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Freda D Miller - One of the best experts on this subject based on the ideXlab platform.

  • the p75 neurotrophin receptor mediates Neuronal apoptosis and is essential for naturally occurring sympathetic Neuron death
    Journal of Cell Biology, 1998
    Co-Authors: Shernaz X Bamji, Carrie G Causing, Raquel Aloyz, Marta Majdan, Christine D Pozniak, Daniel J Belliveau, Judi Kohn, Freda D Miller
    Abstract:

    Abstract. To determine whether the p75 neurotrophin receptor (p75NTR) plays a role in naturally occurring Neuronal death, we examined neonatal sympathetic Neurons that express both the TrkA tyrosine kinase receptor and p75NTR. When sympathetic Neuron survival is maintained with low quantities of NGF or KCl, the neurotrophin brain-derived neurotrophic factor (BDNF), which does not activate Trk receptors on sympathetic Neurons, causes Neuronal apoptosis and increased phosphorylation of c-jun. Function-blocking antibody studies indicate that this apoptosis is due to BDNF-mediated activation of p75NTR. To determine the physiological relevance of these culture findings, we examined sympathetic Neurons in BDNF−/− and p75NTR−/− mice. In BDNF−/− mice, sympathetic Neuron number is increased relative to BDNF+/+ littermates, and in p75NTR−/− mice, the normal period of sympathetic Neuron death does not occur, with Neuronal attrition occurring later in life. This deficit in apoptosis is intrinsic to sympathetic Neurons, since cultured p75NTR−/− Neurons die more slowly than do their wild-type counterparts. Together, these data indicate that p75NTR can signal to mediate apoptosis, and that this mechanism is essential for naturally occurring sympathetic Neuron death.

  • synaptic innervation density is regulated by Neuron derived bdnf
    Neuron, 1997
    Co-Authors: Carrie G Causing, Andrew T Gloster, Raquel Aloyz, Shernaz X Bamji, Eddie Chang, Jim Fawcett, George A Kuchel, Freda D Miller
    Abstract:

    Abstract In this report, we have examined the role of Neuron-derived BDNF at an accessible synapse, that of preganglionic Neurons onto their sympathetic Neuron targets. Developing and mature sympathetic Neurons synthesize BDNF, and preganglionic Neurons express the full-length BDNF/TrkB receptor. When sympathetic Neuron-derived BDNF is increased 2- to 4-fold in transgenic mice, preganglionic cell bodies and axons hypertrophy, and the synaptic innervation to sympathetic Neurons is increased. Conversely, when BDNF synthesis is eliminated in BDNF −/− mice, preganglionic synaptic innervation to sympathetic Neurons is decreased. Together these results indicate that variations in Neuronal neurotrophin synthesis directly regulate Neuronal circuitry by selectively modulating synaptic innervation density.

David J. Maxwell - One of the best experts on this subject based on the ideXlab platform.

  • Serotoninergic and noradrenergic axons make contacts with Neurons of the ventral spinocerebellar tract in the cat
    The Journal of comparative neurology, 2002
    Co-Authors: Ingela Hammar, David J. Maxwell
    Abstract:

    Contacts between monoaminergic fibers and electrophysiologically identified Neurons of the ventral spinocerebellar tract were investigated in the cat. Five Neurons were labeled intracellularly with rhodamine dextran, and monoaminergic fibers were revealed with antibodies against serotonin and dopamine beta-hydroxylase. The distribution of appositions between monoaminergic varicosities and the soma and the whole length of dendrites of these Neurons was examined by using a three-channel confocal microscope. The analysis showed that close appositions between monoaminergic fibers and labeled processes occurred over the whole surface of the Neurons. The highest percentage of such appositions was found on proximal dendrites, for both serotonin (37%) and noradrenaline (57%). The total number of serotoninergic contacts (66–134 per Neuron) by far exceeded that of noradrenergic contacts (3–36 per Neuron). Contacts between serotoninergic fibers and two Neurons were analyzed by using electron microscopy. These Neurons were labeled intracellularly with horseradish peroxidase, and serotoninergic varicosities were identified by immunocytochemistry. Six of 10 serially analyzed boutons in apposition to proximal dendrites were found to form morphologic synapses. The identification of the remaining four was inconclusive. These results indicate that many of the appositions seen in confocal microscopy may represent direct synaptic contacts. They also indicate that monoaminergic Neurons may modulate activity of Neurons of the ventral spinocerebellar tract by direct postsynaptic actions in addition to any effects evoked by means of volume transmission. J. Comp. Neurol. 443:310–319, 2002. © 2002 Wiley-Liss, Inc.

Carrie G Causing - One of the best experts on this subject based on the ideXlab platform.

  • the p75 neurotrophin receptor mediates Neuronal apoptosis and is essential for naturally occurring sympathetic Neuron death
    Journal of Cell Biology, 1998
    Co-Authors: Shernaz X Bamji, Carrie G Causing, Raquel Aloyz, Marta Majdan, Christine D Pozniak, Daniel J Belliveau, Judi Kohn, Freda D Miller
    Abstract:

    Abstract. To determine whether the p75 neurotrophin receptor (p75NTR) plays a role in naturally occurring Neuronal death, we examined neonatal sympathetic Neurons that express both the TrkA tyrosine kinase receptor and p75NTR. When sympathetic Neuron survival is maintained with low quantities of NGF or KCl, the neurotrophin brain-derived neurotrophic factor (BDNF), which does not activate Trk receptors on sympathetic Neurons, causes Neuronal apoptosis and increased phosphorylation of c-jun. Function-blocking antibody studies indicate that this apoptosis is due to BDNF-mediated activation of p75NTR. To determine the physiological relevance of these culture findings, we examined sympathetic Neurons in BDNF−/− and p75NTR−/− mice. In BDNF−/− mice, sympathetic Neuron number is increased relative to BDNF+/+ littermates, and in p75NTR−/− mice, the normal period of sympathetic Neuron death does not occur, with Neuronal attrition occurring later in life. This deficit in apoptosis is intrinsic to sympathetic Neurons, since cultured p75NTR−/− Neurons die more slowly than do their wild-type counterparts. Together, these data indicate that p75NTR can signal to mediate apoptosis, and that this mechanism is essential for naturally occurring sympathetic Neuron death.

  • synaptic innervation density is regulated by Neuron derived bdnf
    Neuron, 1997
    Co-Authors: Carrie G Causing, Andrew T Gloster, Raquel Aloyz, Shernaz X Bamji, Eddie Chang, Jim Fawcett, George A Kuchel, Freda D Miller
    Abstract:

    Abstract In this report, we have examined the role of Neuron-derived BDNF at an accessible synapse, that of preganglionic Neurons onto their sympathetic Neuron targets. Developing and mature sympathetic Neurons synthesize BDNF, and preganglionic Neurons express the full-length BDNF/TrkB receptor. When sympathetic Neuron-derived BDNF is increased 2- to 4-fold in transgenic mice, preganglionic cell bodies and axons hypertrophy, and the synaptic innervation to sympathetic Neurons is increased. Conversely, when BDNF synthesis is eliminated in BDNF −/− mice, preganglionic synaptic innervation to sympathetic Neurons is decreased. Together these results indicate that variations in Neuronal neurotrophin synthesis directly regulate Neuronal circuitry by selectively modulating synaptic innervation density.

Shernaz X Bamji - One of the best experts on this subject based on the ideXlab platform.

  • the p75 neurotrophin receptor mediates Neuronal apoptosis and is essential for naturally occurring sympathetic Neuron death
    Journal of Cell Biology, 1998
    Co-Authors: Shernaz X Bamji, Carrie G Causing, Raquel Aloyz, Marta Majdan, Christine D Pozniak, Daniel J Belliveau, Judi Kohn, Freda D Miller
    Abstract:

    Abstract. To determine whether the p75 neurotrophin receptor (p75NTR) plays a role in naturally occurring Neuronal death, we examined neonatal sympathetic Neurons that express both the TrkA tyrosine kinase receptor and p75NTR. When sympathetic Neuron survival is maintained with low quantities of NGF or KCl, the neurotrophin brain-derived neurotrophic factor (BDNF), which does not activate Trk receptors on sympathetic Neurons, causes Neuronal apoptosis and increased phosphorylation of c-jun. Function-blocking antibody studies indicate that this apoptosis is due to BDNF-mediated activation of p75NTR. To determine the physiological relevance of these culture findings, we examined sympathetic Neurons in BDNF−/− and p75NTR−/− mice. In BDNF−/− mice, sympathetic Neuron number is increased relative to BDNF+/+ littermates, and in p75NTR−/− mice, the normal period of sympathetic Neuron death does not occur, with Neuronal attrition occurring later in life. This deficit in apoptosis is intrinsic to sympathetic Neurons, since cultured p75NTR−/− Neurons die more slowly than do their wild-type counterparts. Together, these data indicate that p75NTR can signal to mediate apoptosis, and that this mechanism is essential for naturally occurring sympathetic Neuron death.

  • synaptic innervation density is regulated by Neuron derived bdnf
    Neuron, 1997
    Co-Authors: Carrie G Causing, Andrew T Gloster, Raquel Aloyz, Shernaz X Bamji, Eddie Chang, Jim Fawcett, George A Kuchel, Freda D Miller
    Abstract:

    Abstract In this report, we have examined the role of Neuron-derived BDNF at an accessible synapse, that of preganglionic Neurons onto their sympathetic Neuron targets. Developing and mature sympathetic Neurons synthesize BDNF, and preganglionic Neurons express the full-length BDNF/TrkB receptor. When sympathetic Neuron-derived BDNF is increased 2- to 4-fold in transgenic mice, preganglionic cell bodies and axons hypertrophy, and the synaptic innervation to sympathetic Neurons is increased. Conversely, when BDNF synthesis is eliminated in BDNF −/− mice, preganglionic synaptic innervation to sympathetic Neurons is decreased. Together these results indicate that variations in Neuronal neurotrophin synthesis directly regulate Neuronal circuitry by selectively modulating synaptic innervation density.

Kamal Masaki - One of the best experts on this subject based on the ideXlab platform.

  • parkinsonian signs and substantia nigra Neuron density in decendents elders without pd
    Annals of Neurology, 2004
    Co-Authors: Webster G Ross, Helen Petrovitch, Robert D Abbott, James S Nelson, William R Markesbery, Daron G Davis, John Hardman, Lenore J Launer, Kamal Masaki
    Abstract:

    Substantia nigra (SN) Neurons were counted on single, transverse caudal midbrain sections from 217 male participants in the Honolulu-Asia Aging Study, aged 74–97 years at death. Quadrants areas within the SN were determined with a planimeter and Neuronal density was expressed as Neurons/mm2 for 10 Parkinson's disease (PD) cases, 29 incidental Lewy body cases, and 178 controls with neither condition. Mean densities in all quadrants were significantly lower in the PD group compared with the other groups (p = 0.006). This relationship was strongest in the ventrolateral quadrant. In a subgroup of 50 controls who were examined with the Unified Parkinson's Disease Rating Scale an average of 2.1 years prior to death, there was an association of stooped posture (p = 0.009), postural instability (p = 0.013), body bradykinesia (p = 0.048), and gait disturbance (p = 0.05) with Neuron density in the dorsolateral quadrant; and impaired speech (p = 0.014), abnormal facial expression (p = 0.022), and difficulty rising from a chair (p = 0.032) with Neuron density in the dorsomedial quadrant. There was a significant association of increasing number of signs present with decreasing Neuron density in both quadrants (p = 0.001 for trend). Low SN Neuron density may be the basis for parkinsonian signs in the elderly without PD. Ann Neurol 2004