Na+,K(+)-ATPase and Mg(2+)-ATPase activities were studied in neurons and glial cells of the olfactory cortex of the rat by quantitative cytophotometry in conditions of long-term potentiation (LTP), and significant changes in direction and extent were found. Na+,K(+)-ATPase activity decreased in neurons in the first 15 min after LTP, with subsequent elevation by 30 min. Mg(2+)-ATPase activity remained unchanged in these conditions. Glial cells showed significant increases in Na+,K(+)-ATPase activity in the initial period after LTP, with return to control by 30 min. Again, there were no significant changes in Mg(2+)-ATPase activity. The formation and persistence of LTP in neurons and glial cells was accompanied by significant changes in Na+,K(+)-ATPase activity, which were reciprocal in nature.
Cell membrane recordings were made in conditions of voltage clamping with tight attachment of the microelectrode-patch clamping--to study the effects of morphine on tetrodotoxin-resistant (TTXr) sodium channels in rat spinal ganglion neurons in culture. The effects of a number of biologically active substances which regulate the receptor-mediated actions of morphine were studied. The effects of morphine were found to involve a chain of sequential reactions leading to decreases in the transfer of effective charge (Zeff) by the activatory gate system of TTXr sodium channels, depending on the concentration of agonist in the extracellular solution. A value of 8 nM was obtained for KD. with a Hill coefficient of X = 0.5. Non-specific antagonists of opioid receptors blocked the actions of morphine; these included ouabain at a concentration of 100 microM. An inhibitor, and activator, and a blocker of G-proteins had no effect on the effective charge. These data provide evidence that morphine decreases the voltage sensitivity of TTXr sodium channels.
Enzymatic methods were used to demonstrate an increase in the activity of G-proteins and protein kinase A in the brain of the common snail at early stages of learning. There were no differences in the activity of G-proteins in the brain between young (unable to learn) and adult snails. Snail brain protein kinase C activity was unchanged compared to controls 20-40 minutes after the end of the training procedure. It is concluded that cAMP-dependent phosphorylation and cAMP-dependent activation of early gene expression have active roles in learning in the snail. The question of the role of additional intracellular regulatory systems in learning in the snail is discussed.
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