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Wang Haitao

Wang Haitao. Research area:

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Wang Haitao

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  1. Wang Haitao

  2. 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.

  3. Ca++ palys important role in trigger presynaptic transmitter release

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

  5. Methods • Cultured SCG(superior cervical ganglion )neuron form fast cholinergic synaptic transmission between them cDNAstransfection to exogenous express WT or Mutant P/Q type Calcium channels in SCG • Whole cell recording • Sharp electrode intracellular reocording

  6. P/Q-Type Ca2+ Currents in SCG Neurons

  7. Calcium Dependent Facilitation and Inactivation of CaV2.1 Channels EPSP = k*(ICa)n k = 1 ,n = 3.5

  8. PPF and PPD Mediated by CaV2.1 Channels

  9. PPF and PPD Mediated by CaV2.1 Channels

  10. Plasticity of Synaptic Transmission Mediated by CaV2.1 Channels during Bursts of Neuronal Activity

  11. Augmentation and PTP Mediated by CaV2.1 Channels

  12. 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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