Brain-derived neurotrophic factor (BDNF) is involved in the differentiation and the survival of neurons. It has also been shown to be associated with the regrowth of neurons of damaged spinal cord and the modulation of ionic currents by acting on sodium channels and NMDA receptors through tyrosine kinase B (TrkB) receptors. We investigated the effects of BDNF on rhythm generation induced by disinhibition in dissociated cultures from embryonic rat spinal cord (E14), with extracellular multisite recordings (MultiElectrode Arrays, MEAs) or intracellular patch-clamp recordings. Exogenous BDNF had only minor effects on the bursting by increasing the activity during the burst. This increase of activity is suggested to be mediated by a potentiation of the postsynaptic NMDA receptors because it has been found that BDNF potentiates the NMDA-evoked depolarization in cultures incubated with BDNF for 10 min. Possible direct effects of BDNF on sodium channels were also investigated by local application of BDNF to the soma of patched neurons but no depolarization was observed. Long-term application of BDNF strongly decreased the activity during the burst and also the number of active electrodes, possibly due to a decrease in network density. 相似文献
To enhance medical cooperation between the hospitals and clinics around Osaka local area, the healthcare network system, named Osaka Community Healthcare Information System (OCHIS), was established with support of a supplementary budget from the Japanese government in fiscal year 2002. Although the system has been based on healthcare public key infrastructure (PKI), there remain security issues to be solved technically and operationally. An experimental study was conducted to elucidate the central and the local function in terms of a registration authority and a time stamp authority in contract with the Japanese Medical Information Systems Organization (MEDIS) in 2003. This paper describes the experimental design and the results of the study concerning message security. 相似文献
In vitro experiments were performed on brainstem – spinal cord preparations from mouse neonates to compare the noradrenergic regulations of the respiratory network in the control C3H/HeJ strain and the transgenic Tg8 strain which has been created from the C3H/HeJ strain by deletion of the gene encoding monoamine oxidase A (MAOA), the main enzyme for serotonin degradation. In both control and MAOA-deficient strains, we show: (i) that the pontine A5 area exerts a potent inhibitory modulation on the respiratory rhythm generator; (ii) that noradrenaline application induces a tonic phrenic activity; and (iii) that noradrenaline increases the respiratory rhythm. The latter effect is however delayed and weak in the Tg8 strain. Therefore, MAOA-deficiency has only slightly altered the noradrenergic regulations of the respiratory network. 相似文献
Many eukaryotic cells depend on proper cell polarization for their development and physiological function. The establishment of these polarities often involve the subcellular localization of a specific subset of proteins, RNAs and organelles. In Drosophila, the microtubule-dependent BicD (BicaudalD) localization machinery is involved in the proper localization of mRNA during oogenesis and embryogenesis and the proper positioning of the oocyte and photoreceptor nuclei. BicD acts together with the minus-end directed motor dynein as well as Egl and Lis-1. The finding that the mammalian homologs of BicD function in retrograde Golgi-to-ER transport has supported the view that BicD may be part of a repeatedly used and evolutionary conserved localization machinery. In this review we focus on the various processes in which BicD is involved during Drosophilian development and in mammals. In addition, we evaluate the interactions between BicD, the dynein localization machinery and associated factors. 相似文献
Neural dynamics in organotypic cortex-striatum co-cultures grown for three to six weeks under conditions of dopamine deficiency are described. Single neuron activities were recorded intra- and extracellularly, and spatiotemporal spreading of population activity was mapped using voltage-sensitive dyes. The temporal properties of spike firing were characterized by interspike interval histograms, autocorrelation and crosscorrelation.
Cortical pyramidal neurons (n = 40) showed irregular firing with a weak tendency to burst or to oscillate. Crosscorrelations revealed strong near-coincident firing and synaptic interactions. Disinhibition was a notable feature in a strongly firing cortical interneuron. Cortical activity spread in the co-culture, thus inducing an overall, homogeneous depolarization in the striatal part. Striatal cells were divided into principal cells and type I and II secondary cells. Principal cells (n = 40) were similar to those reported previously in vivo. Spiking activity ranged from irregular spiking at very low rates to episodic bursting, with an average burst duration of 1 s. Interspike intervals were single-peaked. Intracellular recordings revealed characteristic, long-lasting subthreshold depolarizations (“enabled state”) that were shortened by local muscarinic receptor blockade. During prolonged time periods in the “enabled state”, locally applied bicuculline induced strong firing in most principal neurons. Striatal secondary type I neurons (n = 25) showed high spiking rates, single- and double-peaked interval histograms and low-threshold, short-lasting stereotyped bursting activity and occasional rhythmic bursting. The firing of these neurons was increased by bicuculline. Crosscorrelations showed synchronization of these cells with principal cell activity. Secondary type II neurons (n = 15) revealed tonic, irregular firing patterns similar to cortical neurons, except with occasional firing in doublet spikes.
We conclude that under conditions of dopamine deficiency in corticostriatal co-cultures (i) the cortex induces the “enabled” state and typical bursting mode in striatal principal neurons; (ii) principal neurons are strongly inhibited during the “enabled” state; (iii) muscarinic activity, presumably from tonically active striatal cholinergic interneurons, stabilizes the “enabled” state; (iv) striatal GABAergic interneurons receive synaptic inhibition and take part in synchronized activity among striatal principal cells. Our results favor the view of the striatum as a lateral inhibition network. 相似文献