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Stem Nuclei (stem + nucleus)

Distribution by Scientific Domains
Life Sciences60%
Medical Sciences40%

Kinds of Stem Nuclei

  • brain stem nucleus
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    Selected Abstracts

    Splice-isoform specific immunolocalization of neuronal nitric oxide synthase in mouse and rat brain reveals that the PDZ-complex-building nNOS, ,-finger is largely exposed to antibodies

    DEVELOPMENTAL NEUROBIOLOGY, Issue 4 2007
    Kristina Langnaese
    Abstract Knock out mice deficient for the splice-isoform ,, of neuronal nitric oxide synthase (nNOS,,) display residual nitric oxide synthase activity and immunosignal. To attribute this signal to the two minor neuronal nitric oxide synthase splice variants, ,, and ,,, we generated isoform-specific anti-peptide antibodies against the nNOS,, specific ,,-finger motif involved in PDZ domain scaffolding and the nNOS,, specific N-terminus. The nNOS,, ,,-finger-specific antibody clearly recognized the 160-kDa band of recombinant nNOS,, on Western blots. Using immunocytochemistry, this antibody displayed, in rats and wild-type mice, a labeling pattern similar to but not identical with that obtained using a commercial pan-nNOS antibody. This similarity indicates that the majority of immunocytochemically detectable nNOS is not likely to be complexed with PDZ-domain proteins via the ,,-finger motif. This conclusion was confirmed by the inhibition of PSD-95/nNOS interaction by the nNOS,, ,,-finger antibody in pull-down assays. By contrast, nNOS,, ,,-finger labeling was clearly reduced in hippocampal and cortical neuropil areas enriched in NMDA receptor complex containing spine synapses. In nNOS,, knock out mice, nNOS,, was not detectable, whereas the pan-nNOS antibody showed a distinct labeling of cell bodies throughout the brain, most likely reflecting ,,/,,-isoforms in these cells. The nNOS,, antibody clearly detected bacterial expressed nNOS,, fusion protein and nNOS,, in overexpressing HEK cells by Western blotting. Immunocytochemically, individual cell bodies in striatum, cerebral cortex, and in some brain stem nuclei were labeled in knock out but not in wild-type mice, indicating an upregulation of nNOS,, in nNOS,, deficient animals. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007 [source]

    Long-range connectivity of mouse primary somatosensory barrel cortex

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2010
    Rachel Aronoff
    Abstract The primary somatosensory barrel cortex processes tactile vibrissae information, allowing rodents to actively perceive spatial and textural features of their immediate surroundings. Each whisker on the snout is individually represented in the neocortex by an anatomically identifiable ,barrel' specified by the segregated termination zones of thalamocortical axons of the ventroposterior medial nucleus, which provide the primary sensory input to the neocortex. The sensory information is subsequently processed within local synaptically connected neocortical microcircuits, which have begun to be investigated in quantitative detail. In addition to these local synaptic microcircuits, the excitatory pyramidal neurons of the barrel cortex send and receive long-range glutamatergic axonal projections to and from a wide variety of specific brain regions. Much less is known about these long-range connections and their contribution to sensory processing. Here, we review current knowledge of the long-range axonal input and output of the mouse primary somatosensory barrel cortex. Prominent reciprocal projections are found between primary somatosensory cortex and secondary somatosensory cortex, motor cortex, perirhinal cortex and thalamus. Primary somatosensory barrel cortex also projects strongly to striatum, thalamic reticular nucleus, zona incerta, anterior pretectal nucleus, superior colliculus, pons, red nucleus and spinal trigeminal brain stem nuclei. These long-range connections of the barrel cortex with other specific cortical and subcortical brain regions are likely to play a crucial role in sensorimotor integration, sensory perception and associative learning. [source]

    Changes in adult olfactory bulb neurogenesis in mice expressing the A30P mutant form of alpha-synuclein

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2009
    Franz Marxreiter
    Abstract In familial and sporadic forms of Parkinson's disease (PD), alpha-synuclein pathology is present in the brain stem nuclei and olfactory bulb (OB) long before Lewy bodies are detected in the substantia nigra. The OB is an active region of adult neurogenesis, where newly generated neurons physiologically integrate. While accumulation of wild-type alpha-synuclein is one of the pathogenic hallmarks of non-genetic forms of PD, the A30P alpha-synuclein mutation results in an earlier disease onset and a severe clinical phenotype. Here, we study the regulation of adult neurogenesis in the subventricular zone (SVZ)/OB system in a tetracycline-suppressive (tet-off) transgenic model of synucleinopathies, expressing human mutant A30P alpha-synuclein under the control of the calcium/calmodulin-dependent protein kinase II alpha (CaMK) promoter. In A30P transgenic mice alpha-synuclein was abundant at the site of integration in the glomerular cell layer of the OB. Without changes in proliferation in the SVZ, significantly fewer newly generated neurons were observed in the OB granule cell and glomerular layers of A30P transgenic mice than in controls, most probably due to increased cell death. By tetracycline-dependent abrogation of A30P alpha-synuclein expression, OB neurogenesis and programmed cell death was restored to control levels. Our results indicate that, using A30P conditional (tet-off) mice, A30P alpha-synuclein has a negative impact on olfactory neurogenesis and suppression of A30P alpha-synuclein enhances survival of newly generated neurons. This finding suggests that interfering with alpha-synuclein pathology can rescue newly generated neurons, possibly leading to new targets for therapeutic interventions in synucleinopathies. [source]

    Guidelines for the pathoanatomical examination of the lower brain stem in ingestive and swallowing disorders and its application to a dysphagic spinocerebellar ataxia type 3 patient

    NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 1 2003
    U. Rüb
    U. Rüb, E. R. Brunt, D. Del Turco, R. A. I. de Vos, K. Gierga, H. Paulson and H. Braak (2003) Neuropathology and Applied Neurobiology 29, 1,13 Guildelines for the pathoanatomical examination of the lower brain stem in ingestive and swallowing disorders and its application to a dysphagic spinocerebellar ataxia type 3 patient Despite the fact that considerable progress has been made in the last 20 years regarding the three-phase process of ingestion and the lower brain stem nuclei involved in it, no comprehensive descriptions of the ingestion-related lower brain stem nuclei are available for neuropathologists confronted with ingestive malfunctions. Here, we propose guidelines for the pathoanatomical investigation of these nuclei based on current knowledge with respect to ingestion and the nuclei responsible for this process. The application of these guidelines is described by drawing upon the example of the lower brain stem of a male patient with spinocerebellar ataxia type 3, also known as Machado-Joseph disease, who displayed malfunctions during the preparatory phase of ingestion, as well as lingual and pharyngeal phases of swallowing. By way of the representative application of the recommended investigation procedure to 100 µm serial sections through the patient's brain stem stained for lipofuscin pigment and Nissl material, we observed neuronal loss together with astrogliosis in nearly all of the ingestion-related lower brain stem nuclei (motor, principal and spinal trigeminal nuclei; facial nucleus; parvocellular reticular nucleus; ambiguus nucleus, motor nucleus of the dorsal glossopharyngeal and vagal area; gelatinous, medial, parvocellular and pigmented solitary nuclei; hypoglossal nucleus). In view of their known functional role in the three-phase process of ingestion, damage to these nuclei not only offers an explanation of the patient's malfunctions related to the preparatory phase of ingestion and lingual and pharyngeal phases of swallowing, but also suggests that the patient may have suffered from additional esophageal phase swallowing malfunctions not mentioned in his medical records. [source]

    Protein aggregation in Parkinson's disease

    ACTA NEUROLOGICA SCANDINAVICA, Issue 2010
    V. Gundersen
    Gundersen V. Protein aggregation in Parkinson's disease. Acta Neurol Scand: 2010: 122 (Suppl. 190): 82,87. © 2010 John Wiley & Sons A/S. Parkinson's disease (PD) is a primary neurodegenerative movement disorder. In most cases it occurs as a sporadic type of disease, but there are also rare familial forms. Pathologically Parkinson's disease is characterized by loss of dopaminergic neurons in the compact part of substantia nigra. As a part of the neurodegenerative process protein aggregates will accumulate as Lewy bodies in dopaminergic neurons (1). In addition, non-dopaminergic neurons are known to be affected in Parkinsons's disease, for example, in several brain stem nuclei and the olfactoric bulb (2,4). The pathogenic process underlying the death of dopaminergic neurons is far from fully understood. Along with mitochondrial dysfunction, excitotoxicity, neuroinflammation and oxidative stress (5,8), recent evidence indicates that accumulation of protein filaments in Lewy bodies actively takes part in the degeneration of neurons. This will be further discussed below. [source]