J Physiol Wellcome Trust-funded researchers
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Physiol Vol 275 pp 283-301
Copyright © 1978 by The Physiological Society
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gustafsson, B
Right arrow Articles by Takata, M
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gustafsson, B
Right arrow Articles by Takata, M

Afterhyperpolarization mechanism in the dorsal spinocerebellar tract cells of the cat.

B Gustafsson, S Linström and M Takata

1. The longlasting afterhyperpolarization (a.h.p.) following single or short trains of spikes in dorsal spinocerebellar tract (DSCT) neurons of the cat has been studied with intracellular recording techniques. 2. The a.h.p. amplitude was found to be potential dependent, increasing with depolarization and decreasing with hyperpolarization of the membrane. With large membrane hyperpolarization, the a.h.p. could be reversed in direction, the estimated reversal level being around 30 mV more negative than the threshold potential for spike initiation. The a.h.p. amplitude was also little affected by Cl- ions injected into the cell. 3. The a.h.p. was associated with an increase in the membrane conductance, as measured with short current pulses. The major part of the conductance change was related to the a.h.p. itself and not secondary to the hyperpolarization, i.e. to an anomalous rectification. A conductance change was also found when the membrane potential was polarized close to the a.h.p. reversal level. There was a clear correlation between the a.h.p. amplitude and the measured conductance changes. 4. It is concluded that the a.h.p. in DSCT neurones, as in spinal motoneurones, is caused primarily by an increase in membrane conductance to potassium ions. 5. The time course of the conductance change underlying the a.h.p. was calculated from the a.h.p. voltage and a mathematical expression describing this time course is given. The properties of the a.h.p. in DSCT cells are compared with those in spinal motoneurones and the functional significance of the differences is discussed briefly.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1978 The Physiological Society.