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  • 1
    Abstract: The transcription factor Nkx2-1 belongs to the homeobox-encoding family of proteins that have essential functions in prenatal brain development. Nkx2-1 is required for the specification of cortical interneurons and several neuronal subtypes of the ventral forebrain. Moreover, this transcription factor is involved in migratory processes by regulating the expression of guidance molecules. Interestingly, Nkx2-1 expression was recently detected in the mouse brain at postnatal stages. Using two transgenic mouse lines that allow prenatal or postnatal cell type-specific deletion of Nkx2-1, we show that continuous expression of the transcription factor is essential for the maturation and maintenance of cholinergic basal forebrain neurons in mice. Notably, prenatal deletion of Nkx2-1 in GAD67-expressing neurons leads to a nearly complete loss of cholinergic neurons and parvalbumin-containing GABAergic neurons in the basal forebrain. We also show that postnatal mutation of Nkx2-1 in choline acetyltransferase-expressing cells causes a striking reduction in their number. These degenerative changes are accompanied by partial denervation of their target structures and results in a discrete impairment of spatial memory.
    Type of Publication: Journal article published
    PubMed ID: 22098391
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    ISSN: 0304-8853
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Perfusion-fixed tissue blocks were incubated in high molar sucrose solutions, shock frozen in melting isopentane, and sectioned on a conventional cryostat. Semithin sections (2–4 μm) alternatingly stained for parvalbumin and glutamate decarboxylase enabled us to demonstrate the coexistence of both antigens in the same cell. Thick sections (40 μm) of central and peripheral nervous system tissue were immunostained and processed for correlated light and electron microscopic studies. At the electron microscopic level, the preservation of ultrastructural features such as membranes and synaptic contacts was comparable to that normally seen in vibratome sectioned material. Hence, this technique can successfully be used for preembedding coexistence studies and electron microscopic preembedding immunocytochemistry when vibratome sectioning is problematic.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1106
    Keywords: Key words Hippocampus ; Commissural fibers ; Reactive sprouting ; Synaptogenesis ; Synaptophysin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Expression of the synaptic vesicle protein synaptophysin was studied in lesion-induced sprouting neurons of the contralateral entorhinal cortex and in the contralateral dentate gyrus using immunocytochemistry at the light- and electron-microscopic level. Perikaryal immunoreactivity for synaptophysin was found between 8 and 10 days postlesion. Light microscopy revealed that synaptophysin immunostaining was present in almost all neurons of layers II and III of the contralateral medial entorhinal cortex. These neurons give rise to the sprouting, crossed temporodentate pathway. In addition, some hilar neurons of the contralateral dentate gyrus, which are the parent cells of sprouting commissural fibers, were immunostained for synaptophysin. Transient immunostaining for synaptophysin was observed within cell bodies and dendrites. Additionally, the cell bodies were outlined by immunoreactive puncta, identified by electron microscopy as nerve terminals. Our results revealed that sprouting neurons express the major synaptic vesicle protein synaptophysin during reactive synaptogenesis in a pattern that reflects biosynthesis and sorting of this protein as seen in developing neurons during synapse formation.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0568
    Keywords: Key words Neurodegeneration ; Entorhinal cortex ; Hippocampus ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The transentorhinal cortex (TEC) is a primate-specific transition zone between the entorhinal allocortex and the temporal isocortex. Neurons in the lamina pre-alpha of TEC are known to be the first to develop intraneuronal changes in the course of Alzheimer’s disease. In order to shed light on this important feature, we studied as yet unknown morphological and neurochemical characteristics of the TEC of the African green monkey (Cercopithecus aethiops sabaeus). Using light- and electron-microscopic immunocytochemistry, the distribution and morphology of neurons containing calcium-binding proteins were described and compared with those in the adjacent cortices. Light-microscopic analysis revealed that parvalbumin-containing neurons were distributed in all cortical layers. Calbindin-containing cells were fewer but also present in each layer. Calretinin-containing neurons were largely confined to the upper layers of the TEC. All three types of neuron showed pyramidal-like, multipolar and bipolar shapes; their dendrites were smooth or beaded. Ultrastructural studies revealed immunopositive somata with infolded nuclei and large amounts of cytoplasm. The somata were only sparsely innervated by symmetric synapses. Immunopositive dendrites were almost exclusively covered with immunonegative axon terminals establishing symmetric and asymmetric synapses. Immunopositive terminals established symmetric contacts with immunonegative dendrites and somata. Only occasionally, could synaptic contacts between immunopositive pre- and postsynaptic structures be observed. The comparison of neurons in the TEC and adjacent cortices revealed no striking differences. In summary, the morphological and neurochemical characteristics of TEC neurons as analyzed in our study do not provide an explanation for the early onset of neurodegenerative changes in the TEC.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1435-1463
    Keywords: Keywords: Dementia ; biochemical markers ; heavy metals ; neurodegeneration.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Alzheimer's disease (AD) is a common neurodegenerative disorder that leads to dementia and death. In addition to several genetic parameters, various environmental factors may influence the risk of getting AD. In order to test whether blood levels of the heavy metal mercury are increased in AD, we measured blood mercury concentrations in AD patients (n = 33), and compared them to age-matched control patients with major depression (MD) (n = 45), as well as to an additional control group of patients with various non-psychiatric disorders (n = 65). Blood mercury levels were more than two-fold higher in AD patients as compared to both control groups (p = 0.0005, and p = 0.0000, respectively). In early onset AD patients (n = 13), blood mercury levels were almost three-fold higher as compared to controls (p = 0.0002, and p = 0.0000, respectively). These increases were unrelated to the patients' dental status. Linear regression analysis of blood mercury concentrations and CSF levels of amyloid β-peptide (Aβ) revealed a significant correlation of these measures in AD patients (n = 15, r = 0.7440, p = 0.0015, Pearson type of correlation). These results demonstrate elevated blood levels of mercury in AD, and they suggest that this increase of mercury levels is associated with high CSF levels of Aβ, whereas tau levels were unrelated. Possible explanations of increased blood mercury levels in AD include yet unidentified environmental sources or release from brain tissue with the advance in neuronal death.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: The role of brain amyloid in the pathogenesis of Alzheimer's disease (AD) is discussed controversially, but combined genetic and biochemical evidence points to a central role of the gene encoding the amyloid precursor APP in at least some forms of AD. This article proposes that preventing brain amyloid formation is a rational concept for drug treatment of AD. We suggest that pharmacologically active ligands for specific cell surface receptor subtypes—normally stimulated by neurotransmitters, growth factors, and cytokines—constitute a class of chemicals that might be useful to accelerate processing of APP into non-amyloidogenic, and biologically active, derivatives. This class of agents includes muscarinic m1 and m3 agonists, serotoninergic 5-HT2a and 5-HT2c agonists, glutamatergic mGluR1 agonists, as well as agonists for bradykinin and vasopressin receptors.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 286 (1996), S. 293-303 
    ISSN: 1432-0878
    Keywords: Key words: Phaseolus vulgaris leucoagglutinin ; Anterograde tracing ; Entorhinal cortex ; Crossed temporo-ammonic pathway ; Crossed temporo-dentate pathway ; Rat (Sprague Dawley)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Neurons of the entorhinal cortex project to the hippocampus proper and dentate gyrus. This projection is called the ”perforant pathway” because it perforates the subiculum; current usage applies this term to all entorhino-hippocampal fibers. However, entorhinal fibers also reach Ammon’s horn via the alveus (”alvear pathway”), an alternative route first described by Cajal. The anterograde tracer Phaseolus vulgaris leucoagglutinin (PHAL) was used in order to analyze the contribution of this pathway to the temporo-ammonic projection. In the temporal portion of the rat hippocampus, most of the entorhinal fibers reach Ammon’s horn after perforating the subiculum (classical perforant pathway). At more septal levels, the number of entorhinal fibers that take the alvear pathway increases; in the septal portion of the hippocampal formation, most of the entorhinal fibers to hippocampal subfield CA1 reach this subfield via the alveus. These fibers make sharp right-angle turns in the alveus, perforate the pyramidal cell layer, and finally terminate in the stratum lacunosum-moleculare. The crossed temporo-ammonic fibers reach their termination area in the stratum lacunosum-moleculare of CA1 almost exclusively via the alveus. These data indicate that the alveus is a major route by which entorhinal fibers reach their targets in CA1.
    Type of Medium: Electronic Resource
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