Time dependence of Li+ action on acetylcholinesterase activity in correlation with spontaneous quantal release of acetylcholine in rat diaphragm.

Abstract

The mean miniature end-plate potential (m.e.p.p.) frequency and the acetylcholinesterase (AChE) activity have been examined in the rat diaphragm, in relation to the time of Li+ action. Substitution of LiCI for NaCI caused increase in m.e.p.p. frequency, the final level of which depended on Li + concentration in the bath solution. Incubation of diaphragm homogenate with NaCI caused initially a slight increase of AChE activity, reaching a plateau after 20 min. Substitution of LiCI for NaCI produced an increase in AChE activity to a maximum, followed by a decrease to a minimum. The activity consequently returned to a steady level. During complete substitution of LiCI for NaCI, the maximum value of AChE activity coincided with the maximum m.e.p.p. frequency (Finax) induced by Li +; the minimum value correlated with the precise instant that the frequency reached a plateau. The addition of prostigmine caused: a) blockade of AChE activity, and b) prostigmine concentration-dependent decrease of Fmax and/or disappearance of m.e.p.p.s from neuromuscular junctions treated with Li+. These results are discussed in terms of correlation between changes of AChE activity induced by Li+ and variations of spontaneous quantal release of the transmitter from nerve terminals of the rat diaphragm treated with Li + . It is almost 40 years since CADE (1949) rediscovered the therapeutic properties of Li in the treatment of manic excitement, and Li salts are now firmly established in modern psychiatric treatment. Since OVERTON (1902) first showed that muscle retained its excitability in Li solution, there has been much interest devoted to the effect of Li + on the electrical properties of excitable cells. It was found that the action potential is little affected when the Na+ of the external solution is replaced by Li + (HODGKIN and KATZ, 1949;HUXLEY and STAMPFLI, 1951) and the Na +

The impact of hydroquinone on acetylcholine esterase and certain human carbonic anhydrase isoenzymes (hCA I, II, IX, and XII)

“…Also, ACh induces contraction of skeletal muscle; it acts via a different type of receptor to inhibit contraction of cardiac muscle fibres 1,2 . AChE plays a very important role in the ACh-cycle, including the release of ACh 3 . Disturbance of cholinergic transmission was found in many clinical and neuropathological studies 4,5 .…”

The human carbonic anhydrase isoenzymes I and II (hCA I and II) inhibition effects of trimethoxyindane derivatives

“…Also, ACh induces contraction of skeletal muscle; it acts via a different type of receptor to inhibit contraction of cardiac muscle fibers 26 . AChE plays a crucial role in the ACh-cycle, including the release of ACh 27 . Disturbance of cholinergic transmission was found in many clinical and neuropathological studies 28,29 .…”

Effect of Aging on the Activities of Acetylcholinesterase, Na+, K+-ATPase and Mg2+-ATPase in Rat Pituitary and Hypothalamus

“…It is known that the role of AChE is very impor tant in ACh cycle, including ACh release (Kouniniotou-Krontiri and Tsakiris, 1989) and cholinergic mechanisms are implicated in neuroendocrine functions. Moreover, Na+, K +-ATPase is impli cated in neural excitability (Sastry and Phillis, 1977), activity-dependent metabolism of energy (Mata et al, 1980), Na+-dependent tryptophan up take system (Herrero et al, 1983) and its activity can be regulated by noradrenergic and/or serotoninergic mechanisms (Swann, 1984;Hernandez, 1987).…”