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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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CaM-binding domain (CBD)CaS dependent inactivation
IQ-like motif(IM)CaS ( Ca sensor)dependent faciliation
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
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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