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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Biological cybernetics 72 (1995), S. 371-378 
    ISSN: 1432-0770
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Computer Science , Physics
    Notes: Abstract Sensory input to the central nervous system begins with a transduction step, specialized to the sensory modality involved, resulting in the production of postsynaptic electrical input to the outermost branches of a dendritic tree. Spatiotemporal summation of this ‘slow’ input as it converges upon the axon then initiates the production of or modulates the rate of ongoing production of ‘fast’ neural spikes destined for the central nervous system. We present a novel circuit design consisting of an operational amplifier, a tunnel diode and linear passive components, intended to model the spike generation zone at which the transformation of neural input from slow to fast format takes place. Our circuit is shown to be a relaxation oscillator of the van der Pol type. Simulated postsynaptic current modulates the frequency of spike production by the relaxation oscillator model, producing a stimulus-response characteristic which can be compared with those observed in vivo. Stimulus-response data for our model match data available in the literature for the ampullary electroreceptor of elasmobranch fish.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Biological cybernetics 72 (1995), S. 379-387 
    ISSN: 1432-0770
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Computer Science , Physics
    Notes: Abstract Our preceding paper presented a relaxation oscillator model generally applicable to the description of the spike generation zone of an afferent nerve fiber. This model was shown to reproduce the measured stimulus-response characteristics of the elasmobranch ampullary electroreceptor. In this paper, our optimized model is shown to resolve input stimulus currents or current shifts as small as 50 fA. The fractional spike generator frequency shift produced by injection of this minimum resolvable current is Δf/f≈2×10−3. Arguments based upon known properties of both glutamatergic postsynaptic membrane channels and the electroreceptor organ suggest that this resolvability substantially exceeds that required to account for the known sensitivity of elasmobranch fish to marine electric fields. Our estimates of synaptic input current noise indicate that it will limit the minimum resolvable fractional change of synaptic input current to the range 10−1–10−2 and will thereby limit the minimum resolvable in vivo spike generator fractional frequency shift to the same range. For our optimized model, increase of the minimum resolvable fractional shift of spike generator frequency into this range can be accomplished by injection of ‘white’ stimulus current noise of ≈ 1 pA rms, over a bandwidth of 4–200 Hz. These results lead to the conclusion that synaptic input current noise, rather than inherent spike generator stability, limits electroreceptive sensitivity in vivo. This noise limit is also consistent with the Weber-Fechner criterion derived from psychophysical studies, which places the minimum resolvable fractional change of input stimulus in this same range. We suggest that synaptic current noise provides the physiological basis for the Weber-Fechner criterion. The model studies of this and the preceding paper indicate that the remarkable electroreceptive sensitivity exhibited by marine elasmobranches can be accounted for within the framework of well-known physical principles, with no requirement of ad hoc assumptions relating to the structure or function of the electroreceptor organ.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Biological cybernetics 72 (1995), S. 371-378 
    ISSN: 1432-0770
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Computer Science , Physics
    Notes: Abstract.  Sensory input to the central nervous system begins with a transduction step, specialized to the sensory modality involved, resulting in the production of postsynaptic electrical input to the outermost branches of a dendritic tree. Spatiotemporal summation of this ‘slow’ input as it converges upon the axon then initiates the production of or modulates the rate of ongoing production of ‘fast’ neural spikes destined for the central nervous system. We present a novel circuit design consisting of an operational amplifier, a tunnel diode and linear passive components, intended to model the spike generation zone at which the transformation of neural input from slow to fast format takes place. Our circuit is shown to be a relaxation oscillator of the van der Pol type. Simulated postsynaptic current modulates the frequency of spike production by the relaxation oscillator model, producing a stimulus-response characteristic which can be compared with those observed in vivo. Stimulus-response data for our model match data available in the literature for the ampullary electroreceptor of elasmobranch fish.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Biological cybernetics 72 (1995), S. 379-387 
    ISSN: 1432-0770
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Computer Science , Physics
    Notes: Abstract.  Our preceding paper presented a relaxation oscillator model generally applicable to the description of the spike generation zone of an afferent nerve fiber. This model was shown to reproduce the measured stimulus-response characteristics of the elasmobranch ampullary electroreceptor. In this paper, our optimized model is shown to resolve input stimulus currents or current shifts as small as 50 fA. The fractional spike generator frequency shift produced by injection of this minimum resolvable current is Δ f / f≈2×10-3. Arguments based upon known properties of both glutamatergic postsynaptic membrane channels and the electroreceptor organ suggest that this resolvability substantially exceeds that required to account for the known sensitivity of elasmobranch fish to marine electric fields. Our estimates of synaptic input current noise indicate that it will limit the minimum resolvable fractional change of synaptic input current to the range 10-1−10-2 and will thereby limit the minimum resolvable in vivo spike generator fractional frequency shift to the same range. For our optimized model, increase of the minimum resolvable fractional shift of spike generator frequency into this range can be accomplished by injection of ‘white’ stimulus current noise of ≈1 pA rms, over a bandwidth of 4–200 Hz. These results lead to the conclusion that synaptic input current noise, rather than inherent spike generator stability, limits electroreceptive sensitivity in vivo. This noise limit is also consistent with the Weber-Fechner criterion derived from psychophysical studies, which places the minimum resolvable fractional change of input stimulus in this same range. We suggest that synaptic current noise provides the physiological basis for the Weber-Fechner criterion. The model studies of this and the preceding paper indicate that the remarkable electroreceptive sensitivity exhibited by marine elasmobranches can be accounted for within the framework of well-known physical principles, with no requirement of ad hoc assumptions relating to the structure or function of the electroreceptor organ.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Biological cybernetics 76 (1997), S. 409-418 
    ISSN: 1432-0770
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Computer Science , Physics
    Notes: Abstract.  It has been known for 30 years that the output of a repetitively firing neuron or pacemaker can be synchronized (locked) to regularly spaced inhibitory or excitatory postsynaptic input potentials. Conditions for stable locking have been determined mathematically, demonstrated in computer simulation, and locking has been observed in vivo. We have developed a neural spike generator circuit model which exhibits stable locking to externally derived simulated inhibitory or excitatory post-synaptic inputs. Conditions for stable 1 : 1 lock, in which pacemaker output frequency matches that of the periodic input, are derived. These take the form of expressions for stable delay and convergence factor which incorporate known or measurable parameters of the circuit model. The expressions have been evaluated and shown to compare satisfactorily with experimental observations of locking by our circuit model.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 19 (2004), S. 0 
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A subset of myenteric neurons in the intestine (AH neurons) generate prolonged (〉5 s) post-spike afterhyperpolarizations (slow AHPs) that are insensitive to apamin and tetraethylammonium. Generation of slow AHPs depends critically on Ca2+ entry and intracellular release of Ca2+ from stores, which then leads to the activation of a K+ conductance that underlies the slow AHP (gsAHP). Slow AHPs are inhibited by stimulation of the cAMP/protein kinase A (PKA) pathway, suggesting that phosphorylation of the K+-channels that mediate the gsAHP (KsAHP-channels) is responsible for suppression of slow AHPs and possibly for the repolarization phase of slow AHPs. In the present study, we investigated the possibility that the rising phase of the slow AHP is mediated by dephosphorylation of KsAHP-channels by calcineurin (CaN), a Ca2+-calmodulin-dependent protein phosphatase, leading to an increase in gsAHP and activation of the associated current IsAHP. Slow AHPs and IsAHP were recorded using conventional recording techniques, and we tested the actions of two inhibitors of CaN, FK506 and cyclosporin A, and also the effect of the CaN autoinhibitory peptide applied intracellularly, on these events. We report here that all three treatments inhibited the slow AHP and IsAHP (〉70%) without significantly affecting the ability of neurons to fire action potentials. In addition, the slow AHP and IsAHP were suppressed by okadaic acid, an inhibitor of protein phosphatases 1 and 2A. Our results indicate that activation of the gsAHP that underlies the post-depolarization slow AHPs in AH neurons is mediated by the actions CaN and non-Ca2+-dependent phosphatases.
    Type of Medium: Electronic Resource
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  • 7
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    Unknown
    Oxford : Periodicals Archive Online (PAO)
    Cambridge quarterly. 2:3 (1967:Summer) 237 
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  • 8
    facet.materialart.
    Unknown
    Oxford : Periodicals Archive Online (PAO)
    Cambridge quarterly. 8:1 (1978) 72 
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  • 9
    facet.materialart.
    Unknown
    Oxford : Periodicals Archive Online (PAO)
    Cambridge quarterly. 4:4 (1969/1970:Autumn/Winter) 419 
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  • 10
    facet.materialart.
    Unknown
    Oxford : Periodicals Archive Online (PAO)
    Cambridge quarterly. 1:4 (1966:Autumn) 384 
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