The Experts below are selected from a list of 108 Experts worldwide ranked by ideXlab platform

Ranney R Mize - One of the best experts on this subject based on the ideXlab platform.

  • failure to disrupt development of Cholinergic Fiber patches in the superior colliculus in nitric oxide synthase deficient mice
    Developmental Brain Research, 1999
    Co-Authors: Christopher A Scheiner, John R Cork, Ranney R Mize
    Abstract:

    Abstract Nitric oxide (NO) has been shown to mediate refinement of glutamatergic axonal pathways during development. In this study, we investigated whether the development of a Cholinergic pathway in the intermediate gray layer (IGL) of the mouse superior colliculus (SC) is also mediated by NO. The pathway was labeled using an antibody directed against choline acetyltransferase (ChAT) and its distribution examined in normal C57/BL6 mice and in knockout mice in which the genes for the neuronal isoform of nitric oxide synthase (NOS) or both the endothelial and neuronal isoforms of NOS had been disrupted. We also examined the development of expression of NOS using nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) staining. NADPHd labeled cells were found within the IGL by P8 and formed loose clusters of cells by P12–P15. ChAT and NADPHd labeled Fibers were first observed at P12 and gradually established their characteristic two-tiered patchy pattern between P14 and P21. Comparison of the ChAT labeled Fiber distribution in normal, single nNOS and double e,nNOS knockout mice revealed no differences between these three groups. We therefore conclude that nitric oxide does not mediate refinement of this Cholinergic pathway.

  • inhibition of nitric oxide synthase fails to disrupt the development of Cholinergic Fiber patches in the rat superior colliculus
    Developmental Neuroscience, 1997
    Co-Authors: Ranney R Mize, Christopher A Scheiner, Michael F Salvatore, R J Cork
    Abstract:

    Nitric oxide may serve as a retrograde messenger to refine or stabilize synapses in the developing nervous system. Whether this action is dependent upon glutamate and the N-methyl- D

R J Cork - One of the best experts on this subject based on the ideXlab platform.

P.g.m. Luiten - One of the best experts on this subject based on the ideXlab platform.

  • 17β-Estradiol enhances cortical Cholinergic innervation and preserves synaptic density following excitotoxic lesions to the rat nucleus basalis magnocellularis
    Neuroscience, 2002
    Co-Authors: Katalin Horváth, Wolfgang Härtig, R.a. Van Der Veen, Johannes Keijser, Jan Mulder, M Ziegert, Van Der Eddy Zee, Tibor Harkany, P.g.m. Luiten
    Abstract:

    Estradiol exerts beneficial effects on neurodegenerative disorders associated with the decline of cognitive performance. The present study was designed to further investigate the effect of 17beta-estradiol on learning and memory, and to evaluate its neuroprotective action on Cholinergic cells of the nucleus basalis magnocellularis, a neural substrate of cognitive performance. Female rats were ovariectomized at an age of 6 months. Three weeks later they received injections of either a mid-physiological dose of 17beta-estradiol or vehicle (oil), every other day for 2 weeks. The effect of estradiol on cognitive performance was tested in two associative learning paradigms. In the two-way active shock avoidance task estradiol-replaced animals learned significantly faster, while in the passive shock avoidance test no differences were observed between the experimental groups. Subsequent unilateral infusion of N-methyl-D-aspartate in the nucleus basalis magnocellularis resulted in a significant loss of Cholinergic neurons concomitant with the loss of their Fibers invading the somatosensory cortex. Estradiol treatment did not affect the total number of choline-acetyltransferase-immunoreactive neurons and their coexpression of the p75 low-affinity neurotrophin receptor either contralateral or ipsilateral to the lesion. In contrast, Cholinergic Fiber densities in estradiol-treated animals were greater both in the contralateral and ipsilateral somatosensory cortices as was detected by quantitative choline-acetyltransferase and vesicular acetylcholine transporter immunocytochemistry. However, estradiol treatment did not affect the lesion-induced relative percentage loss of Cholinergic Fibers. A significant decline of synaptophysin immunoreactivity paralleled the Cholinergic damage in the somatosensory cortex of oil-treated animals, whereas an almost complete preservation of synaptic density was determined in estradiol-treated rats. Our results indicate that estradiol treatment enhances the cortical Cholinergic innervation but has no rescuing effect on Cholinergic nerve cells in the basal forebrain against excitotoxic damage. Nevertheless, estradiol may restore or maintain synaptic density in the cerebral cortex following Cholinergic Fiber loss. This estradiol effect may outweigh the lack of cellular protection on Cholinergic cells at the functional level.

  • Cholinergic Fiber aberrations in nucleus basalis lesioned rat and Alzheimer's disease.
    Neurobiology of aging, 1992
    Co-Authors: Ronald P.a. Gaykema, Louis B. Hersh, Csaba Nyakas, E. Horvath, C. Majtenyi, P.g.m. Luiten
    Abstract:

    Innervation density and morphological aberrations of Cholinergic Fibers were studied with choline acetyltransferase (ChAT) immunocytochemistry and acetylcholinesterase (AChE) histochemistry in 30-35 month-old aged rats and rats with long-term bilateral lesions of the magnocellular basal nucleus (MBN). In addition, AChE histochemistry was performed on human cortical sections derived from autopsy brains of normal aged and Alzheimer's disease (AD) patients. A limited but variable number of morphological alterations were observed in ChAT-immunoreactive Fibers in the cortex and the hippocampus of the aged control rats. The aged MBN-lesioned rats displayed a severely reduced number of Cholinergic Fibers in the denervated areas of the neocortex, whereas the surviving Fibers showed a strongly increased number of aberrations. Fiber anomalies were also observed in the cortex of the aged human subjects and Alzheimer patients, the latter showing a higher incidence of such aberrations. Only a part of these distended profiles were seen in close association with senile plaques as detected in the AChE-stained material. These findings suggest that experimental MBN lesions combined with aging share with AD the induction of large quantities of Fiber malformations. Implications of possible mechanisms in both conditions are discussed.

Christopher A Scheiner - One of the best experts on this subject based on the ideXlab platform.

  • failure to disrupt development of Cholinergic Fiber patches in the superior colliculus in nitric oxide synthase deficient mice
    Developmental Brain Research, 1999
    Co-Authors: Christopher A Scheiner, John R Cork, Ranney R Mize
    Abstract:

    Abstract Nitric oxide (NO) has been shown to mediate refinement of glutamatergic axonal pathways during development. In this study, we investigated whether the development of a Cholinergic pathway in the intermediate gray layer (IGL) of the mouse superior colliculus (SC) is also mediated by NO. The pathway was labeled using an antibody directed against choline acetyltransferase (ChAT) and its distribution examined in normal C57/BL6 mice and in knockout mice in which the genes for the neuronal isoform of nitric oxide synthase (NOS) or both the endothelial and neuronal isoforms of NOS had been disrupted. We also examined the development of expression of NOS using nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) staining. NADPHd labeled cells were found within the IGL by P8 and formed loose clusters of cells by P12–P15. ChAT and NADPHd labeled Fibers were first observed at P12 and gradually established their characteristic two-tiered patchy pattern between P14 and P21. Comparison of the ChAT labeled Fiber distribution in normal, single nNOS and double e,nNOS knockout mice revealed no differences between these three groups. We therefore conclude that nitric oxide does not mediate refinement of this Cholinergic pathway.

  • inhibition of nitric oxide synthase fails to disrupt the development of Cholinergic Fiber patches in the rat superior colliculus
    Developmental Neuroscience, 1997
    Co-Authors: Ranney R Mize, Christopher A Scheiner, Michael F Salvatore, R J Cork
    Abstract:

    Nitric oxide may serve as a retrograde messenger to refine or stabilize synapses in the developing nervous system. Whether this action is dependent upon glutamate and the N-methyl- D

Mary Lou Voytko - One of the best experts on this subject based on the ideXlab platform.

  • Effects of two years of estrogen loss or replacement on nucleus basalis Cholinergic neurons and Cholinergic Fibers to the dorsolateral prefrontal and inferior parietal cortex of monkeys.
    The Journal of comparative neurology, 2004
    Co-Authors: Gregory Paul Tinkler, Joseph R. Tobin, Mary Lou Voytko
    Abstract:

    The present study examined the long-term (2 years) effects of estrogen loss or estrogen replacement therapy (ERT) on Cholinergic neurons in the nucleus basalis of Meynert and on Cholinergic Fibers in the prefrontal and parietal cortex of adult female cynomolgus monkeys. Cholinergic Fiber density in layer II of the prefrontal cortex was decreased in monkeys who were ovariectomized and treated with placebo for 2 years. In contrast, ovariectomized monkeys receiving ERT for 2 years had Fiber densities that were comparable to those of intact controls. No differences in parietal Cholinergic Fiber density or nucleus basalis Cholinergic neuron number or volume were found among intact, ovariectomized, or ERT monkeys. Our results suggest that ERT is effective in preventing region-specific changes in cortical Cholinergic Fibers that result from the loss of circulating ovarian hormones. These modest but appreciable effects on Cholinergic neurobiology following long-term estrogen loss and ERT may contribute to changes in visuospatial attention function that is mediated by the prefrontal cortex. J. Comp. Neurol. 469:507–521, 2004. © 2004 Wiley-Liss, Inc.