Acetylcholine Content Of Rat Brain Research Articles

The estimation of the "free" and "bound" acetylcholine content of rat brain.

Abstract Rat brains, not frozen, were homogenized in saline solution containing physostigmine, and also cupric chloride to inhibit choline acetyl-transferase. When brains were homogenized for periods of up to 3 min, the amount of acetylcholine extracted was proportional to the duration of homogenization. After 3 min, there was no further significant increase in acetylcholine. The acetylcholine extracted in this way was termed “free”; whereas that remaining in the brain tissue and extracted by acid-ethanol solution was termed “bound”. The total amount obtained from each brain was not significantly different from the total amount extracted by a more conventional method from the brains of rats killed by rapid freezing in liquid air. This observation applied also to brains removed from animals during anaesthesia and convulsions.

Effect of Hachimi-jio-gan on scopolamine-induced memory impairment and on acetylcholine content in rat brain

The effect of Hachimi-jio-gan (HJ) on scopolamine induced memory impairment was studied using a radial maze performance, the effect of HJ on the central cholinergic system as measured by acetylcholine (ACh) content, choline acetyltransferase (CAT) and acetylcholinesterase (AChE) activities was also examined. HJ (0.01–1.0 g/kg, p.o.) showed no influence on the radial maze performance. However, with the administration of scopolamine (0.5 mg/kg, i.p.), the number of the correct choices decreased and the number of the error choices increased. HJ (0.1 and 0.5 g/kg, p.o.) reduced this scopolamine-induced cognitive disturbance. The effect of HJ on ACh content and enzyme activities in the brain, frontal cortex, hippocampus and striatum was also investigated. In normal rats, HJ (0.1 and 0.5 g/kg, p.o. × 7 days) significantly increased ACh content in the frontal cortex, although it did not increased ACh content in the hippocampus. In scopolamine-treated rats, ACh content decreased in the brain regions examined. HJ (0.5 g/kg, p.o.) inhibited a decrease in ACh content in the frontal cortex, and with the same dosage of HJ increased CAT activity in the frontal cortex and AChE activity in the hippocampus. These results suggest that the behavioral effects of HJ may be related to its effect on the central cholinergic system.

The effect of 6-aminonicotinamide on the concentration and synthesis of acetylcholine in rat brain

Abstract The acetylcholine content of rat brain determined by a radio-receptor method was 10.87 ± 0.63 nmol/g of whole brain. It showed no significant change following a blockade of the hexose monophosphate shunt by administration of 6-aminocotinamide (6-AN). For measurement of the radioactive acetylcholine formed after injection of radioactive glucose as a precursor, acetylcholine was isolated quantitatively from brain extracts in a fraction free from other major radioactive compounds. The radioactivity of acetylcholine in the fraction was determined by the method as described by Fonnum (1975). The treatment of rats with 6-AN resulted in non-significant decreases of yields of radioactive acetylcholine in brain after injection of [1- 14 C]glucose, [1- 3 H]glucose and [2- 3 H]glucose.

Acetylcholine content in rat brain is elevated by status epilepticus induced by lithium and pilocarpine.

The effects of status epilepticus on the concentration, synthesis, release, and subcellular localization of acetylcholine, the concentration of choline, and the activity of acetylcholinesterase in rat brain regions were studied. Generalized convulsive status epilepticus was induced by the administration of pilocarpine to lithium-treated rats. The concentration of acetylcholine in the cortex, hippocampus, and striatum decreased prior to the onset of spike activity or status epilepticus. Once status epilepticus began, the concentration of acetylcholine increased over time in the cortex and hippocampus, reaching peak levels that were 461% and 304% of control levels, respectively, after 2 h of seizures. Such high in vivo levels of acetylcholine had not been reported previously following any treatment. During status epilepticus, the concentration of acetylcholine in the striatum returned to control levels after the initial depression, but did not accumulate to high levels as it did in the other two regions. The in vivo cortical efflux of acetylcholine was also increased during the seizures. Choline levels were increased by status epilepticus in all three brain regions. Inhibition of seizures by pretreatment with atropine blocked the increases of acetylcholine and choline. Synaptosomes prepared from the cortex and from the hippocampus of rats with status epilepticus had elevated concentrations of acetylcholine: in the hippocampus the acetylcholine was principally in the cytoplasmic fraction, whereas in the cortex the acetylcholine was elevated in both the cytoplasmic and the vesicular fractions. The extra acetylcholine was in a releasable compartment, since increased K+ in the media or ouabain increased the release of acetylcholine from cortical slices to a greater extent in tissue from seized rats than from controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of anesthetic doses of γ-hydroxybutyrate on the acetylcholine content of rat brain

Gamma-hydroxybutyrate administered in anesthetic doses produces a time dependent increase in the levels of rat barin acetylcholine. A maximal increase in whole brain and subcortical levels of acetylcholine is observed about 15 min after administration of the lactone form of the drug. A similar GHB-induced increase in acetylcholine is observed in the striatum and a 75% increase in the hippocampus 15 min after administration of the drug. A good temporal correlation was not obtained between the increase in acetylcholine and the depth of anesthesia produced by the drug. Gamma-hydroxybutyrate did not cause a significant change in the striatal or hippocampal levels of choline. Possible mechanisms involved in the production of this increase in acetylcholine are discussed.

The effect of lithium treatment on the acetylcholine content of rat brain

The effect of lithium treatment on the acetylcholine content of rat brain

Changes in acetylcholine content in rat brain after bilateral olfactory bulbectomy in relation to mouse-killing behavior

Acetylcholine (Ach) content was measured in 5 discrete areas of rat brain following bilateral olfactory bulbectomy. The rats with olfactory bulbectomy (O.B. rat) exhibited significantly lower Ach levels in the cortex than intact and sham-operated controls. However, there was no significant difference in Ach level of all brain areas between the killer and non-killer O.B. rats. These results may suggest that cortical cholinergic function is activated by bulbectomy, but the change in cortical Ach level is not related to muricide.

Effects of physostigmine on brain acetylcholine content and release

The content and release of acetylcholine (ACh) from cat brain and ACh content of rat brain was measured using the frog rectus and leech muscle bioassays before and after physostigmine 100 μg kg i.v. or i.p. The drug elevates steady state levels of brain ACh of awake animals especially in the neocortex, caudate nucleus and hippocampus but much less so in the lateral geniculate and superior colliculus. Physostigmine was shown to produce neocortical release of ACh through a subcortical mechanism in brainstem transected cats and to decrease ACh neocortical content in pentobarbital anesthetized cats and rats. The neocortical release of ACh seems to be mediated primarily through a subcortical brain mechanism which is activated by physostigmine. It is postulated that the ascending reticular formation is involved. Local application of scopolamine (1 μg ml ) into the collecting cup did not antagonize the effects of 100 μg kg of physostigmine i.v. as much as l mg kg of scopolamine i.v. On the other hand, 2 mg kg of mecamylamine given i.v. not only did not antagonize physostigmine-induced neocortical release of ACh, but seemed to enhance it. The results indicate a complex action of physostigmine on the cholinergic system of the brain.

The acute effect of some chlorinated hydrocarbon insecticides on the acetylcholine content of rat brain.

Changes in total brain acetylcholine (ACh) levels as related to convulsive activity were followed after the intracarotid administration of four structurally unrelated chlorinated hydrocarbon insecticides to rats. ACh levels were determined by gas chromatography. The level of ACh found in cannulated controls was 4.7 ± 0.5 (S.E.M.) μg/g fresh tissue. Lindane raised the ACh level (μg/g) to 3.5–6.7, dieldrin to 8.5–9.7, heptachlor to 6.5–10.7, and DDT to 8.8–10.9. The order of neurotoxic signs was lindane > dieldrin > heptachlor > DDT.

Changes in acetylcholine content of rat brain by toxic doses of di-isopropyl phosphofluoridate.

Die Behandlung mit Phosphorsaure-Di-Isopropylester-Fluorid ergibt im Rattengehirn eine 100 prozentige Erhohung des totalen ACh-Gehaltes. Der ACh-Anstieg in den Synaptosomen war nur gering.

CORRELATION BETWEEN ELECTROENCEPHALOGRAPHIC (EEG) EFFECTS AND ACETYLCHOLINE CONTENT OF BRAIN AFTER CHOLINOLYTIG HALLUCINOGENS

The cholinolytic hallucinogens (atropine and hyoscine) reduce the acetylcholine content of rat brain (1) and certain parts of rabbit brain (2). The reduction in the acetylcholine content of the brain caused by these drugs may be related not only to their psychotomimetic effects (1, 3) but also to their amnesic effect (4) and electroencephalographic (EEG) effects (5, 6). The reduction in the acetylcholine content of certain parts of rabbit brain (2) may be related to the sleep like EEG pattern seen in these animals (5) but the corresponding EEG changes in rats have not been reported though atropine and hyoscine reduced the total acetylcholine content of rat brain (1) without any evidence of excitation or behavioural alerting. The purpose of the present paper has been to gather further information on the correlation between the EEG changes and the total acetylcholine content of the rat brain after the administration of atropine, hyoscine and total alkaloids of Datura alba. Total alkaloids of Datura alba were included in the study as the plant grows extensively all over India, contains mainly atropine and hyoscine (7) and frequently causes toxic effects like delirium, tremors, hallucinations and confusion similar to atropine poisoning.

The effects of triethylcholine and hemicholinium-3 on the acetylcholine content of rat brain.

Intraventricular injections of triethylcholine made in conscious rats produced catatonia preceded in a number of animals by a seizure. Hemicholinium-3 also produced a brief period of catatonia but any seizures which occurred did so only after an interval of about 1 hr. Both compounds reduced the total amount of brain acetylcholine and this effect was prevented when choline was administered at the same time. A small intraventricular dose of triethylcholine, which was not sufficient to affect the total amount of brain acetylcholine, did reduce the amount of free acetylcholine. A larger dose decreased both the free and bound components. An intraperitoneal injection of triethylcholine had no effect on brain acetylcholine. The catatonia and seizures produced by triethylcholine and hemicholinium-3 cannot be related to any apparent changes in either brain acetylcholine content or acetylcholinesterase activity.

The effect of some drugs on the "free" and "bound" acetylcholine content of rat brain.

The effect of some drugs on the "free" and "bound" acetylcholine content of rat brain.

Effect of alpha-methyl dopa on acetylcholine content of rat brain, heart and intestine.

RESERPINE, guanethidine and syrosingopine, which are potent hypotensive drugs, have been shown to produce side effects suggestive of increased parasympathetic activity. Some of these effects, such as bradycardia and diarrhoea, are attributable to an increased acetylcholine content of heart and intestine1, 2.

Effect of Anesthetics and Convulsants on Brain Acetylcholine Content

Conclusions1. Both free and total acetylcholine content of the whole rat brain are higher after nembutal or chloroform anesthesia (diffuse diminution of activity) than in the unanesthetized animal. The free acetylcholine change is more convincing after chloroform, whereas the total acetylcholine change is more convincing after nembutal. The total acetylcholine content of the frog brain is similarly elevated after nembutal.2. Neither free nor total acetylcholine content of rat brain differed significantly after the onset of strychnine or picrotoxin convulsions (diffuse increase of activity) from that found in quiet animals awake. Nor did strychnine alter total acetylcholine content of the frog brain.3. With the methods used, normal whole rat brain has been found to contain about 0.7 μg of free and 2.9 μg of total acetylcholine per gram wet weight; frog brain about 4.9 μg of total acetylcholine per gram.