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  • Biodiversity Research  (132)
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  • 1
    Online Resource
    Online Resource
    Elsevier BV ; 2012
    In:  Progress in Neurobiology Vol. 98, No. 3 ( 2012-9), p. 316-318
    In: Progress in Neurobiology, Elsevier BV, Vol. 98, No. 3 ( 2012-9), p. 316-318
    Type of Medium: Online Resource
    ISSN: 0301-0082
    RVK:
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2012
    detail.hit.zdb_id: 1500673-6
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Elsevier BV ; 2012
    In:  Progress in Neurobiology Vol. 98, No. 3 ( 2012-9), p. 241-249
    In: Progress in Neurobiology, Elsevier BV, Vol. 98, No. 3 ( 2012-9), p. 241-249
    Type of Medium: Online Resource
    ISSN: 0301-0082
    RVK:
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2012
    detail.hit.zdb_id: 1500673-6
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  • 3
    In: European Journal of Neuroscience, Wiley, Vol. 12, No. 7 ( 2000-07), p. 2333-2344
    Abstract: Reactive gliosis is a prominent morphological feature of mesial temporal lobe epilepsy. Because astrocytes express glutamate receptors, we examined changes in metabotropic glutamate receptor (mGluR) 2/3, mGluR5 and transforming growth factor (TGF)‐β in glial cells of the hippocampal regions in an experimental rat model of spontaneous seizures. Rats that exhibited behavioural status epilepticus (SE) directly after 1 h of electrical angular bundle stimulation, displayed chronic spontaneous seizures after a latent period of 1–2 weeks as observed using continuous electrographic monitoring. SE resulted in hypertrophy of astrocytes and microglia activation throughout the hippocampus as revealed by immunolabelling studies. A dramatic, seizure intensity‐dependent increase in vimentin immunoreactivity (a marker for reactive astrocytes) was revealed in CA3 and hilar regions where prominent neuronal loss occurs. Increased vimentin labelling was first apparent 24 h after onset of SE and persisted up to 3 months. mGluR2/3 and mGluR5 protein expression increased markedly in glial cells of CA3 and hilus by 1 week after SE, and persisted up to 3 months after SE. Double immunolabelling of brain sections with vimentin confirmed co‐localization with glial fibrillary acidic protein (GFAP), mGluR2/3 and mGluR5 in reactive astrocytes. TGF‐β, a cytokine implicated in mGluR3‐mediated neuroprotection, was also upregulated during the first 3 weeks after SE throughout the hippocampus. This study demonstrates seizure‐induced upregulation of two mGluR subtypes in reactive astrocytes, which − together with the increased production of TGF‐β − may represent a novel mechanism for modulation of glial function and for changes in glial‐neuronal communication in the course of epileptogenesis.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    Language: English
    Publisher: Wiley
    Publication Date: 2000
    detail.hit.zdb_id: 2005178-5
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  • 4
    In: Acta Botanica Brasilica, FapUNIFESP (SciELO), Vol. 20, No. 1 ( 2006-03), p. 49-59
    Abstract: We estimate litter production and leaf decomposition rate in a cerradão area, physiognomy little studied and very threatened in São Paulo State. During the period of study, litter production was 5646.9 kg.ha-1.year-1, which the 'leaf' fraction corresponded to 4081.2 kg.ha¹.year¹; the 'branch' fraction, to 1066.1 kg.ha-1.year-1; the 'reproductive structures' fraction, to 434.1 kg.ha-1.year-1; and the 'miscellaneous' fraction to 65.5 kg.ha-1.year-1. Litter production was highly seasonal and negatively correlated with relative humidity and air temperature. Leaf production was negatively correlated with relative humidity, rainfall, and air temperature. There was no significant difference between litter production found in this study and those in two other sites with cerradão and semideciduous forest, but these physiognomies differed significantly from the cerrado sensu stricto. Leaf decomposition rate (K) was 0.56. Half-life of the decomposing material was 1.8 years and turnover time was 2.3 years.
    Type of Medium: Online Resource
    ISSN: 0102-3306
    Language: Unknown
    Publisher: FapUNIFESP (SciELO)
    Publication Date: 2006
    detail.hit.zdb_id: 2055440-0
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  • 5
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 25, No. 38 ( 2005-09-21), p. 8755-8765
    Abstract: The characteristic cell loss in layer III of the medial entorhinal area (MEA-III) in human mesial temporal lobe epilepsy is reproduced in the rat kainate model of the disease. To understand how this cell loss affects the functional properties of the MEA, we investigated whether projections from the presubiculum (prS), providing a main input to the MEA-III, are altered in this epileptic rat model. Injections of an anterograde tracer in the prS revealed bilateral projection fibers mainly to the MEA-III in both control and chronic epileptic rats. We further examined the prS–MEA circuitry using a 16-channel electrode probe covering the MEA in anesthetized control and chronic epileptic rats. With a second 16-channel probe, we recorded signals in the hippocampus. Current source density analysis indicated that, after prS double-pulse stimulation, afterdischarges in the form of oscillations (20–45 Hz) occurred that were confined to the superficial layers of the MEA in all epileptic rats displaying MEA-III neuronal loss. Slower oscillations (theta range) were occasionally observed in the deep MEA layers and the dentate gyrus. This kind of oscillation was never observed in control rats. We conclude that dynamical changes occur in an extensive network within the temporal lobe in epileptic rats, manifested as different kinds of oscillations, the characteristics of which depend on local properties of particular subareas. These findings emphasize the significance of the entorhinal cortex in temporal lobe epilepsy and suggest that the superficial cell layers could play an important role in distributing oscillatory activity.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2005
    detail.hit.zdb_id: 1475274-8
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  • 6
    In: European Journal of Neuroscience, Wiley, Vol. 14, No. 9 ( 2001-11), p. 1475-1484
    Abstract: Neuronal loss, gliosis and axonal sprouting in the hippocampal formation are characteristics of the syndrome of mesial temporal sclerosis (MTS). In the post‐status epilepticus (SE) rat model of spontaneous seizures these features of the MTS syndrome can be reproduced. To get a global view of the changes in gene expression in the hippocampus we applied serial analysis of gene expression (SAGE) during the early phase of epileptogenesis (latent period), prior to the onset of the first spontaneous seizure. A total of 10 000 SAGE tags were analyzed per experimental group, resulting in 5053 (SE) and 5918 (control group) unique tags (genes), each representing a specific mRNA transcript. Of these, 92 genes were differentially expressed in the hippocampus of post‐SE rats in comparison to controls. These genes appeared to be mainly associated with ribosomal proteins, protein processing, axonal growth and glial proliferation proteins. Verification of two of the differentially expressed genes by in situ hybridization confirmed the changes found by SAGE. Histological analysis of hippocampal sections obtained 8 days after SE showed extensive cell loss, mossy fibre sprouting and gliosis in hippocampal sub regions. This study identifies new high‐abundant genes that may play an important role in post‐SE epileptogenesis.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    Language: English
    Publisher: Wiley
    Publication Date: 2001
    detail.hit.zdb_id: 2005178-5
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  • 7
    Online Resource
    Online Resource
    American Society for Cell Biology (ASCB) ; 2001
    In:  Molecular Biology of the Cell Vol. 12, No. 10 ( 2001-10), p. 3095-3102
    In: Molecular Biology of the Cell, American Society for Cell Biology (ASCB), Vol. 12, No. 10 ( 2001-10), p. 3095-3102
    Abstract: The rab family of GTP-binding proteins regulates membrane transport between intracellular compartments. The major rab protein in brain, rab3A, associates with synaptic vesicles. However, rab3A was shown to regulate the fusion probability of synaptic vesicles, rather than their transport and docking. We tested whether rab3A has a transport function by analyzing synaptic vesicle distribution and exocytosis in rab3A null-mutant mice. Rab3A deletion did not affect the number of vesicles and their distribution in resting nerve terminals. The secretion response upon a single depolarization was also unaffected. In normal mice, a depolarization pulse in the presence of Ca 2+ induces an accumulation of vesicles close to and docked at the active zone (recruitment). Rab3A deletion completely abolished this activity-dependent recruitment, without affecting the total number of vesicles. Concomitantly, the secretion response in the rab3A-deficient terminals recovered slowly and incompletely after exhaustive stimulation, and the replenishment of docked vesicles after exhaustive stimulation was also impaired in the absence of rab3A. These data indicate that rab3A has a function upstream of vesicle fusion in the activity-dependent transport of synaptic vesicles to and their docking at the active zone.
    Type of Medium: Online Resource
    ISSN: 1059-1524 , 1939-4586
    Language: English
    Publisher: American Society for Cell Biology (ASCB)
    Publication Date: 2001
    detail.hit.zdb_id: 1474922-1
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  • 8
    In: European Journal of Neuroscience, Wiley, Vol. 16, No. 2 ( 2002-07), p. 360-364
    Abstract: As several epilepsy syndromes are associated with changes in sodium channel subunits we investigated the expression of β1 sodium channel protein in a rat epilepsy model. In this model a chronic epileptic syndrome develops after electrically induced status epilepticus (SE). Many neuropathological characteristics of mesial temporal lobe epilepsy can be reproduced (cell loss, gliosis and synaptic reorganization). In control hippocampus β1 subunit protein was moderately expressed in neurons and weakly expressed in resting astrocytes. β1 sodium channel immunoreactivity increased markedly within 1 week after SE mainly in astrocytes that were colocalized with vimentin (marker for reactive astrocytes). This up‐regulation was still present in reactive astrocytes of chronic epileptic rats ( 〉  3 months after SE). Considering the fact that the β1 subunits may function as cell adhesion molecules interacting with extracellular matrix, the observed increase in reactive astrocytes might subserve a function in cellular and synaptic reorganization during epileptogenesis.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    Language: English
    Publisher: Wiley
    Publication Date: 2002
    detail.hit.zdb_id: 2005178-5
    SSG: 12
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  • 9
    In: European Journal of Neuroscience, Wiley, Vol. 16, No. 4 ( 2002-08), p. 701-712
    Abstract: The effects on high‐voltage activated (HVA) calcium currents were examined in hippocampal CA1 cells and dentate gyrus (DG) granule neurons, 2 days (short‐term; ST) and 2–3 months (long‐term; LT) after electrically induced, limbic electrographic and behavioural seizures in rats. Whole‐cell voltage‐clamp recordings in dissociated CA1 neurons of LT rats showed a decrease in the sustained HVA calcium current amplitude and a faster inactivation of the current both in rats that had experienced a status epilepticus (post‐SE rats) and those in which the stimulation did not lead to SE (non‐SE rats). In CA1 neurons of LT–SE rats this resulted in a reduced Ca 2+ entry through the HVA channels. Perforated‐patch voltage‐clamp recordings in dissociated DG granule neurons of LT–SE rats showed an increased sustained HVA current amplitude compared to controls and non‐SE rats, leading to an increased Ca 2+ entry via HVA calcium channels. Two days after SE, we observed an increased Ca 2+ entry for a defined depolarization, although the change in HVA current amplitude and inactivation rate did not reach significance. We also observed a decrease in calbindin‐D 28k staining in DG post‐SE neurons, but this change was not associated with a change in HVA current inactivation. The opposite changes in neuronal Ca 2+ entry through HVA channels in CA1 vs. DG cells depended strongly on whether rats had experienced SE and later spontaneous seizure activity. These changes are likely to contribute to regionally different effects on local network excitability.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    Language: English
    Publisher: Wiley
    Publication Date: 2002
    detail.hit.zdb_id: 2005178-5
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  • 10
    In: European Journal of Neuroscience, Wiley, Vol. 11, No. 12 ( 1999-12), p. 4269-4277
    Abstract: In central nerve terminals transmitter release is tightly regulated and thought to occur in a number of steps. These steps include vesicle mobilization and docking prior to neurotransmitter release. Intrasynaptic changes in vesicle distribution were determined by electron microscopical analysis and neurotransmitter release was monitored by biochemical measurements. We correlated K + ‐induced changes in distribution of small and large vesicles with the release of their transmitters. For small synaptic vesicles, amino acid release as well as recruitment to and docking at the active zone were activated within 1 s of depolarization. In contrast, the disappearance of large dense‐cored vesicles and the release of the neuropeptide cholecystokinin were much slower, and no docking was observed. Studies with diverse Ca 2  +  channel blockers indicated that mobilization and neurotransmitter release from both vesicle types were regulated by multiple Ca 2  +  channels, although in different ways. Neurotransmitter release from small synaptic vesicles was predominantly regulated by P‐type Ca 2  +  channels, whereas primarily Q‐type Ca 2  +  channels regulated neurotransmitter release from large dense‐cored vesicles. The different Ca 2  +  channnel types directly regulated mobilization of and neurotransmitter release from small synaptic vesicles whereas, by their cooperativity in raising the intracellular Ca 2  +  concentration above release threshold, they more indirectly regulated large dense‐cored vesicle exocytosis.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    Language: English
    Publisher: Wiley
    Publication Date: 1999
    detail.hit.zdb_id: 2005178-5
    SSG: 12
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