Relationship between acetylcholine content and release in the cat's cerebral cortex.
01 Nov 1970-Canadian Journal of Physiology and Pharmacology (NRC Research Press Ottawa, Canada)-Vol. 48, Iss: 11, pp 780-790
TL;DR: Cortical acetylcholine (ACh) release and content were measured in non-anesthetized pretrigeminally sectioned or in Dial-ansthetized cats.
Abstract: Cortical acetylcholine (ACh) release and content were measured in non-anesthetized pretrigeminally sectioned or in Dial-anesthetized cats. In 28 pretrigerninally sectioned cats a very highly significant negative correlation between ACh content and output was found. In the same preparations, 15 mg/kg pentobarbital or electrolytic lesion in the rostral midbrain decreased ACh output and increased content. Atropine (1 mg/kg i.v. or 1 μg/ml topically) increased ACh output fourfold without significantly altering content. A larger dose of atropine (25 mg/kg i.v.) increased output ninefold and decreased ACh content. In Dial-anesthetized preparations, picrotoxin-induced ACh release was accompanied by a decrease in ACh content. Pretreatment with atropine in the same preparation resulted in an enhanced effect of picrotoxin on both output and content while atropine alone (1 mg/kg i.v.) raised ACh output without decreasing content. In pretrigerminally sectioned non-anesthetized preparations, hemicholinium-3 (HC-3) did...
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01 Jan 1972
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TL;DR: This review will focus on choline transport into cholinergic neurons, especially by means of the sodium-dependent, high affinity choline uptake system (SDHACU) which appears to be involved in ACh synthesis and its regulation.
Abstract: MANY experiments in a variety of systems have revealed that the rate of synthesis of ACh adjusts to changes in the rate of release of ACh. From this follows the universal belief that the synthesis of ACh is regulated by some biochemical mechanism. All of the factors in the regulation of synthesis of ACh are not understood Most models of regulation deal with ChAc and/or the supply of acetylCoA and choline. Important questions dealing with choline have been formulated. What are the sources of choline? How is it utilized? What is the fate of choline derived from released ACh? All of these questions cannot be answered here for practical reasons, and there are several recent reviews dealing with the sources of choline for ACh synthesis and with overall aspects of its acetylation in neuronal tissue (HEBB, 1972; WHITTAKER et al., 1972; FONNUM, 1973, 1975; BROWNING, 1976; FREEMAN & JENDEN, 1976; HAUBRKH & CHIPPENDALE, 1977). This review will focus on choline transport into cholinergic neurons, especially by means of the sodium-dependent, high affinity choline uptake system (SDHACU) which appears to be involved in ACh synthesis and its regulation. Transport of choline through the blood-brain barrier has been discussed elsewhere (PARDRIDGE & OLDENWRF, 1977).
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TL;DR: The fact that patterns characteristic of sleep, arousal, and waking behavior continue in decorticate animals indicates that reticulo-cortical mechanisms are not essential for these aspects of behavior.
Abstract: It is traditionally believed that cerebral activation (the presence of low voltage fast electrical activity in the neocortex and rhythmical slow activity in the hippocampus) is correlated with arousal, while deactivation (the presence of large amplitude irregular slow waves or spindles in both the neocortex and the hippocampus) is correlated with sleep or coma However, since there are many exceptions, these generalizations have only limited validity Activated patterns occur in normal sleep (active or paradoxical sleep) and during states of anesthesia and coma Deactivated patterns occur, at times, during normal waking, or during behavior in awake animals treated with atropinic drugs Also, the fact that patterns characteristic of sleep, arousal, and waking behavior continue in decorticate animals indicates that reticulo-cortical mechanisms are not essential for these aspects of behavior These puzzles have been largely resolved by recent research indicating that there are two different kinds of input from the reticular activating system to the hippocampus and neocortex One input is probably cholinergic; it may play a role in stimulus control of behavior The second input is noncholinergic and appears to be related to motor activity; movement-related input to the neocortex may be dependent on a trace amine Reticulo-cortical systems are not related to arousal in the traditional sense, but may play a role in the control of adaptive behavior by influencing the activity of the cerebral cortex, which in turn exerts control over subcortical circuits that co-ordinate muscle activity to produce behavior
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TL;DR: It has been found that excitation of the cortex, either through sensory nerves or by direct electrical stimulation, increases the ACh output and the most important step in the identification of cholinergic transmission has been the demonstration of the release of ACh during stimulation of the appropriate nerve.
Abstract: The possibility that acetylcholine (ACh) acts as a mediator of synaptic transmission in the cerebral cortex of mammals has been suggested both by experiment and by argument. It has, however, been difficult to obtain direct evidence in support of this view although many of the characteristics that might be expected of a central nervous transmitter have been clearly demonstrated for ACh in the cortex (Feldberg, 1945b, 1950, 1957; Crossland, 1960). They include the demonstration of enzymes for the synthesis and rapid destruction of ACh and the natural occurrence of this substance in the brain. ACh and drugs which are known to affect its action have been shown to influence the electrical activity of the cortex, and recently single cells in the cortex have been selectively activated by the iontophoretic application of ACh through micropipettes (Krnjevid & Phillis, 1961). However, at peripheral synapses the most important step in the identification of cholinergic transmission has been the demonstration of the release of ACh during stimulation of the appropriate nerve. Experiments of this kind, on the intact brain, offer certain difficulties and attempts by several groups of workers to demonstrate a central release of ACh during nervous stimulation have produced conflicting results (see Feldberg, 1945 b): but in 1950 Elliott, Swank & Henderson detected a release ofACh from the surface of the intact cortex and MacIntosh & Oborin (1953) showed that this release was related to the spontaneous electrical activity of the cortex. A technique similar to that of MacIntosh & Oborin has been used in the present experiments to study the effect of direct and indirect stimulation of the cortex on the local release of ACh, in an attempt to assess its significance. It has been found that excitation ofthe cortex, either through sensory nerves or by direct electrical stimulation, increases the ACh output
368 citations