The effect of central stimulant drugs on acetylcholine release from rat cerebral cortex

Abstract

1. The effects of central stimulant drugs injected intraperitoneally were examined on the release of acetylcholine (ACh) from the cerebral cortex of the anaesthetized rat. The effects of the drugs in increasing ACh release were approximately parallel to the increases produced in the electrical activity of the brain. 2. Leptazol in a dose of 150 mg/kg increased the release of ACh by 2.9 times the resting release and in a dose of 300 mg/kg by 7.5 times; on the e.e.g. the injection produced a large increase in the electrical activity. 3. Picrotoxin in a dose of 12 mg/kg increased the release of ACh by 7.5 times and on the e.e.g. caused a large increase in activity. 4. Strychnine in doses of 8 mg/kg and 12 mg/kg increased the release of ACh by 2.0 and 2.4 times and produced a small increase in the activity of the e.e.g. 5. Dexamphetamine in a dose of 100 mg/kg increased the release of ACh by 1.9 times and had no appreciable effect on the e.e.g. 6. Nikethamide in a dose of 2 g/kg increased the release of ACh by 2.3 times and produced no appreciable change in the e.e.g. 7. Caffeine in a dose of 100 mg/kg produced no significant effect on the release of ACh.In the present experiments central stimulant drugs with different sites of action in the neuraxis were used to investigate, in the anaesthetized rat, the relationship between increased neuronal activity in the brain produced by drugs and release of acetylcholine (ACh) from the cerebral cortex.

Effects of nicotine on electrocortical activity and acetylcholine release from the cat cerebral cortex

“…Convulsant drugs such as leptazol have been shown to increase ACh output in cats (Mitchell, 1963;Beleslin et al, 1965;Celesia & Jasper, 1966), and rats (Hemsworth & Neal, 1968). That nicotine caused the opposite effect may result from differences in site of action because nicotine induces seizure discharge by an action on the hippocampus (Floris et al, 1964) whereas leptazol exerts its effects on other cortical and subcortical structures.…”

The Output Per Stimulus of Acetylcholine From Cerebral Cortical Slices in the Presence or Absence of Cholinesterase Inhibition

“…In previous studies on the release of ACh from the cerebral cortex in vivo, the activity of cholinergic neurones was influenced through indirect means, such as drugs that stimulate or depress the central nervous system (Hemsworth & Neal, 1968;Szerb, Malik & Hunter, 1970) or by peripheiral stimulation (Mitchell, 1963) which affects the cortical cholinergic neurones through multisynaptic pathways. In studies on the release of ACh in vitro, on the other hand, release was augmented either by increasing the potassium conte nt of the medium (Mann, Tennenbaum & Quastel, 1939;Bertels-Meeuws & Polak, 1968) or by electrical stimulation at a single frequency (100 Hz) (Rowsell, 1954;Bowers, 1967).…”

Effects of some sympathomimetic drugs and their antagonists on afterdischarges elicited in chronically isolated slabs of cerebral cortex

“…Atropine prevents the action of amphetamine, but pretreatment with a-adrenoceptor blocking agents does not prevent the decrease in duration of EADs produced by cholinomimetics. There is evidence that amphetamine increases cortical ACh release (Pepeu & Bartolini, 1968;Beani, Bianchi, Santinoceto & Marchetti, 1968;Hemsworth & Neal, 1968) and that this increase in release can be prevented in the rat by a-adrenoceptor blocking agents (Hemsworth & Neal, 1968). Bartolini & Pepeu (1970) were able to prevent the increase in ACh release produced by amphetamine in the cat with 8-adrenoceptor blocking agents only, while with aadrenoceptor blocking agents which they used did not modify cortical ACh output.…”