TY  - JOUR
AB  - The aim of this study was to indentify the involvement of leptin receptors (LepR) in astrocytes in hippocampal synaptic transmission and plasticity and metabolism. To this end we used a genetic mouse model (GFAP-LepR(-/-)) of specific LepR ablation in GFAP positive cells and recorded excitatory postsynaptic potentials (fEPSPs) within the CA1 area. Glutamate (Glu) uptake and the expression of Glu transporters (EEAT3, GLT-1 and GLAST) and enzymes involved in Glu metabolism (glutamine synthase, GABA decarboxylase 65 and 67) were quantified. Modifications in the expression of GFAP, the glucose transporter (GLUT)-1, and the monocarboxylate transporters MCT-2 and MCT-4, were also analyzed. The results show that depletion of LepR in GFAP positive cells reduced basal synaptic transmission within the CA1 area and impaired N-methyl-D-aspartate (NMDA)-evoked long-term depression (NMDA-LTD). Hippocampal slices from GFAP-LepR(-/-) mice displayed lower Glu uptake efficacy together with up-regulation of GLT-1, glutamine synthase, GFAP and GLUT-1. In conclusion, astrocyte LepRs are involved in the maintenance of Glu homeostasis and Glu neurotransmission within the hippocampus. Our findings support a role of hippocampal LepRs in synaptic plasticity, which could have an impact on memory and learning processes.This article is part of a Special Issue entitled: The Neuroscience of Energy Balance and Eating Behavior (C) 2019 IBRO.
AU  - Naranjo, V.*
AU  - Contreras, A.*
AU  - Merino, B.*
AU  - Plaza, A.*
AU  - Lorenzo, M.P.*
AU  - García-Cáceres, C.
AU  - García, A.*
AU  - Chowen, J.A.*
AU  - Ruiz-Gayo, M.*
AU  - Del Olmo, N.*
AU  - Cano, V.*
C1  - 57458
C2  - 47798
CY  - The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, England
SP  - 182-190
TI  - Specific deletion of the astrocyte leptin receptor induces changes in hippocampus glutamate metabolism, synaptic transmission and plasticity.
JO  - Neuroscience
VL  - 447
PB  - Pergamon-elsevier Science Ltd
PY  - 2020
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - Clinical evidence and pathological studies suggest a bidirectional link between temporal lobe epilepsy and Alzheimer's disease (AD). Data analysis from omic studies offers an excellent opportunity to identify the overlap in molecular alterations between the two pathologies. We have subjected proteomic data sets from a rat model of epileptogenesis to a bioinformatics analysis focused on proteins functionally linked with AD. The data sets have been obtained for hippocampus (HC) and parahippocampal cortex samples collected during the course of epileptogenesis. Our study confirmed a relevant dysregulation of proteins linked with Alzheimer pathogenesis. When comparing the two brain areas, a more prominent regulation was evident in parahippocampal cortex samples as compared to the HC. Dysregulated protein groups comprised those affecting mitochondrial function and calcium homeostasis. Differentially expressed mitochondrial proteins included proteins of the mitochondrial complexes I, III, IV, and V as well as of the accessory subunit of complex I. The analysis also revealed a regulation of the microtubule associated protein Tau in parahippocampal cortex tissue during the latency phase. This was further confirmed by immunohistochemistry. Moreover, we demonstrated a complex epileptogenesis-associated dysregulation of proteins involved in amyloid beta processing and its regulation. Among others, the amyloid precursor protein and the alpha-secretase alpha disintegrin metalloproteinase 17 were included. Our analysis revealed a relevant regulation of key proteins known to be associated with AD pathogenesis. The analysis provides a comprehensive overview of shared molecular alterations characterizing epilepsy development and manifestation as well as AD development and progression.
AU  - von Rüden, E.L.*
AU  - Zellinger, C.*
AU  - Gedon, J.*
AU  - Walker, A.*
AU  - Bierling, V.*
AU  - Deeg, C.A.*
AU  - Hauck, S.M.
AU  - Potschka, H.*
C1  - 57627
C2  - 47845
CY  - The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, England
SP  - 102-120
TI  - Regulation of Alzheimer's disease-associated proteins during epileptogenesis.
JO  - Neuroscience
VL  - 424
PB  - Pergamon-elsevier Science Ltd
PY  - 2020
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - Agrin is a multi-domain protein best known for its essential function during formation of the neuromuscular junction. Alternative mRNA splicing at sites named y and z in the C-terminal part of agrin regulates its interaction with a receptor complex consisting of the agrin-binding low-density lipoprotein receptor-related protein 4 (Lrp4) and the muscle-specific kinase (MuSK). Isoforms with inserts at both splice sites bind to Lrp4, activate MuSK and are synaptogenic at the neuromuscular junction. Agrin is also expressed as a transmembrane protein in the central nervous system (CNS) but its function during interneuronal synapse formation is unclear. Recently we demonstrated that transfection of a full-length cDNA coding for transmembrane agrin (TM-agrin) in cultured embryonic cortical neurons induced an Lrp4-dependent but MuSK-independent increase in dendritic glutamatergic synapses and an Lrp4- and MuSK-independent reduction of inhibitory synapses. Here we show that presynaptic specializations were similarly affected by TM-agrin overexpression. In addition, we mapped the regions within TM-agrin responsible for TM-agrin's effects on dendritic aggregates of synapse-associated proteins. We show that the presence of a four amino acid insert at splice site y is essential for the increase in the density of puncta containing the postsynaptic density protein 95 kDa. This effect was independent of splice site z. The reduction of the gephyrin puncta density was independent of the entire extracellular part of TM-agrin but required a highly conserved serine residue in the intracellular domain of TM-agrin. These results provide further evidence for a function of TM-agrin during CNS synaptogenesis and demonstrate that different domains and alternative splicing of TM-agrin differentially affect excitatory and inhibitory synapse formation in cultured embryonic CNS neurons.
AU  - Handara, G.
AU  - Kröger, S.*
C1  - 57325
C2  - 47698
CY  - The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, England
SP  - 60-71
TI  - Alternative splicing and the intracellular domain mediate TM-agrin's ability to differentially regulate the density of excitatory and inhibitory synapse-like specializations in developing CNS neurons.
JO  - Neuroscience
VL  - 419
PB  - Pergamon-elsevier Science Ltd
PY  - 2019
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - IBRO. A 62-year-old diabetologist diagnosed himself to have diabetes type-2, with an HbA1c of 9.5. Five months after lifestyle intervention and a multi-drug approach, HbA1c was 6.3, systolic blood pressure was below 135. mmHg and BMI reduced to 27. But he suffered from severe painful diabetic neuropathy. Therefore he decided to visit his friend, a famous neuroscientist at an even more famous university. He asked him several plain questions: 1. What is the natural course of painful diabetic neuropathy? 2. Why do I have, despite almost normalizing HbA1c, more problems than before? 3. Are you sure my problems are due to diabetes or should we do a nerve biopsy? 4. Are there imaging techniques helpful for the diagnosis of this diabetic complication, starting in the distal nerve endings of the foot and slowly moving ahead? 5. Can you suggest any drug, specific and effective, for relieving painful diabetic neuropathy?This review will use the experts' answers to the questions of the diabetologist, not only to give a summary of the current knowledge, but even more to highlight areas of research needed for improving the fate of patients with painful diabetic neuropathy. Based on the unknowns, which exceed the knowns in diabetic neuropathy, a quest for more public support of research is made.
AU  - Nawroth, P.P.
AU  - Bendszus, M.*
AU  - Pham, M.*
AU  - Jende, J.*
AU  - Heiland, S.*
AU  - Ries, S.*
AU  - Schumann, C.*
AU  - Schmelz, M.*
AU  - Schuh-Hofer, S.*
AU  - Treede, R.D.*
AU  - Kuner, R.*
AU  - Oikonomou, D.*
AU  - Groener, J.B.*
AU  - Kopf, S.*
C1  - 52103
C2  - 43736
TI  - The quest for more research on painful diabetic neuropathy.
JO  - Neuroscience
PY  - 2017
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - Elevated levels of oxidative stress and neuronal inflammation in the hypothalamus or ventral midbrain, respectively, represent common denominators for obesity and Parkinson’s Disease (PD). However, little is known about defense mechanisms that protect neurons in these regions from oxidative damage. Here, we aimed to assess whether murine Gpx4, a crucial antioxidant enzyme that protects neurons from membrane damage and ferroptosis, is critical for the protection from neuronal inflammation in two distinct pathophysiologic diseases, namely metabolic dysfunction in diet-induced obesity or PD. Gpx4 was deleted from either AgRP or POMC neurons in the hypothalamus, essential for metabolic homeostasis, or from dopaminergic neurons in the ventral midbrain, governing behaviors such as anxiety or voluntary movement. To induce a pro-inflammatory environment, AgRP and POMC neuron-specific Gpx4 knockout mice were subjected to high-fat high-sucrose (HFHS) diet. To exacerbate oxidative stress in dopaminergic neurons of the ventral midbrain, we systemically co-deleted the PD-related gene DJ-1. Gpx4 was dispensable for the maintenance of cellular health and function of POMC neurons, even in mice exposed to obesogenic conditions. In contrast, HFHS-fed mice with Gpx4 deletion from AgRP neurons displayed increased body adiposity. Gpx4 expression and activity were diminished in the hypothalamus of HFHS-fed mice compared to standard diet-fed controls. Gpx4 deletion from dopaminergic neurons induced anxiety behavior, and diminished spontaneous locomotor activity when DJ-1 was co-deleted. Overall, these data suggest a physiological role for Gpx4 in balancing metabolic control signals and inflammation in AgRP but not POMC neurons. Moreover, Gpx4 appears to constitute an important rheostat against neuronal dysfunction and PD-like symptoms in dopaminergic circuitry within the ventral midbrain.
AU  - Schriever, S.C.
AU  - Zimprich, A.
AU  - Pfuhlmann, K.
AU  - Baumann, P.
AU  - Giesert, F.
AU  - Klaus, V.
AU  - Kabra, D.*
AU  - Hafen, U.
AU  - Romanov, A.
AU  - Tschöp, M.H.
AU  - Wurst, W.
AU  - Conrad, M.
AU  - Hölter, S.M.*
AU  - Weisenhorn, D.M.
AU  - Pfluger, P.T.
C1  - 50909
C2  - 42897
CY  - Oxford
SP  - 241-254
TI  - Alterations in neuronal control of body weight and anxiety behavior by glutathione peroxidase 4 deficiency.
JO  - Neuroscience
VL  - 357
PB  - Pergamon-elsevier Science Ltd
PY  - 2017
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - Parkinson's disease (PD) is the second most common neurodegenerative disorder, characterized by alterations of nigrostriatal dopaminergic neurotransmission. Compared to the wealth of data on the impairment of the dopamine system, relatively limited evidence is available concerning the role of major non-dopaminergic neurotransmitter systems in PD. Therefore, we comprehensively investigated the density and distribution of neurotransmitter receptors for glutamate, GABA, acetylcholine, adrenaline, serotonin, dopamine and adenosine in brains of homozygous aphakia mice being characterized by mutations affecting the Pitx3 gene. This genetic model exhibits crucial hallmarks of PD on the neuropathological, symptomatic and pharmacological level. Quantitative receptor autoradiography was used to characterize 19 different receptor binding sites in eleven brain regions in order to understand receptor changes on a systemic level. We demonstrated striking differential changes of neurotransmitter receptor densities for numerous receptor types and brain regions, respectively. Most prominent, a strong up-regulation of GABA receptors and associated benzodiazepine binding sites in different brain regions and concomitant down-regulations of striatal nicotinic acetylcholine and serotonergic receptor densities were found. Furthermore, the densities of glutamatergic kainate, muscarinic acetylcholine, adrenergic α1 and dopaminergic D2/D3 receptors were differentially altered. These results present novel insights into the expression of neurotransmitter receptors in Pitx3(ak) mice supporting findings on PD pathology in patients and indicating on the possible underlying mechanisms. The data suggest Pitx3(ak) mice as an appropriate new model to investigate the role of neurotransmitter receptors in PD. Our study highlights the relevance of non-dopaminergic systems in PD and for the understanding of its molecular pathology.
AU  - Cremer, J.N.*
AU  - Amunts, K.*
AU  - Graw, J.
AU  - Piel, M.*
AU  - Rösch, F.*
AU  - Zilles, K.*
C1  - 42892
C2  - 35725
SP  - 11-23
TI  - Neurotransmitter receptor density changes in Pitx3AK mice - a model relevant to Parkinson's disease.
JO  - Neuroscience
VL  - 285
PY  - 2015
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - The homeobox-containing transcription factor Otx2 controls the identity, fate and proliferation of mesencephalic dopaminergic (mesDA) neurons. Transgenic mice, in which Otx2 was conditionally overexpressed by a Cre recombinase expressed under the transcriptional control of the Engrailed1 gene (En1(Cre/+); tOtx2(ov/+)), show an increased number of mesDA neurons during development. In adult mice, Otx2 is expressed in a subset of neurons in the ventral tegmental area (VTA) and its overexpression renders mesDA more resistant to MPTP neurotoxin. Here we further investigated the neurological consequences of the increased number of mesDA neurons in En1(Cre/+); tOtx2(ov/+) adult mice. Immunohistochemistry for the active, glycosylated form of the dopamine transporter (glyco-Dat) showed that En1(Cre/+); tOtx2(ov/+) adult mice display an increased density of mesocortical DAergic fibers, as compared to control animals. Increased glyco-Dat staining was accompanied by a marked hypolocomotion in En1(Cre/+); tOtx2(ov/+) mice, as detected in the open field test. Since conditional knockout mice lacking Otx2 in mesDA precursors (En1(Cre/+); Otx2(floxv/flox) mice) show a marked resistance to kainic acid (KA) induced seizures, we investigated the behavioural response to KA in En1(Cre/+); tOtx2(ov/+) and control mice. No difference was observed between mutant and control mice, but En1(Cre/+); tOtx2(ov/+) mice showed a markedly different c-fos mRNA induction profile in the cerebral cortex and hippocampus after KA seizures, as compared to controls. Accordingly, an increased density of parvalbumin (PV) positive inhibitory interneurons was detected in deep layers of the frontal cortex of naïve En1(Cre/+); tOtx2(ov/+) mice, as compared to controls. These data indicate that Otx2 overexpression results in increased DAergic innervation and PV cell density in the fronto-parietal cortex, with important consequences on spontaneous locomotor activity and seizure-induced gene expression. Our results strengthen the notion that Otx2 mutant mouse models are a powerful genetic tool to unravel the molecular and behavioural consequences of altered development of the DAergic system.
AU  - Tripathi, P.P.*
AU  - Giovannantonio, L.G.*
AU  - Sanguinetti, E.*
AU  - Acampora, D.*
AU  - Allegra, M.*
AU  - Caleo, M.*
AU  - Wurst, W.
AU  - Simeone, A.*
AU  - Bozzi, Y.*
C1  - 28867
C2  - 33553
SP  - 173-183
TI  - Increased dopaminergic innervation in the brain of conditional mutant mice overexpressing Otx2: Effects on locomotor behaviour and seizure susceptibility.
JO  - Neuroscience
VL  - 261
PY  - 2014
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - Osmotic swelling of retinal neurons and glial cells is an important pathogenic factor of retinal edema formation. Here, we show that the neuroprotective factor osteopontin (OPN), which is released from retinal glial (Müller) cells after stimulation of the cells with glial cell line-derived neurotrophic factor (Del Río et al., 2011, Glia 59:821-832), inhibits the swelling of rat Müller cells induced by hypoosmotic exposure of retinal slices in the presence of barium ions and H2O2, respectively, and in slices of postischemic retinas. OPN did not inhibit the hypoosmotic swelling of bipolar cells in slices of control and postischemic retinas. The inhibitory effect of OPN on Müller cell swelling was dose-dependent, with a half-maximal effect at ∼0.6ng/ml. The effect of OPN was abrogated in the presence of pharmacological blockers of vascular endothelial growth factor (VEGF) receptor-2, metabotropic glutamate receptors, and purinergic receptors (P2Y1, adenosine A1 receptors), as well as of a neutralizing anti-VEGF antibody. The data suggest that OPN induces the release of VEGF, glutamate, ATP, and adenosine from Müller cells. The effect of OPN was also prevented by blockers of voltage-gated sodium channels (tetrodotoxin), T-type voltage-gated calcium channels (kurtoxin), potassium channels (clofilium), and chloride channels 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB). The swelling-inhibitory effect of OPN was dependent on intracellular calcium signaling, activation of phospholipase C and protein kinase C, and vesicular exocytosis of glutamate. In retinal slices, Müller glial cells display immunoreactivity of OPN. The data suggest that Müller cell-derived OPN has (in addition to the effects on photoreceptors and retinal neurons) autocrine effects. The neuroprotective effects of OPN may be in part mediated by the prevention of cytotoxic Müller cell swelling and the release of VEGF and adenosine from Müller cells.
AU  - Wahl, V.*
AU  - Vogler, S.*
AU  - Grosche, A.*
AU  - Pannicke, T.*
AU  - Ueffing, M.
AU  - Wiedemann, P.*
AU  - Reichenbach, A.*
AU  - Hauck, S.M.
AU  - Bringmann, A.*
C1  - 26268
C2  - 32153
SP  - 59-72
TI  - Osteopontin inhibits osmotic swelling of retinal glial (Müller) cells by inducing release of VEGF.
JO  - Neuroscience
VL  - 246
PB  - Pergamon-Elsevier
PY  - 2013
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - The concept that intestinal microbial composition not only affects the health of the gut, but also influences centrally-mediated systems involved in mood, is supported by a growing body of literature. Despite the emergent interest in brain-gut communication and its possible role in the pathogenesis of psychiatric disorders such as depression, particularly subtypes with accompanying gastrointestinal (GI) symptoms, there are few studies dedicated to the search for therapeutic solutions that address both central and peripheral facets of these illnesses. This study aims to assess the potential benefits of the probiotic Bifidobacterium infantis in the rat maternal separation (MS) model, a paradigm that has proven to be of value in the study of stress-related GI and mood disorders. MS adult rat offsprings were chronically treated with bifidobacteria or citalopram and subjected to the forced swim test (FST) to assess motivational state. Cytokine concentrations in stimulated whole blood samples, monoamine levels in the brain, and central and peripheral hypothalamic-pituitary-adrenal (HPA) axis measures were also analysed. MS reduced swim behavior and increased immobility in the FST, decreased noradrenaline (NA) content in the brain, and enhanced peripheral interleukin (IL)-6 release and amygdala corticotrophin-releasing factor mRNA levels. Probiotic treatment resulted in normalization of the immune response, reversal of behavioral deficits, and restoration of basal NA concentrations in the brainstem. These findings point to a more influential role for bifidobacteria in neural function, and suggest that probiotics may have broader therapeutic applications than previously considered.
AU  - Desbonnet, L.*
AU  - Garrett, L.
AU  - Clarke, G.*
AU  - Kiely, B.*
AU  - Cryan, J.F.*
AU  - Dinan, T.G.*
C1  - 5370
C2  - 27937
CY  - Oxford
SP  - 1179-1188
TI  - Effects of the probiotic Bifidobacterium infantis in the maternal separation model of depression.
JO  - Neuroscience
VL  - 170
IS  - 4
PB  - Pergamon-Elsevier Sci. Ltd.
PY  - 2010
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - Corticotropin-releasing hormone (CRH) coordinates neuroendocrine and behavioral adaptations to stress. Acute CRH administration in vivo activates extracellular signal-regulated kinase 1/2 (ERK1/2) in limbic brain areas, acting through the CRH receptor type 1 (CRH-R1). In the present study, we used CRH-COE-Cam mice that overexpress CRH in limbic-restricted areas, to analyze the effect of chronic CRH overexpression on ERK1/2 activation. By immunohistochemistry and confocal microscopy analysis we found that pERK1/2 levels in the basolateral amygdala (BLA) were similar in control and CRH overexpressing mice under basal conditions. Acute stress caused comparably increased levels of corticosterone in both control (CRH-COEcon-Cam) and CRH overexpressing (CRH-COEhom-Cam) animals. CRH-COEhom-Cam mice after stress showed reduced pERK1/2 immunoreactivity in the BLA compared to CRH-COEhom-Cam animals under basal conditions. Radioligand binding and in situ hybridization revealed higher density of CRH-R1 in the amygdala of CRH-COEhom mice under basal conditions compared to control littermates. A significant reduction of the receptor levels was observed in this area after acute stress, suggesting that stress may trigger CRH-R1 internalization/downregulation in these CRH overexpressing mice. Chronic CRH overexpression leads to reduced ERK1/2 activation in response to acute stress in the BLA.
AU  - Silberstein, S.*
AU  - Vogl, A.M.*
AU  - Refojo, D.*
AU  - Senin, S.A.*
AU  - Wurst, W.
AU  - Holsboer, F.*
AU  - Deussing, J.M.*
AU  - Arzt, E.*
C1  - 574
C2  - 26250
SP  - 610-617
TI  - Amygdaloid pERK1/2 in corticotropin-releasing hormone overexpressing mice under basal and acute stress conditions.
JO  - Neuroscience
VL  - 159
IS  - 2
PB  - Pergamon-Elsevier Science Ltd
PY  - 2009
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - Corticotropin releasing hormone (CRH) is the central modulator of the mammalian hypothalamic-pituitaryadrenal (HPA) axis. In addition, CRH affects other processes in the brain including learning, memory, and synaptic plasticity. Moreover, CRH has been shown to play a role in nerve cell survival under apoptotic conditions and to serve as an endogenous neuroprotectant in vitro. Employing mice over-expressing murine CRH in the CNS, we observed a differential response of CRH-overexpressing mice (CRH-COEhom-Nes) to acute excitotoxic stress induced by kainate compared with controls (CRH-COEcon-Nes). Interestingly, CRH-overexpression reduced the duration of epileptic seizures and prevented kainate-induced neurodegeneration and neuro-inflammation in the hippocampus. Our findings highlight a neuroprotective action of CRH in vivo. This neuroprotective effect was accompanied by increased levels of brain-derived neurotrophic factor (BDNF) in CRH-COEhom-Nes mice, suggesting a potential role for BDNF in mediating CRH-induced neuroprotective actions against acute excitotoxicity in vivo.
AU  - Hanstein, R.*
AU  - Lu, A.*
AU  - Wurst, W.
AU  - Holsboer, F.*
AU  - Deussing, J.M.*
AU  - Clement, A.B.*
AU  - Behl, C.*
C1  - 1936
C2  - 25901
SP  - 712-721
TI  - Transgenic overexpression of corticotropin releasing hormone provides partial protection against neurodegeneration in an in vivo model of acute excitotoxic stress.
JO  - Neuroscience
VL  - 156
IS  - 3
PB  - Elsevier
PY  - 2008
SN  - 0306-4522
ER  - 

TY  - JOUR
AB  - The establishment of the regional subdivisions of the vertebrate CNS is accomplished through the activity of different neuroepithelial organizing centers. The wingless/int (Wnt) family of secreted glycoproteins, among other factors, plays a crucial role in signaling from these centers. Wnt1 secreted from the boundary between the mid- and hindbrain, for instance, controls the development of this brain region and of associated neuronal populations. Different Wnts secreted from the caudomedial pallium, the cortical hem, pattern the adjacent hippocampal field. The first step in Wnt signal transduction is binding of the Wnt ligand to its receptors, the seven-pass transmembrane Frizzled proteins. Inactivation of different Frizzled genes in mice have revealed an extensive functional redundancy between these receptors. In order to discriminate between a possible participation of different Frizzled receptors in the transduction of Wnt signals at the mid-/hindbrain boundary and the cortical hem, we have performed a detailed expression study of the 10 known murine Frizzled genes at crucial stages of mouse embryonic development. Our analysis reveals a highly dynamic yet distinct expression pattern of individual Frizzled genes in the anterior neural tube of the developing mouse embryo. The overlapping spatio-temporal expression of at least two and up to six Frizzled genes in any region of the developing mouse brain, however, also suggests a vast functional redundancy of the murine Frizzled receptors. This redundancy has to be taken into consideration for future analyses of Frizzled receptor function at these signaling centers in the mouse.
AU  - Fischer, T.
AU  - Guimera, J.
AU  - Wurst, W.
AU  - Prakash, N.
C1  - 3384
C2  - 24850
SP  - 693-711
TI  - Distinct but redundant expression of the Frizzled Wnt receptor genes at signaling centers of the developing mouse brain.
JO  - Neuroscience
VL  - 147
IS  - 3
PB  - Elsevier
PY  - 2007
SN  - 0306-4522
ER  - 

TY  - JOUR
AU  - Schmidt, M.*
AU  - Oitzl, M.S.*
AU  - Müller, M.B.*
AU  - Ohl, F.*
AU  - Wurst, W.
AU  - Holsboer, F.*
AU  - Levine, S.*
AU  - de Kloet, E.R.*
C1  - 9975
C2  - 21092
SP  - 589-595
TI  - Regulation of the developing hypothalmic-pituitary-adrenal axis in corticotropin releasing hormone receptor 1-deficient mice. 
JO  - Neuroscience
VL  - 119
PY  - 2003
SN  - 0306-4522
ER  -