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  • Formation of perineuronal nets in organotypic mouse brain slice cultures is independent of neuronal glutamatergic activity. 17561838

    Perineuronal nets (PNs) are a specialized form of the extracellular matrix and cover specific sets of neurons in distinct brain areas. Animal experiments on sensory visual deprivation have demonstrated that the generation of PNs around neurons of the visual cortex is dependent on neuronal activity during the critical period of visual experience. The importance of the activity of specific neurotransmitter systems for PN formation has, however, not yet been demonstrated. Based on the predominantly glutamatergic innervation of the visual cortex we hypothesized that reduced glutamatergic activity impairs the development of PNs. To address this question, genetic mouse models with compromised glutamate release [Munc13-1-knockout (KO) and Munc13-1/2 double-KO (DKO)] and chronic pharmacological treatments interfering with specific steps of glutamatergic transmission were used. Under experimental conditions of glutamatergic hypofunction PN formation was studied in organotypic brain slice cultures with Wisteria floribunda lectin binding and with aggrecan immunohistochemistry. After cultivation for 21 days a regular PN formation was observed in brain slices (i) derived from Munc13-1-KO and Munc13-1/2-DKO mice, (ii) after blockade of metabotropic and ionotropic glutamate receptors with MCPG and kynurenate, and (iii) after suppression of glutamate release by blockade of presynaptic Ca++ channels with riluzole. Nonselective suppression of neuronal activity by blockade of voltage-gated sodium channels with tetrodotoxin clearly inhibited PN formation. These results indicate that neuronal activity is required but that the glutamatergic system is not essential for PN development.
    Document Type:
    Reference
    Product Catalog Number:
    AB1031
    Product Catalog Name:
    Anti-Aggrecan Antibody

  • Brain-derived neurotrophic factor mediates activity-dependent dendritic growth in nonpyramidal neocortical interneurons in developing organotypic cultures. 12843269

    Brain-derived neurotrophic factor (BDNF) promotes postnatal maturation of GABAergic inhibition in the cerebral and cerebellar cortices, and its expression and release are enhanced by neuronal activity, suggesting that it acts in a feedback manner to maintain a balance between excitation and inhibition during development. BDNF promotes differentiation of cerebellar, hippocampal, and neostriatal inhibitory neurons, but its effects on the dendritic development of neocortical inhibitory interneurons remain unknown. Here, we show that BDNF mediates depolarization-induced dendritic growth and branching in neocortical interneurons. To visualize inhibitory interneurons, we biolistically transfected organotypic cortical slice cultures from neonatal mice with green fluorescent protein (GFP) driven by the glutamic acid decarboxylase (GAD)67 promoter. Nearly all GAD67-GFP-expressing neurons were nonpyramidal, many contained GABA, and some expressed markers of neurochemically defined GABAergic subtypes, indicating that GAD67-GFP-expressing neurons were GABAergic. We traced dendritic trees from confocal images of the same GAD67-GFP-expressing neurons before and after a 5 d growth period, and quantified the change in total dendritic length (TDL) and total dendritic branch points (TDBPs) for each neuron. GAD67-GFP-expressing neurons growing in control medium exhibited a 20% increase in TDL, but in 200 ng/ml BDNF or 10 mm KCl, this increase nearly doubled and was accompanied by a significant increase in TDBPs. Blocking action potentials with TTX did not prevent the BDNF-induced growth, but antibodies against BDNF blocked the growth-promoting effect of KCl. We conclude that BDNF, released by neocortical pyramidal neurons in response to depolarization, enhances dendritic growth and branching in nearby inhibitory interneurons.
    Document Type:
    Reference
    Product Catalog Number:
    AB1778