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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 54 (1984), S. 567-570 
    ISSN: 1432-1106
    Keywords: Hippocampus ; Frequency potentiation ; Transmembrane potential ; Ephaptic transmission
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The contribution of ephaptic interactions to potentiation of the hippocampal CA1 extracellular population spike during paired pulse or frequency stimulation of stratum radiatum (SR) inputs was investigated using the in vitro hippocampal slice preparation. Records of the transmembrane potential revealed a depolarizing wave with an amplitude and latency that varied directly with that of the extracellular population spike. Paired pulse or repetitive stimulation of SR resulted in a potentiation of the population spike amplitude and a corresponding increase in the amplitude of the TMP depolarizing wave. Action potentials generated during the stimulus train consistently arose from the peak of the depolarizing wave. It is proposed that ephaptic interactions contribute to potentiation of the extracellular population spike through recruitment of subthreshold neurons within the population during repetitive afferent stimulation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 56 (1984), S. 243-256 
    ISSN: 1432-1106
    Keywords: Medial septum ; Hippocampus ; Dentate gyrus ; Evoked potentials
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previous electrophysiological experiments in rabbits have suggested that medial septal stimulation activates dentate granule cells and evokes an associated negative field response at the granule cell layer, without an associated “dendritic” response. Anatomical studies have suggested that septal input to the granule cells may be to stratum moleculare, or close to the cell layer, or may not exist at all. The present experiments confirmed in rats anaesthetised with urethane that medial septal stimulation elicits single action potentials from cells in the granule layer. The associated negative field potential was maximal in the granule cell layer and there was no sign of a separate dendritic potential. The fibres responsible for this potential travel to the dorsal hippocampus in the fornix superior rather than the fimbria, taking the same course as the fibres which contribute to the dense cholinesterase staining just above the granule cell layer. Stimulation at 100 Hz for 1 s of either medial septal, or perforant path, input to the dentate granule cell layer produced long term potentiation of the subsequent evoked field responses to the stimulated pathway. The responses to the non-stimulated pathway were unchanged. Paired pulse stimulation produced both homosynaptic and heterosynaptic potentiation. These data suggest that medial septal input synapses close to granule cell bodies and produces a negative field potential which is a combination of dendritic and population spike potentials. Medial septal input also appeared to produce direct activation of hilar neurones, some of which may be basket cells or other interneurones. The data also show that long term potentiation is specific to this input, perhaps dependent on presynaptic mechanisms. Paired pulse potentiation, at least in the heterosynaptic case appears to depend on postsynaptic mechanisms.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1076
    Keywords: Complement, neonatal concentrations and activation ; Susceptibility to infection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Determinations of C3, C4, and C5 concentrations by radial immunodiffusion, and assays for the activation products of C3, C3c and C3d by counter-immunoelectrophoresis, were performed on 80 infants. Seven nonbacteremic preterm infants with necrotizing enterocolitis (NEC) or probable NEC (PNEC) were found at the time of diagnosis to have a significantly lower mean concentration of C3 (P〈0.05, 1-tailed) without C3 activation when compared to other noninfected preterm infants. Ten full-term and 63 preterm infants were studied prospectively during the first days of life, and were then followed for the postnatal development of localized or systemic infection. Assays for the detection of C3 activation products were negative in all these infants. Four preterm infants who developed PNEC after 5 or more days without clinical illness had low original concentrations of complement components. The pathogenesis of NEC may not involve primarily complement activation, and susceptibility to this condition may be related to pre-existing deficiencies in complement component concentrations relative to gestational age, or to defective activation of C3 in the presence of certain bacterial species and strains.
    Type of Medium: Electronic Resource
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