Acetylcholine inhibition in the intact and chronically isolated cerebral cortex

Jordan, Larry M.; Phillis, John W.

doi:10.1111/j.1476-5381.1972.tb08116.x

Cited by 55 publications

(8 citation statements)

References 32 publications

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“…It is known that iontophoretically applied ACh causes a long-lasting excitation of units in the deeper layers of the cortex (Kmjevic & Phillis, 1963) or long-lasting inhibition in the more superficial layers (Jordan & Phillis, 1972). Therefore, a decrease in the output of ACh per stimulus with increasing frequencies of stimulation would result in a rather constant postsynaptic action of released ACh on cholinoceptive units in the cortex in spite of variations in the rate of firing of cholinergic neurones.…”

Section: Resultsmentioning

confidence: 99%

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

Bourdois

Mitchell

Somogyi

et al. 1974

British J Pharmacology

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1 The release of endogenous acetylcholine (ACh) from cerebral cortical slices stimulated at 0.25, 1, 4, 16 and 64 Hz was measured in the presence either of physostigmine or of physostigmine and atropine. 2 Atropine potentiated the evoked release of endogenous ACh especially at low frequencies resulting in an output per stimulus which sharply declined with increasing frequency of stimulation, while in the absence of atropine the output of ACh per stimulus was low and fairly constant.3 The evoked release of [3 H]-ACh per stimulus following the incubation of the slices with [3 H] -choline, as estimated by means of rate constants of the evoked release of total radioactivity, showed a frequency dependence similar to endogenous ACh when the two were tested under identical conditions. 4 In the absence of an anticholinesterase the evoked release of [3H]-ACh per stimulus was dependent on frequency of stimulation in a similar way to that in the presence of physostigmine and atropine. 5 Results suggest that under physiological conditions, i.e. in the absence of an anticholinesterase, the release of ACh per stimulus decreases with increasing frequency of stimulation and that this decrease is due to a lag in the mobilization of stored ACh rather than in the synthesis of new ACh.

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Section: Resultsmentioning

confidence: 99%

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

Bourdois

Mitchell

Somogyi

et al. 1974

British J Pharmacology

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“…BEN-ARI AND OTHERS type, as found in other regions of the thalamus (Andersen & Curtis, 1964b) and cerebral cortex (Jordan & Phillis, 1972).…”

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confidence: 90%

“…evoked inhibitions in the cerebral cortex were reported to be blocked by iontophoretic applications of strychnine and could not be differentiated by strychnine from inhibitions caused by either glycine or 5-hydroxytryptamine (Phillis & York, 1967a, b;Jordan & Phillis, 1972). Stone (1972), however, was unable to block ACh-evoked inhibitions in the cerebral cortex with iontophoretic strychnine.…”

Section: /12mentioning

confidence: 99%

“…Phillis (1971), however, has also suggested that there may be inhibitory cholinergic terminals on cells inhibited by ACh (cf. Jordan & Phillis, 1972).…”

Section: /12mentioning

confidence: 99%

“…The possibility that ACh-evoked inhibition is artifactual in the sense that it might be caused by spread of ACh to neighbouring cells, the excitation of which leads to inhibition of the neurone under study by release of a transmitter other than ACh, has been discussed by several groups (Randic, Siminoff & Straughan, 1964;Phillis & York, 1967a, b, 1968Jordan & Phillis, 1972;Duggan & Hall, 1975a, b). Indeed, ACh- …”

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confidence: 99%

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Inhibitory effects of acetylcholine on neurones in the feline nucleus reticularis thalami.

Ben-Ari¹,

Dingledine²,

Kanazawa³

et al. 1976

The Journal of Physiology

136

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SUMMARY1. Short iontophoretic pulses of acetylcholine (ACh) inhibited almost every spontaneously active cell encountered in the nucleus reticularis thalami of cats anaesthetized with a mixture of halothane, nitrous oxide and oxygen. On 200 cells the mean current needed to eject an effective inhibitory dose of ACh was 67 + 2 nA. When the ACh-evoked inhibition was mimicked by y-aminobutyric acid (GABA) or glycine on the same cell, the current required to release ACh was found to be approximately twice as great as that required to release an equally effective dose of GABA or glycine.2. The ACh inhibitions developed with a latency which was very much shorter than that for ACh excitation in cells of the ventrobasal complex. The latency of the ACh-evoked inhibition was as rapid as the onset and offset of the excitation of the same cells by glutamate and their inhibition by GABA or glycine.3. The firing pattern of ACh-inhibited neurones in the nucleus reticularis was characterized by periods of prolonged, high frequency bursts, and their mean firing frequency was 22 Hz. Raster dot displays and interspike interval histograms showed that whereas ACh suppressed the spikes that occurred between bursts much more readily than those that occurred during bursts, all spikes were equally sensitive to the depressant action of GABA and glycine. Large doses of ACh provoked or exaggerated burst activity.4. ACh-evoked inhibition was extremely sensitive to blockade by short iontophoretic applications of atropine, which had no effect on the inhibitions evoked on the same cell by equipotent doses of GABA or glycine. The Y. BEN-ARI AND OTHERSACh-evoked inhibitions were also antagonized by dihydro-fl-erythroidine released with slightly larger currents. When tested on the same cell, small iontophoretic applications of picrotoxin and bicuculline methoiodide blocked the inhibition evoked by GABA but had no effect on that evoked by ACh. Iontophoretic strychnine only rarely affected the inhibition evoked by ACh, while readily blocking the inhibition evoked on the same cell by an equipotent dose of glycine. In two cats, intravenous strychnine (1.2 mg/kg) had no effect on the ACh-evoked inhibition, while greatly reducing the sensitivity of the cell under study to glycine.5

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Immunocytochemical localization of choline acetyltransferase in rat cerebral cortex: A study of cholinergic neurons and synapses

Houser

Crawford

Salvaterra

et al. 1985

J of Comparative Neurology

373

159

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Choline acetyltransferase (ChAT), the acetylcholine-synthesizing enzyme and a definitive marker for cholinergic neurons, was localized immunocytochemically in the motor and somatic sensory regions of rat cerebral cortex with monoclonal antibodies. ChAT-positive (ChAT+) varicose fibers and terminal-like structures were distributed in a loose network throughout the cortex. Some immunoreactive cortical fibers were continuous with those in the white matter underlying the cortex, and many of these fibers presumably originated from subcortical cholinergic neurons. ChAT+ fibers appeared to be rather evenly distributed throughout all layers of the motor cortex, but a subtle laminar pattern was evident in the somatic sensory cortex, where lower concentrations of fibers in layer IV contrasted with higher concentrations in layer V. Electron microscopy demonstrated that immunoreaction product was concentrated in synaptic vesicle-filled profiles and that many of these structures formed synaptic contacts. ChAT+ synapses were present in all cortical layers, and the majority were of the symmetric type, although a few asymmetric ones were also observed. The most common postsynaptic elements were small to medium-sized dendritic shafts of unidentified origin. In addition, ChAT + terminals formed synaptic contacts with apical and, probably, basilar dendrites of pyramidal neurons, as well as with the somata of ChAT-negative nonpyramidal neurons.ChAT+ cell bodies were present throughout cortical layers 11-VI, but were most concentrated in layers 11-111. The somata were small in size, and the majority of ChAT-t neurons were bipolar in form, displaying vertically oriented dendrites that often extended across several cortical layers. Electron microscopy confirmed the presence of immunoreaction product within the cytoplasm of small neurons and revealed that they received both symmetric and asymmetric synapses on their somata and proximal dendrites. These observations support an identification of ChAT+ cells as nonpyramidal intrinsic neurons and thus indicate that there is an intrinsic source of cholinergic innervation of the rat cerebral cortex, as well as the previously described extrinsic sources.

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Acetylcholine inhibition in the intact and chronically isolated cerebral cortex

Cited by 55 publications

References 32 publications

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

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

Inhibitory effects of acetylcholine on neurones in the feline nucleus reticularis thalami.

Immunocytochemical localization of choline acetyltransferase in rat cerebral cortex: A study of cholinergic neurons and synapses

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