TY - JOUR
T1 - Diamide, a thiol oxidizing agent, uncouples the electrotonic junctions of crayfish septate axons, but not those of Navanax motoneurons
AU - Giaume, C.
AU - Spira, M. E.
AU - Korn, H.
PY - 1981/11
Y1 - 1981/11
N2 - Diamide, a thiol oxidizing agent, uncouples the crayfish septate axons. This uncoupling is indicated by a hundred-fold increase of the junctional membrane resistance and a much less significant decrease of the non-junctional membrane resistance. By contrast, the junctional conductance of electrotonically-coupled motoneurons from the buccal ganglion of Navanax inermis is not affected by this substance. The different effect of diamide upon the junctional membrane of the two preparations, strongly suggests that oxidation (if any) of thiol groups present at their level is not enough to account for alteration of their conductances. The uncoupling of the septate axons is most likely due to an increase of the intracellular free Ca++ concentration, this cation being released from internal stores such as microchondria. Evidence reported in the literature that mitochondria of Navanax motoneurons do not release under normal conditions sufficient Ca++ to uncouple adjacent cells and data showing that at low internal pH coupling is decreased in both preparations, favor this hypothesis for the mechanism of diamide action.
AB - Diamide, a thiol oxidizing agent, uncouples the crayfish septate axons. This uncoupling is indicated by a hundred-fold increase of the junctional membrane resistance and a much less significant decrease of the non-junctional membrane resistance. By contrast, the junctional conductance of electrotonically-coupled motoneurons from the buccal ganglion of Navanax inermis is not affected by this substance. The different effect of diamide upon the junctional membrane of the two preparations, strongly suggests that oxidation (if any) of thiol groups present at their level is not enough to account for alteration of their conductances. The uncoupling of the septate axons is most likely due to an increase of the intracellular free Ca++ concentration, this cation being released from internal stores such as microchondria. Evidence reported in the literature that mitochondria of Navanax motoneurons do not release under normal conditions sufficient Ca++ to uncouple adjacent cells and data showing that at low internal pH coupling is decreased in both preparations, favor this hypothesis for the mechanism of diamide action.
UR - http://www.scopus.com/inward/record.url?scp=0019820009&partnerID=8YFLogxK
U2 - 10.1016/0306-4522(81)90012-9
DO - 10.1016/0306-4522(81)90012-9
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C2 - 6276811
AN - SCOPUS:0019820009
SN - 0306-4522
VL - 6
SP - 2239
EP - 2247
JO - Neuroscience
JF - Neuroscience
IS - 11
ER -