Adult Neurons (adult + neuron)

Distribution by Scientific Domains


Selected Abstracts


Extracellular matrix molecules and synaptic plasticity: immunomapping of intracellular and secreted Reelin in the adult rat brain

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2006
Tania Ramos-Moreno
Abstract Reelin, a large extracellular matrix glycoprotein, is secreted by several neuron populations in the developing and adult rodent brain. Secreted Reelin triggers a complex signaling pathway by binding lipoprotein and integrin membrane receptors in target cells. Reelin signaling regulates migration and dendritic growth in developing neurons, while it can modulate synaptic plasticity in adult neurons. To identify which adult neural circuits can be modulated by Reelin-mediated signaling, we systematically mapped the distribution of Reelin in adult rat brain using sensitive immunolabeling techniques. Results show that the distribution of intracellular and secreted Reelin is both very widespread and specific. Some interneuron and projection neuron populations in the cerebral cortex contain Reelin. Numerous striatal neurons are weakly immunoreactive for Reelin and these cells are preferentially located in striosomes. Some thalamic nuclei contain Reelin-immunoreactive cells. Double-immunolabeling for GABA and Reelin reveals that the Reelin-immunoreactive cells in the visual thalamus are the intrinsic thalamic interneurons. High local concentrations of extracellular Reelin selectively outline several dendrite spine-rich neuropils. Together with previous mRNA data, our observations suggest abundant axoplasmic transport and secretion in pathways such as the retino-collicular tract, the entorhino-hippocampal (,perforant') path, the lateral olfactory tract or the parallel fiber system of the cerebellum. A preferential secretion of Reelin in these neuropils is consistent with reports of rapid, activity-induced structural changes in adult brain circuits. [source]


Cholesterol homeostasis markers are localized to mouse hippocampal pyramidal and granule layers

HIPPOCAMPUS, Issue 8 2010
Chris M. Valdez
Abstract Changes in brain cholesterol homeostasis are associated with multiple diseases, such as Alzheimer's and Huntington's; however, controversy persists as to whether adult neurons produce their own cholesterol, or if it is outsourced to astrocytes. To address this issue, we analyzed 25 genes most immediately involved in cholesterol homeostasis from in situ data provided by the Allen Brain Mouse Atlas. We compared the relative mRNA expression in the pyramidal and granule layers, populated with neurons, with the rest of the hippocampus which is populated with neuronal processes and glia. Comparing the expression of the individual genes to markers for neurons and astrocytes, we found that cholesterol homeostasis genes are preferentially targeted to neuronal layers. Therefore, changes in gene expression levels might affect neuronal populations directly. © 2010 Wiley-Liss, Inc. [source]


Isoflurane enhances spontaneous Ca2+ oscillations in developing rat hippocampal neurons in vitro

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2009
Q. XIANG
Background: During the nervous system development, spontaneous synchronized Ca2+ oscillations are thought to possess integrative properties because their amplitude and frequency can influence the patterning of neuronal connection, neuronal differentiation, axon outgrowth, and long-distance wiring. Accumulating studies have confirmed that some drugs such as volatile anesthetic isoflurane produced histopathologic changes in the central nervous system in juvenile animal models. Because the hippocampus plays an important role in learning and memory, the present work was designed to characterize the Ca2+ oscillations regulated by volatile anesthetic isoflurane in primary cultures of developing hippocampal neurons (5-day-cultured). Methods: Primary cultures of rat hippocampal neurons (5-day-cultured) were loaded with the Ca2+ indicator Fluo-4AM (4 ,M) and were studied with a confocal laser microscope. Results: Approximately 22% of 5-day-cultured hippocampal neurons exhibited typical Ca2+ oscillations. These oscillations were dose-dependently enhanced by isoflurane (EC50 0.5 MAC, minimum alveolar concentration) and this effect could be reverted by bicuculline (50 ,M), a specific ,-aminobutyric acid (GABAA) receptor antagonist. Conclusion: Unlike its depressant effect on the Ca2+ oscillations in adult neurons in previous researches, isoflurane dose-dependently enhanced calcium oscillations in developing hippocampal neurons by activating GABAA receptors, a major excitatory receptor in synergy with N -methyl- d -aspartate receptors at the early stages of development. It may be involved in the mechanism of an isoflurane-induced neurotoxic effect in the developing rodent brain. [source]


Rho-associated kinase (ROCK) inhibitor, Y27632, promotes neurite outgrowth in PC12 cells in the absence of NGF

JOURNAL OF NEUROCHEMISTRY, Issue 2002
R. Nath
Neurite extension and retraction are very important processes in the formation of neuronal networks. A strategy for fostering axonal regrowth/regeneration of injured adult neurons is attractive therapeutically for various diseases such as traumatic brain injury, stroke and Alzheimer's disease. The Rho family of small GTPases, including Rac and Cdc42 have been shown to be involved in promoting neurite outgrowth. On the other hand, activation of RhoA induces collapse of growth cone and retraction of neurites. Rho-associated kinase (ROCK) an effector molecule of RhoA, is downstream of a number of axonal outgrowth and growth cone collapse inhibition mechanisms. In the present study, we sought to identify the role of ROCK in neurite outgrowth in PC12 cells. Y27632, a specific inhibitor of ROCK, induced a robust increase in neurite outgrowth in these cells within 24,48 h as visualized by phase contrast microscopy. Staining with FITC-tubulin or phalloidin show extended neurites in PC12 cells treated with Y27632, comparable to that with 100 ng/mL of NGF. Assessment of other biochemical markers of neurite outgrowth such as GAP43, neurofilament and tyrosine hydroxylase phosphorylation further indicates that inhibition of ROCK in PC12 cells causes differentiation of these cells to a neuronal phenotype. [source]


Glucose-dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion-affected expression, and impaired regenerative axonal growth

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2009
Bettina A. Buhren
Abstract Glucose-dependent insulinotropic polypeptide (GIP) was initially described to be rapidly regulated by endocrine cells in response to nutrient ingestion, with stimulatory effects on insulin synthesis and release. Previously, we demonstrated a significant up-regulation of GIP mRNA in the rat subiculum after fornix injury. To gain more insight into the lesion-induced expression of GIP and its receptor (GIPR), expression profiles of the mRNAs were studied after rat sciatic nerve crush injury in 1) affected lumbar dorsal root ganglia (DRG), 2) spinal cord segments, and 3) proximal and distal nerve fragments by means of quantitative RT-PCR. Our results clearly identified lesion-induced as well as tissue type-specific mRNA regulation of GIP and its receptor. Furthermore, comprehensive immunohistochemical stainings not only confirmed and exceeded the previous observation of neuronal GIP expression but also revealed corresponding GIPR expression, implying putative modulatory functions of GIP/GIPR signaling in adult neurons. In complement, we also observed expression of GIP and its receptor in myelinating Schwann cells and oligodendrocytes. Polarized localization of GIPR in the abaxonal Schwann cell membranes, plasma membrane-associated GIPR expression of satellite cells, and ependymal GIPR expression strongly suggests complex cell type-specific functions of GIP and GIPR in the adult nervous system that are presumably mediated by autocrine and paracrine interactions, respectively. Notably, in vivo analyses with GIPR-deficient mice suggest a critical role of GIP/GIPR signal transduction in promoting spontaneous recovery after nerve crush, insofar as traumatic injury of GIPR-deficient mouse sciatic nerve revealed impaired axonal regeneration compared with wild-type mice. © 2009 Wiley-Liss, Inc. [source]


Statistical morphological analysis of hippocampal principal neurons indicates cell-specific repulsion of dendrites from their own cell

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2003
Alexei V. Samsonovich
Abstract Traditionally, the sources of guidance cues for dendritic outgrowth are mainly associated with external bodies (A) rather than with the same neuron from which dendrites originate (B). To quantify the relationship between factors A and B as determinants of the adult dendritic shape, the morphology of 83 intracellularly characterized, stained, completely reconstructed, and digitized principal neurons of the rat hippocampus was statistically analyzed using Bayesian optimization. It was found that the dominant directional preference (tropism) manifested in dendritic turns is to grow away from the soma rather than toward the incoming fibers or in any other fixed direction; therefore, B is predominant. Results are robust and consistent for all examined morphological classes (dentate gyrus granule cells, basal and apical trees of CA3 and CA1 pyramidal cells). In addition, computer remodeling of neurons based on the measured parameters produced virtual structures consistent with real morphologies, as confirmed by measurement of several global emergent parameters. Thus, the simple description of dendritic shape based on dendrites' tendency to grow straight, away from their own soma, and with additional random deflections, proves remarkably accurate and complete. Although based on adult neurons, these results suggest that dendritic guidance during development may be associated primarily with the host cell. This possibility challenges the traditional concept of dendritic guidance: in that hippocampal cells are densely packed and have highly overlapping dendritic fields, the somatodendritic repulsion must be cell specific. Plausible mechanisms involving extracellular effects of spikes are discussed, together with feasible experimental tests and predicted results. © 2002 Wiley-Liss, Inc. [source]


Diabetic neuropathy: therapies on the horizon

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 9 2009
Danish Mahmood
Abstract Objectives This is a review of emerging interventions from the recent preclinical and clinical literature that demonstrate the potential for effectiveness in the therapy of diabetic neuropathy (DN). DN is the most common complication of diabetes mellitus and up to 50% of patients with type 1 and type 2 forms have some or other form of neuropathy. The pathology of DN is characterized by progressive nerve fibre loss that gives rise to positive and negative clinical signs and symptoms such as pain, paraesthesiae and loss of sensation. Key findings There are very few drugs available to directly treat DN. Those that are clinically indicated provide symptomatic relief but do not repair or reverse underlying nerve damage. However, some agents are in clinical development that may support adult neurons and direct reparative processes after injury stages. Several disease modifying drugs such as aldose reductase inhibitors and protein kinase C inhibitors are in phase III development. Agents on the horizon include neurotrophic factors, growth factors, gene therapy, immunotherapy, poly(ADP-ribose) polymerase inhibitors and non-immunosuppressive immunophilin ligands. Summary Progress has been made toward understanding the biochemical mechanisms leading to diabetic neuropathy, and as a result, new treatment modalities are being explored. The pathogenesis, types and approaches for treating DN together with the newer therapeutic interventions on the horizon are discussed. [source]


Life-span phenotypes of elav and Rbp9 in Drosophila suggest functional cooperation of the two elav-family protein genes

ARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 4 2010
Gakuta Toba
Abstract The ELAV family of RNA-binding proteins is involved in various aspects of the post-transcriptional regulation of gene expression, from alternative splicing to translation. The members of this family have been shown to interact with each other and have been suggested to function as homo- and/or hetero-multimers. However, the functional interactions among them have not been demonstrated in vivo. In this study, we examined the genetic interaction between elav and Rbp9, two of the three genes encoding ELAV-family proteins in Drosophila. Mutants of both elav and Rbp9 showed shorter life spans than the control, with elav showing a shorter life span than Rbp9. The survival curve of elav-Rbp9 double-mutant flies was indistinguishable from that of elav single-mutant flies, suggesting that both mutations affect longevity through the same pathway. Considering the fact that both genes are co-expressed in adult neurons, we hypothesize that ELAV and Rbp9 cooperate to maintain the functional integrity of the adult nervous system. © 2010 Wiley Periodicals, Inc. [source]