Neuron channels

CNS, many types of channels are known with differential patterns of distj-ib tion Opening of neuronal channels generally... 

Cummins An important factor in understanding inactivation and the generation of persistent currents may be subtle differences between the skeletal muscle and neuronal channels or isoforms. Patlak Ortiz (1986) found that noninactivating or persistent Na currents in skeletal muscle cells were very small, whereas in the squid axons persistent Na+ currents are much larger. There seem to be subtle but important differences between the different isoforms. There may be differences in cooperativity. All of this has to be worked out very carefully. 

Cummins The striking feature to me of that closed state inactivation is the difference between, say, the PNl neuronal channel and the skeletal muscle. It is a major difference, but 1 don t know what the underlying mechanism is. 

Cummins At least from my evidence concerning closed state inactivation of Na channels (Cummins et al 1998), it might be that the inactivation is dependent on the channels opening for the peripheral neuronal channels, as opposed to skeletal muscle channels, which are more likely to inactivate from the closed states. This may be why you see such a concordance between the Hinf (steady-state inactivation curve) and the voltage-dependence of the persistent current the peripheral neuronal Na channels may have to open if they are going to inactivate. 

One of the problems with the sensory neuronal channels is getting them functionally expressed. There is a feeling that there is some J subunit or other factor that we are missing. 

Cummins To follow up on this, it is certainly not the same for all the isoforms. With the skeletal muscle channel you can knock out much of the fast inactivation with the F1304Q mutation and it doesn t affect the biophysically distinct slow inactivation, either the entry or the exit. This doesn t mean that this isn t the case for some of the neuronal channels. 

A second reason is that empirical work on color vision traces the phenomenology of color experiences to opponent processing channels in the brain. Differences in color experience phenomenology are explained by reference to different activation levels in these neuronal channels (Pautz, 2006). So, again, if you fix the brain events, you fix the phenomenal character or at least the phenomenal character of color experience. 

Biological ejfects Tetrodotoxin is a powerful neurotoxin (paralytic poison, which prevents the function of neuronal channels for Na+ ions). More than 60% of poisonings are fatal. About as toxic as tetrodotoxin (LDjq = 8-10 xg/kg in mice) is chiriquitoxin, while... 

Maintenance of electrical potential between the cell membrane exterior and interior is a necessity for the proper functioning of excitable neuronal and muscle cells. Chemical compounds can disturb ion fluxes that are essential for the maintenance of the membrane potentials. Fluxes of ions into the cells or out of the cells can be blocked by ion channel blockers (for example, some marine tox-... 

FIGURE 17.26 The o i-subuiiit of the t-tubule Ca" chainiel/DHP receptor contains six peptide segments that may associate to form the Ca" channel. This Ca" channel polypeptide is homologous with the voltage-sensitive Na channel of neuronal tissue. 

Antiepileptics Na+, Ca2+ channels GABA receptors l Na+currents l Ca2+ currents GABA receptor activity l Excitability of peripheral and central neurons l Release of excitatory neurotransmitters Sedation, dizziness, cognitive impairment, ataxia, hepatotoxicity, thrombocytopenia... 

Antidepressants Noradrenaline/5-HT transporters Na+, K+ channels l Noradrenaline/ 5-HT reuptake l Na+ currents t K+ currents l Excitability of peripheral and central neurons Cardiac arrhythmia, myocardial infarction, sedation, nausea, dry mouth, constipation, dizziness, sleep disturbance, blurred vision... 

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