Title: Wang Haitao
1 2Research 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.
3Ca palys important role in trigger presynaptic
transmitter release
4Ca2.1, (P/Q type Ca channel)
5Methods
- 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
6P/Q-Type Ca2 Currents in SCG Neurons
7Calcium Dependent Facilitation and Inactivation
of CaV2.1 Channels
EPSP k(ICa)n
k 1 ,n 3.5
8PPF and PPD Mediated by CaV2.1 Channels
9PPF and PPD Mediated by CaV2.1 Channels
10Plasticity of Synaptic Transmission Mediated by
CaV2.1 Channels during Bursts of Neuronal
Activity
11Augmentation and PTP Mediated by CaV2.1 Channels
12Summary
- 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