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  • Collateral specificity  (1)
  • Susceptibility to infection  (1)
  • Transmembrane potential  (1)
  • 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 62 (1986), S. 250-258 
    ISSN: 1432-1106
    Keywords: Longterm potentiation ; Hippocampus ; Collateral specificity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Long term potentiation (LTP) in response to brief high frequency trains has been reported for many pathways in the hippocampus. The mechanisms involved are still unclear. The present experiments set out to confirm reports in the literature that LTP of output from CA3 neurons can be specific to particular collaterals. Single pulses delivered to area CA3 produced field responses nearly simultaneously in area CA1 and in the lateral septum (LS). High frequency stimulation of CA3 produced long term potentiation of CA1 but not LS responses. The CA1 response to stimulation of the contralateral hippocampus did not potentiate when the CA1 response to CA3 stimulation showed long term potentiation. The CA1 and LS responses to CA3 stimulation showed similar strength-duration, strength-amplitude and frequency following characteristics. Their latencies were comparable to the latencies of antidromic activation of CA3 cells from CA1 and LS. Movement of stimulating electrodes to the region of the Schaffer collaterals increased the latency of the LS response and decreased the latency of the CA1 response but left the sum of these latencies unchanged. It was concluded that the CA3 and Schaffer stimulation were activating LS and CA1 collaterals of the same CA3 neurons. CA1 and LS responses to CA3 stimulation showed somewhat different paired pulse and frequency potentiation characteristics. These data confirm reports in the literature that long term potentiation is both input-specific and collateral-specific. The mechanisms of long term potentiation are likely, therefore, to be limited to changes at specific synaptic junctions, e.g. changes in sensitivity of specific postsynaptic receptor sites or changes in transmitter release, which can depend on functional or organisational differences between two collaterals of the same neuron.
    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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