Evidence for a muscarinic inhibitory mechanism in the cerebral cortex

Vazquez, A. J.; Krip, Gordon; Pinsky, Carl M.

doi:10.1016/0014-4886(69)90080-6

Cited by 15 publications

(8 citation statements)

References 20 publications

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“…Atropine antagonized both effects of eserine, indicating that they were due to eserine action on endogenous ACh. The dispersion of epileptiform discharges by eserine and their re-synchronization by atropine might explain the apparent discrepancy between our findings and a report of a muscarinic mechanism which inhibits epileptiform discharges in the isolated cortex (Vazquez et al 1969). This report was based on the observation that eserine shortens and atropine lengthens the duration of epileptiform afterdischarges in the isolated cortex.…”

Section: Discussioncontrasting

confidence: 99%

The Effects of Eserine and Atropine on the Epileptiform Activity of Chronically Isolated Cortex

1971

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SUMMARY Our study was designed to test the hypothesis that the epileptiform activity of chronically isolated cortex is due to supersensitivity to endogenous acetylcholine. Eserine and atropine were administered systemically to cats with chronically isolated occipital cortex and implanted EEG recording electrodes. Eserine usually diminished the amplitude and increased the duration of the epileptiform EEG discharges in the isolated area. These changes were antagonized by a subsequent administration of atropine. Atropine, without a preceding application of eserine, did not abolish the paroxysmal discharges but tended to obscure them by inducing slow waves in the island. In contrast, diazepam was very effective in abolishing the paroxysmal discharges. The effects of both eserine and atropine on the paroxysmal activity of the island occurred only at those dosage levels that produced changes in the EEG from other areas of the brain. These results do not support the hypothesis investigated.

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Section: Discussioncontrasting

confidence: 99%

The Effects of Eserine and Atropine on the Epileptiform Activity of Chronically Isolated Cortex

1971

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“…This phenomenon is quite analogous to atropine's antagonism of long duration inhibition described in this paper. Vazquez and his associates (Vazquez et a-., 1969;Krip & Vazquez, 1971) have confirmed the involvement of cholinergic interneurones in cortical inhibition by demonstrating that cholinergic agents shorten, and anticholinergic muscarinic agents lengthen, the duration of the epileptiform afterdischarge in chronically isolated cortical slabs.…”

Section: Discussionmentioning

confidence: 99%

“…A portion of the left suprasylvian gyrus was surgically isolated in 5 cats, by means of the technique described by Vazquez et al (1969). The surgery was performed under sterile conditions.…”

Section: Methodsmentioning

confidence: 99%

Acetylcholine inhibition in the intact and chronically isolated cerebral cortex

Jordan

Phillis

1972

British J Pharmacology

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Summary1. Some spontaneously firing cells in the cerebral cortex of cats can be depressed by iontophoretically applied acetylcholine or acetyl-P-methylcholine, and this depression is antagonized by atropine. Thirteen per cent of 101 spontaneously active neurones tested were depressed by cholinergic agents and 64%,' were excited.2. Single stimuli applied to the adjacent cortical surface excited 132 neurones orthodromically. Acetylcholine or acetyl-f3-methylcholine depressed this synaptic firing in 18% of the cells. The depression was blocked by atropine.3. The population of neurones in which cholinergic agents depressed spontaneous or synaptic firing was located within the superficial half of the cortex. 4. Glutamate-induced firing was depressed by cholinergic agents in 41% of 211 cells tested; atropine and strychnine strongly antagonized this depressant action, while dihydro-f3-erythroidine was a weaker antagonist.5. Long duration inhibition of glutamate-induced firing evoked by repetitive stimulation of the cortical surface could be blocked by atropine or strychnine in both the intact and chronically isolated cortex. This provides strong evidence for a system of intracortical cholinergic neurones which make direct inhibitory contacts with neurones in the superficial layers of the cortex.

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“…Current histochemical evidence (Dahlstrom, 1969) indicates that there are noradrenergic neurones with cell bodies mainly found in the pons and the medulla oblongata and axons that ascend close to the medial forebrain bundle and innervate the cortex. These neurones may very well synapse with the neurones involved in the cortical cholinergic inhibitory system previously described (Vazquez, et al, 1969). Excitation of the adrenergic neurones would activate the cholinergic inhibitory system.…”

Section: Discussionmentioning

confidence: 99%

“…These authors concluded that there are central 83-adrenoceptors where the catecholamines could act to stimulate cholinergic neurones. It seemed reasonable, therefore, to examine the role of sympathomimetic agents in the maintenance and termination of cortical epileptiform activity in neuronally isolated cortical slabs, and to study their interactions with the cortical cholinergic inhibitory system that we previously postulated (Vaizquez et al, 1969 (Vazquez et al, 1969). This provided a slab of cerebral cortex, completely free of all neuronal connexions with adjacent non-isolated brain, but preserving the pial and arachnoidal blood vessels intact.…”

Section: Introductionmentioning

confidence: 99%

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

Krip

Vázquez

1971

British J Pharmacology

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Summary1. The role of sympathomimetic agents in the maintenance and termination of induced cortical epileptiform activity was studied in chronically neuronally isolated slabs of cerebral cortex in the suprasylvian gyrus of unanaesthetized, unrestrained cats. 2. The administration of the sympathomimetic agents (+)-amphetamine, methamphetamine, tyramine, and ephedrine resulted in a highly significant decrease in the duration of epileptiform afterdischarge (EADs). 3. The a-adrenoceptor blocking drugs phenoxybenzamine, phentolamine and tolazoline did not significantly alter the duration of EADs but prevented the decrease in duration of EADs produced by the sympathomimetic drugs. 4. The effect of atropine and arecoline on the duration of EADs, previously described, were not modified by the a-adrenoceptor blocking drugs, but atropine prevented and reversed the inhibitory action of amphetamine. 5.

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Evidence for a muscarinic inhibitory mechanism in the cerebral cortex

Cited by 15 publications

References 20 publications

The Effects of Eserine and Atropine on the Epileptiform Activity of Chronically Isolated Cortex

The Effects of Eserine and Atropine on the Epileptiform Activity of Chronically Isolated Cortex

Acetylcholine inhibition in the intact and chronically isolated cerebral cortex

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

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