelin, shares several neurochemical and behavioral similarities with patients suffering from schizophrenia. It has been shown that defective reelin signaling influences the mesolimbic dopaminergic pathways in a specific manner. However, there is only little information about the impact of reelin haploinsufficiency on the monoaminergic innervation of different brain areas, known to be involved in the pathophysiology of schizophrenia. In the present study using immunocytochemical procedures, we investigated HRM and wild-type mice (WT) for differences in the densities of tyrosine hydroxylase (TH)-immunoreactive (IR) and serotonin (5-HT)-IR fibers in prefrontal cortex, ventral and dorsal hippocampal formation, amygdala and ventral and dorsal striatum. We found that HRM, compared to WT, shows a significant increase in TH-IR fiber densities in dorsal hippocampal CA1, CA3 and ventral CA1. In contrast, HRM exhibits a significant decrease of TH-IR in the shell of the nucleus accumbens (AcbShell), but no differences in the other brain areas investigated. Overall, no genotype differences were found in the 5-HT-IR fiber densities. In conclusion, these results support the view that reelin haploinsufficiency differentially influences the catecholaminergic (esp. dopaminergic) systems in brain areas associated with schizophrenia. The reelin haploinsufficient mouse may provide a useful model for studying the role of reelin in hippocampal dysfunction and its effect on the dopaminergic system as related to schizophrenia.

AB - The heterozygous reeler mouse (HRM), haploinsufficient for reelin, shares several neurochemical and behavioral similarities with patients suffering from schizophrenia. It has been shown that defective reelin signaling influences the mesolimbic dopaminergic pathways in a specific manner. However, there is only little information about the impact of reelin haploinsufficiency on the monoaminergic innervation of different brain areas, known to be involved in the pathophysiology of schizophrenia. In the present study using immunocytochemical procedures, we investigated HRM and wild-type mice (WT) for differences in the densities of tyrosine hydroxylase (TH)-immunoreactive (IR) and serotonin (5-HT)-IR fibers in prefrontal cortex, ventral and dorsal hippocampal formation, amygdala and ventral and dorsal striatum. We found that HRM, compared to WT, shows a significant increase in TH-IR fiber densities in dorsal hippocampal CA1, CA3 and ventral CA1. In contrast, HRM exhibits a significant decrease of TH-IR in the shell of the nucleus accumbens (AcbShell), but no differences in the other brain areas investigated. Overall, no genotype differences were found in the 5-HT-IR fiber densities. In conclusion, these results support the view that reelin haploinsufficiency differentially influences the catecholaminergic (esp. dopaminergic) systems in brain areas associated with schizophrenia. The reelin haploinsufficient mouse may provide a useful model for studying the role of reelin in hippocampal dysfunction and its effect on the dopaminergic system as related to schizophrenia.

U2 - 10.1016/j.neuroscience.2014.06.027

DO - 10.1016/j.neuroscience.2014.06.027

M3 - SCORING: Journal article

C2 - 24969133

VL - 275

SP - 404

EP - 419

JO - NEUROSCIENCE

JF - NEUROSCIENCE

SN - 0306-4522

ER -