The central release of acetylcholine during stimulation of the visual pathway

Self Cite

The characteristics of the acetylcholine (ACh) release mechanism have been studied in the auditory cortex of rabbits on stimulation of the ipsilateral medial geniculate nucleus. On stimulation of the medial geniculate nucleus the mean release of ACh from the auditory receiving cortex was 6.1 times the spontaneous release; the mean release from other parts of the cortex was 2.2 times the spontaneous release. The frequency of stimulation most effective in evoking ACh release was found to be 10/sec. Both the spontaneous and evoked release of ACh were reduced by 40–65% in the absence of calcium from the solution bathing the auditory cortex, and increased by 15–25% when the calcium concentration in the bathing solution was doubled. The presence of low concentrations of magnesium in the fluid bathing the cortex was essential for the optimal release of ACh, but high magnesium concentrations lowered this release. The presence of triethylcholine (TEC) in the fluid bathing the auditory cortex reduced both the spontaneous and evoked release of ACh. This reduction was reversed in the presence of choline. The effects of calcium, magnesium and TEC on the ACh release mechanism in the cerebral cortex and at the neuromuscular junction are compared.

Section: Discussionsupporting

confidence: 75%

Section: Discussionsupporting

confidence: 58%

The characteristics of acetylcholine release mechanisms in the auditory cortex

Hemsworth¹,

Mitchell²

1969

Self Cite

“…desynchronization by an action on neurones of the pontine reticular formation. An additional contribution to the changes in ACh output may arise by way of a second cholinergic system, the thalamocortical after-discharge pathway (Collier & Mitchell, 1966) from actions of nicotine on brain structures particularly involved with changes in behaviour. This could account for our observations that effects of nicotine on ACh output and electrocortical activity are distinct.…”

Section: Discussionmentioning

confidence: 99%

“…Solutions placed in the cup were pre-warmed to 370 C. The samples removed from the cup were assayed for ACh on the blood pressure of the eviscerated cat treated with physostigmine (Brown & Feldberg, 1936) or on the dorsal muscle of the leech sensitized with physostigmine 20 ,g/ml. The assay procedure for the leech was similar to that described by Collier & Mitchell (1966). To determine the accuracy of the assay procedure, unknown solutions of ACh were assayed by matching as closely as possible the contraction of leech muscle or fall in blood pressure with the response caused by known amounts or concentrations of ACh.…”

Section: Methodsmentioning

confidence: 99%

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

Armitage¹,

Hall²,

Sellers³

1969

115

The effects of small amounts of nicotine on electrocortical activity and central acetylcholine (ACh) release have been studied on anaesthetized cats. The most common effect of nicotine given intravenously in a dose of 2 μg/kg every 30 sec for 20 min was to cause desynchronization of the electrocorticogram, indicating cortical activation, and an increase in the release of cortical ACh. A larger dose given less frequently (4 μg/kg every min for 20 min) caused, in some experiments, an increase and in others a decrease in cortical activity. Such changes were accompanied respectively by an increase or decrease in cortical ACh output. The amounts of nicotine that affected the electrocorticogram and ACh release are probably similar to those absorbed by the cigarette smoker who inhales. The effects of nicotine on the electrocorticogram were transient, but the effects on ACh were prolonged. This suggests that at least two pathways are involved in the nicotine response.

“…The ACh originates from cholinergic nerve terminals of ascending fibres, the cell bodies of which appear to be located in the thalamic nuclei and the reticular formation of the brain stem (Shute & Lewis, 1963;Collier & Mitchell, 1966). The rate of release of ACh from the sensory cortex is dependent on neuronal activity and can be increased by stimulation of the appropriate sensory pathways (Mitchell, 1963 ;Collier & Mitchell, 1966;Neal, Hemsworth & Mitchell, 1968).…”

mentioning

confidence: 99%

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

Hemsworth

Neal

1968

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.