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Learning and Retention of Pattern-Analyzing Skill in Amnesia : Dissociation of Knowing How and Knowing That
| Content Provider | Semantic Scholar |
|---|---|
| Author | Horn, Richard Brodwick, Malcolm S. Dickey, W. Daryl Linder, M. Quastel, J. H. Barry, Peter H. Gage, Peter W. Helden, Dirk F. Van Horn, Michael S. Brodwick, J. Physiol |
| Abstract | These currents were also not influenced by internal anesthetics (Fig. 2C). This is in contrast to the effects of external anesthetics, which cause a marked alteration of the steady-state current-voltage relation for ACh-induced current (6, 7). To determine whether the anesthetics reached the internal membrane surface, the voltage-activated sodium current was examined in two myoballs. At a holding potential of-80 mV, a 30-msec pulse to-40 mV elicited an inward sodium current. In the absence of anesthetic compounds, the sodium current was not affected by stimulating at a frequency of 1 Hz. However, 20 minutes after the addition of 1 mM QX-314 to the internal solution, the sodium current exhibited a use-dependent block, decreasing by about one-third in response to 30 pulses at 1 Hz. Extracellular 1 mM QX-314 was without effect on the current through the sodium channel. A use-dependent inhibition of sodium current by internal QX-3 14 was reported previously (9). It is possible that an asymmetry of surface potentials could explain the asymmetrical effects of QX-314 and QX-222 on the ACh channel. If the extracellular negative surface potential is greater than the intracellular surface potential, it could concentrate the cationic anesthetic at the outer mouth of the ACh channel, thus increasing its effectiveness when applied externally. If the extracellular surface charge density is about 0.002 electron charge per square angstrom (10), then the surface potential can be calculated by use of the Grahame equation (10, 11). The calculated extracellular surface potential,-41 mV, would increase the concentration of the mono-valent cation from 0.1 mM in the bath to 0.5 mM at the outer membrane surface. This concentration is still less than the intracellular concentration, 1 mM. In spite of the fact that the intracellular concentration is greater, these anesthetics have no effect when applied intra-cellularly. It seems to us, therefore, that asymmetry of surface potential cannot explain this result. Extracellular anesthetics appear to block channels by hopping over an extra-cellular barrier and binding to an intra-channel site within the transmembrane electrical field. Apparently the blocker is unable to hop over an even larger intra-cellular barrier to reach the inside of the cell. If the blocker could be driven by voltage over an intracellular barrier, the block would be relieved at sufficiently negative potentials by a "punch-through" mechanism (12), which has not been observed for the ACh channel (6, 7). The large intracellular barrier may prevent access of intemally applied … |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://gureckislab.org/courses/fall13/learnmem/papers/Cohen1980.pdf |
| Alternate Webpage(s) | http://smash.psych.nyu.edu/courses/spring16/learnmem/papers/Cohen1980.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
