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Excitatory Neurons (excitatory + neuron)
Selected AbstractsIdentification of ventricular-side-enriched molecules regulated in a stage-dependent manner during cerebral cortical developmentEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2006Itsuki Ajioka Abstract Radial glial cells are the main component of the embryonic cortical ventricular zone (VZ), producing deep-layer excitatory neurons in the early stage and upper-layer excitatory neurons in the late stage of development. Previous studies have suggested that the laminar fate of deep-layer neurons might be determined by early-stage-specific secretory or transmembrane molecules (S/TMs) in the VZ. However, the different properties required to produce the different types of neurons in early-stage and late-stage VZ cells are largely unknown. Herein, we investigated the stage-dependent transcriptional profiles of the ventricular side of the mouse cortex, which was manually dissected at embryonic day (E)12, E14 and E16, and identified 3985 ,VZ-enriched' genes, regulated stage-dependently, by GeneChip analysis. These molecules were classified into nine types based on stage-dependent regulation patterns. Prediction programs for the S/TMs revealed 659 ,VZ-enriched' S/TMs. In situ hybridization and real-time PCR analysis for several of these molecules showed results consistent with the statistical analysis of the GeneChip experiments. Moreover, we identified 17 cell cycle-related early-stage and ,VZ-enriched' molecules. These molecules included not only those involved in cell cycle progression, but also essential molecules for DNA double-strand break repair, such as Rad51 and Rpa1. These results suggest that the early stage-VZ cells, which produce both deep- and upper-layer neurons, and the late-stage VZ cells, which produce only upper-layer neurons, are intrinsically different. The gene lists presented here will be useful for the investigation of stage-dependent changes in VZ cells and their regulatory mechanisms in the developing cortex. [source] Activity-dependent maturation of excitatory synaptic connections in solitary neuron cultures of mouse neocortexEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2005Naoki Takada Abstract Activity plays important roles in the formation and maturation of synaptic connections. We examined these roles using solitary neocortical excitatory neurons, receiving only self-generated synaptic inputs, cultured in a microisland with and without spontaneous spike activity. The amplitude of excitatory postsynaptic currents (EPSCs), evoked by applying brief depolarizing voltage pulses to the cell soma, continued to increase from 7 to 14 days in culture. Short-term depression of EPSCs in response to paired-pulse or 10-train-pulse stimulation decreased with time in culture. These developmental changes were prevented when neurons were cultured in a solution containing tetrodotoxin (TTX). The number of functional synapses estimated by recycled synaptic vesicles with FM4-64 was significantly smaller in TTX-treated than control neurons. However, the miniature EPSC amplitude remained unchanged during development, irrespective of activity. Transmitter release probability, assessed by use-dependent blockade of N -methyl- d -aspartate receptor-mediated EPSCs with MK-801, was higher in TTX-treated than control neurons. Therefore, the activity-dependent increase in EPSC amplitude was mainly ascribed to the increase in synapse number, while activity-dependent alleviation of short-term depression was mostly ascribed to the decrease in release probability. The effect of activity blockade on short-term depression, but not EPSC amplitude, was reversed after 4 days of TTX removal, indicating that synapse number and release probability are controlled by activity in very different ways. These results demonstrate that activity regulates the conversion of immature synapses transmitting low-frequency input signals preferentially to mature synapses transmitting both low- and high-frequency signals effectively, which may be necessary for information processing in mature cortex. [source] The development of hippocampal interneurons in rodentsHIPPOCAMPUS, Issue 12 2006Lydia Danglot Abstract Interneurons are GABAergic neurons responsible for inhibitory activity in the adult hippocampus, thereby controlling the activity of principal excitatory cells through the activation of postsynaptic GABAA receptors. Subgroups of GABAergic neurons innervate specific parts of excitatory neurons. This specificity indicates that particular interneuron subgroups are able to recognize molecules segregated on the membrane of the pyramidal neuron. Once these specific connections are established, a quantitative regulation of their strength must be performed to achieve the proper balance of excitation and inhibition. We will review when and where interneurons are generated. We will then detail their migration toward and within the hippocampus, and the maturation of their morphological and neurochemical characteristics. We will finally review potential mechanisms underlying the development of GABAergic interneurons. © 2006 Wiley-Liss, Inc. [source] Distinct roles of neuropilin 1 signaling for radial and tangential extension of callosal axonsTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2009Yumiko Hatanaka Abstract Cortical excitatory neurons migrate from their origin in the ventricular zone (VZ) toward the pial surface. During migration, these neurons exhibit a stellate shape in the intermediate zone (IZ), transform into bipolar cells, and then initiate radial migration, extending a trailing process, which may lead to an axon. Here we examined the role of neuropilin 1 (NRP1) in these developmental events. Both NRP1 mRNA and protein were highly expressed in the IZ, where stellate-shaped cells were located. DiI labeling experiments showed that neuronal migration occurred normally in Nrp1 mutant mice up to embryonic day (E) 14.5, the latest day to which the mutant survives, with only subtle axonal defasciculation. However, interference with Nrp1 signaling at a later stage caused pathfinding errors: when a dominant negative form of Nrp1 was electroporated into the cortical VZ cells at E12.5 or E15.5 and examined perinatally, guidance errors were found in tangential axonal extension toward the midline. In contrast, no significant effect was noted on the migration of cortical excitatory neurons. These findings indicate that NRP1 plays an important role in the guidance of callosal axons originating from cortical excitatory neurons but does not support a role in their migration. Moreover, insofar as radial axonal extension within the cortical plate was unaffected, the present findings imply that molecular mechanisms for the axonal extension of excitatory neurons within the cortical plate are distinct from those in the white matter. J. Comp. Neurol. 514:215,225, 2009. © 2009 Wiley-Liss, Inc. [source] Composition of perineuronal nets in the adult rat cerebellum and the cellular origin of their componentsTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2006Daniela Carulli Abstract The decrease in plasticity that occurs in the central nervous system during postnatal development is accompanied by the appearance of perineuronal nets (PNNs) around the cell body and dendrites of many classes of neuron. These structures are composed of extracellular matrix molecules, such as chondroitin sulfate proteoglycans (CSPGs), hyaluronan (HA), tenascin-R, and link proteins. To elucidate the role played by neurons and glial cells in constructing PNNs, we studied the expression of PNN components in the adult rat cerebellum by immunohistochemistry and in situ hybridization. In the deep cerebellar nuclei, only large excitatory neurons were surrounded by nets, which contained the CSPGs aggrecan, neurocan, brevican, versican, and phosphacan, along with tenascin-R and HA. Whereas both net-bearing neurons and glial cells were the sources of CSPGs and tenascin-R, only the neurons expressed the mRNA for HA synthases (HASs), cartilage link protein, and link protein Bral2. In the cerebellar cortex, Golgi neurons possessed PNNs and also synthesized HASs, cartilage link protein, and Bral2 mRNAs. To see whether HA might link PNNs to the neuronal cell surface by binding to a receptor, we investigated the expression of the HA receptors CD44, RHAMM, and LYVE-1. No immunolabelling for HA receptors on the membrane of net-bearing neurons was found. We therefore propose that HASs, which can retain HA on the cell surface, may act as a link between PNNs and neurons. Thus, HAS and link proteins might be key molecules for PNN formation and stability. J. Comp. Neurol. 494:559,577, 2006. © 2005 Wiley-Liss, Inc. [source] Colocalization of GABA and glycine in the ventral nucleus of the lateral lemniscus in rat: An in situ hybridization and semiquantitative immunocytochemical studyTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2001Raquel Riquelme Abstract We have studied by in situ hybridization for GAD65 mRNA in thick sections and by semiquantitative postembedding immunocytochemistry in consecutive semithin sections, the expression of ,-aminobutyric acid (GABA) and glycine in cell bodies and axosomatic puncta of the rat ventral nucleus of the lateral lemniscus (VNLL), a prominent monaural brainstem auditory structure. The in situ hybridization and the densitometric analysis of the immunostaining suggest that the rat VNLL contains two main populations of neurons. Approximately one-third of neurons are unstained with either technique and are presumably excitatory; their cell bodies are enveloped by a large number of glycine-immunoreactive puncta. Most if not all of the remaining two-thirds colocalize GABA and glycine and are assumed to be inhibitory. These two populations show a complementary distribution within the VNLL, with inhibitory neurons located mainly ventrally and excitatory neurons dorsally. In scatterplots of gray values measured from cell bodies, the double-labeled cells appear to form a single cluster in terms of their staining intensities for the two transmitter candidates. However, this cluster may have to be further subdivided because cells with extreme GABA/glycine ratios differ from those with average ratios with respect to location or size. The VNLL seems unique among auditory structures by its large number of neurons that colocalize GABA and glycine. Although the functional significance of this colocalization remains unknown, our results suggest that the VNLL exerts convergent excitatory and inhibitory influences over the inferior colliculus, which may underlie the timing processing in the auditory midbrain. J. Comp. Neurol. 432:409,424, 2001. © 2001 Wiley-Liss, Inc. [source] Pacing of interstitial cells of Cajal in the murine gastric antrum: neurally mediated and direct stimulationTHE JOURNAL OF PHYSIOLOGY, Issue 2 2003Elizabeth A. H. Beckett Phase advancement of electrical slow waves and regulation of pacemaker frequency was investigated in the circular muscle layer of the gastric antra of wild-type and W/WV mice. Slow waves in the murine antrum of wild-type animals had an intrinsic frequency of 4.4 cycles min,1 and were phase advanced and entrained to a maximum of 6.3 cycles min,1 using 0.1 ms pulses of electrical field stimulation (EFS) (three pulses delivered at 3,30 Hz). Pacing of slow waves was blocked by tetrodotoxin (TTX) and atropine, suggesting phase advancement was mediated via intrinsic cholinergic nerves. Phase advancement and entrainment of slow waves via this mechanism was absent in W/WV mutants which lack intramuscular interstitial cells of Cajal (ICC-IM). These data suggest that neural regulation of slow wave frequency and regulation of smooth muscle responses to slow waves are mediated via nerve-ICC-IM interactions. With longer stimulation parameters (1.0,2.0 ms), EFS phase advanced and entrained slow waves in wild-type and W/WV animals. Pacing with 1,2 ms pulses was not inhibited by TTX or atropine. These data suggest that stimulation with longer pulse duration is capable of directly activating the pacemaker mechanism in ICC-MY networks. In summary, intrinsic excitatory neurons can phase advance and increase the frequency of antral slow waves. This form of regulation is mediated via ICC-IM. Longer pulse stimulation can directly activate ICC-MY in the absence of ICC-IM. [source] | ||||||||||