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Wang Haitao

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CaM-binding domain (CBD) CaS dependent inactivation. IQ-like motif(IM) CaS( Ca sensor)dependent faciliation. Ca2.1, (P/Q type Ca channel) – PowerPoint PPT presentation

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Title: Wang Haitao


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  • Wang Haitao

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Research area Voltage-gated Na channels are
responsible for initiation of electrical
signaling in nerve, muscle and other excitable
cells, and voltage-gated Ca channels are
responsible for initiation of synaptic
transmission in neurons, excitation-contraction
in muscle, secretion in endocrine cells, and many
other processes.
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Ca palys important role in trigger presynaptic
transmitter release
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Ca2.1, (P/Q type Ca channel)
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Methods
  • Cultured SCG(superior cervical ganglion )neuron
  • form fast cholinergic synaptic transmission
    between them
  • cDNAs transfection to exogenous express WT or
    Mutant P/Q type Calcium channels in SCG
  • Whole cell recording
  • Sharp electrode intracellular reocording

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P/Q-Type Ca2 Currents in SCG Neurons
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Calcium Dependent Facilitation and Inactivation
of CaV2.1 Channels
EPSP k(ICa)n
k 1 ,n 3.5
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PPF and PPD Mediated by CaV2.1 Channels
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PPF and PPD Mediated by CaV2.1 Channels
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Plasticity of Synaptic Transmission Mediated by
CaV2.1 Channels during Bursts of Neuronal
Activity
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Augmentation and PTP Mediated by CaV2.1 Channels
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Summary
  • A mutation of the Iq-like motif in the C
    terminus that blocks Ca2/CaS dependent
    facilitation of the P/Q-type Ca2 current
    markedly reduces facilitation of synaptic
    transmission.
  • Deletion of the nearby calmodulin-binding
    domain,which inhibits CaS-dependent
    inactivation,substantially reduces depression of
    synaptic transmission.
  • Residual Ca2 in presynaptic terminals can act
    through CaS dependent regulation of CaV2.1
    channels to induce short-term synaptic
    facilitation and rapid synaptic depression.
    Activity-dependent regulation of presynaptic
    CaV2.1 channels by CaS proteins may therefore be
    a primary determinant of short-term synaptic
    plasticity and information-processing
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