Open voltage.

All these results are clear indications that CTx and PbTx have similar modes of action and that they increase the membrane permability of excitable cells to Na ions by opening voltage-dependent Na channels. This action fully accounts for the toxicity of ciguatoxin and brevetoxins. 

FIGURE 10-7 The delay between Ca2+ influx into the nerve terminal and the postsynaptic response is brief. The temporal relationships between the Ca2+ current and the action potential in the nerve terminal and the postsynaptic response in the squid giant synapse are shown. The rapid depolarization (a) and repolarization (b) phases of the action potential are drawn. A major fraction of the synaptic delay results from the slow-opening, voltage-sensitive Ca2+ channels. There is a further delay of approximately 200 is between Ca2+ influx and the postsynaptic response. (With permission from reference [20].)... 

Suppose that a specific neurotransmitter arrives at its ligand-gated ion channel, say a sodium ion channel. It will open and sodium ions will flow into the postsynaptic neuron, depolarizing its membrane. If this depolarization exceeds the threshold level, this will open voltage-gated sodium and potassium ion channels, generating an action potential that will flow down the dendrite to the cell body, and so on. 

The arrival of the action potential at the presynaptic terminal opens voltage-dependent Ca ion channels in the plasma membrane so that the Ca ions enter the cytosol down their concentration gradient. This results in activation of a Ca -binding cytosolic or a membrane protein. This facilitates movement of the vesicles to the membrane and formation of a fusion pore through which the neurotransmitter is discharged into the synaptic cleft (i.e. exocytosis). This occurs within about 0.1 ms of the arrival of the depolarisation (Figure 14.8). The process of exocytosis lasts for only a short time, since the Csl ion concentration in the cytosol is rapidly lowered due to the ion extrusion from the cell (Appendix 14.3). 

These are (3-adrenergic agonists that act by stimulation of the enzyme, adenylyl cyclase, thereby increasing intracellular cAMP. This indirectly increases intracellular calcium, by induction of the active form of protein kinase followed by an influx of Ca2+ through open voltage-dependent Ca2+ channels (Figure 8.4). 

Photovoltaic devices were irradiated at 400 nm through the transparent substrate at a wavelength that gave significant absorption to determine the quantum efficiency, open voltage, and power conversion. Testing results for selected samples provided in Table 1. 

Entry Mesogenic Monomers Used Monomer Ratios Quantum Efficiency (%) Open Voltage (V) Power Conversion (%)... 

Schematic diagram of a generalized noradrenergic junction (not to scale). Tyrosine is transported into the noradrenergic ending or varicosity by a sodium-dependent carrier (A). Tyrosine is converted to dopamine (see Figure 6-5 for details), which is transported into the vesicle by a carrier (B) that can be blocked by reserpine. The same carrier transports norepinephrine (NE) and several other amines into these granules. Dopamine is converted to NE in the vesicle by dopamine-B-hydroxylase. Release of transmitter occurs when an action potential opens voltage-sensitive calcium channels and increases intracellular calcium. Fusion of vesicles with the surface membrane results in expulsion of norepinephrine, cotransmitters, and dopamine-13-hydroxylase.

Fig. 2 Membrane topography of the a-LTX pore. Cross-section of the a-LTX tetramer embedded in a membrane (as observed in liposomes) (Orlova et al. 2000) is shown alongside the cut-open voltage-dependent K+ channel (Kvl.2) (Long et al. 2005) and Ca2+ release channel (ryanodine receptor) (Serysheva et al. 2005). Fully hydrated cations and molecules known to permeate through the respective channels are shown next to each reconstruction (FITC, fluoresceine isothiocyanate NE, norepinephrine). The narrowest part of the a-LTX channel is 10 A. Molecular images were produced using the UCSF Chimera package (Pettersen et al. 2004).

Hagberg GB, Blomstrand F, Nilsson M, Tamir H, Hansson E. Stimulation of 5-HT2A receptors on astrocytes in primary culture opens voltage-independent Ca2+ channels. Neurochem Int 1985 32 153-162. 

This observation suggests that the effect of increased [KC1] depends on an influx of Ca2+ from the extracellular medium, which is required to stimulate cell division. High [KC1] treatment must depolarize the oocyte sufficiently to open voltage-dependent Ca2+ channels in the plasma membrane. 

In skeletal muscle open voltage-gated L-type Ca2+ channels can interact directly with muscle ER (sarcoplasmic reticulum) ryanodine receptors to open the ryanodine receptor Ca2+ channel and thence elevate cytosolic Ca2+ concentration from sarcoplamic. reticulum Ca2+ stores. However in neurons and cardiac muscle activation of PM voltage-gated Ca2+ channels indirectly activates ryanodine receptor Ca2+ channels as outlined in the section on Ligand-gated Ca2+ channels . 

Fig. 7.1. Argon injection via a piezo-electric valve, with the opening voltage waveform shown in the bottom frame along with the Ar16+ X-ray brightness time history. The electron density and temperature, along with the argon density are shown in the top two frames...

Arrival of an action potential at the synaptic knoh opens voltage-gated Ca + channels in the plasma membrane. 

Figure 7.3. Mechanism of transmitter release, a Thepresynap-tic action potential opens voltage-gated Ca channels. Ca triggers exocytosis of neurotransmitters stored in piesynaptic vesicles. b Some proteins (out of mat r more) that are involved in exocytosis. Ca is involved at multiple stages. By binding to calmodulin (CaM), it promotes phosphorylation of synapsin, which primes the transmitter vesicle but does not immediately lead to exocytosis. Adhesion of primed vesicles to the presynap-tic membrane is mediated by synaptobrevin and other SNARE proteins. Synaptotagmin is activated directly by Ca and participates in the final step of secretiom...

---