The mechanism of after‐bursts in cerebral cortex

Burns, B. Delisle

doi:10.1113/jphysiol.1955.sp005247

Cited by 55 publications

(14 citation statements)

References 21 publications

(29 reference statements)

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“…in the developing conditioned reaction. In addition to lowering the threshold of the involved cells (Burns, 1954(Burns, , 1955, the anodal current appears to confer upon these cell populations the property of retaining, at least for a short period of time, a representation of a stimulus imposed during the polarization. Indeed this may be demonstrated even more graphically if one shifts the polarizing electrode to the visual cortex and studies the effect of single or rhythmic stroboscopic stimulation.…”

Section: Discussionmentioning

confidence: 99%

Effect of Anodal Polarization on the Firing Pattern of Single Cortical Cells

Morrell

1961

Annals of the New York Academy of Sciences

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Section: Discussionmentioning

confidence: 99%

Effect of Anodal Polarization on the Firing Pattern of Single Cortical Cells

Morrell

1961

Annals of the New York Academy of Sciences

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“…This suggests that the functional unbalance exists in the organisation of the general regions of the brain and it is not always necessary to postulate a punctate localization of epileptogenic tissue in a definite area. The neurophysiological foundation for the disturbances of the organisation in the general regions of the brain will remain unknown until more precise illustrations of the mechanisms of neuronal nets (Burns, 1955) in which neurons are completely connected with each other and with other cells by their dendrites are made available.…”

Section: Discussionmentioning

confidence: 99%

ABNORMALITY OP PROTEIN DISTRIBUTION ON THE EPILEPTIC BRAIN and ITS SIGNIFICANCE

Kiyota

1961

Psychiatry Clin Neurosci

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Summary 1) Brain samples obtained by biopsy from the frontal lobes in idiopathic epilepsy patients showed an abnormal distribution of proteins in all five cases tested. 2) Following three questions has been discussed: What is the original pattern of abnormal protein distribution found in the brains of idiopathic epilepsy patients? What significance has the abnormal protein distribution in concern with the predisposition toward epileptic seizures or for the mechanism which leads up to epileptic attacks? Is not the original pattern of abnormal protein distribution really induced by some developmental lesions of the brain?

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“…A 200 msec 60 Hz current of 200 mA was applied by means of corneal saline-wick electrodes, This current intensity regularly produced maximal electroshock seizure patterns. These potential differences may arise by differential repolarization properties of contiguous portions of neurons (3,14) or as a result of mechanical deformation of part of a cortical neuron (20,29,30). 10 shows a dose-response curve relating the incidence of maximal seizure with dose.…”

mentioning

confidence: 99%

“…Thus, Schmidt et al (20), Ward (29,30), Burns (3) and Pinsky and Burns (14) have suggested that the probable underlying mechanism in the generation of cortical high frequency nerve activity is a generator potential created by intra-neuronal potential differences. These potential differences may arise by differential repolarization properties of contiguous portions of neurons (3,14) or as a result of mechanical deformation of part of a cortical neuron (20,29,30). In any case the nerve axon, which is capable of rapid recovery, is exposed to some long-lasting cathodal influence and therefore fires repetitively.…”

mentioning

confidence: 99%

Effects of Anticonvulsant Drugs on Nerve Terminals

Raines

Standaert

1969

Epilepsia

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SUMMARY The anticonvulsant agents diphenyrhydantoin(DPH) and diphenylthiohydantoin (DPTH) suppress repetitive after‐discharges originating in the motor nerve endings of the cat soleus nerve. Since these repetitive after‐discharges are responsible for virtually all of the posttetanic potentiation in this neuromuscular junction, DPH, DPTH and to a lesser degree certain other anticonvulsants reduce PTP. The repetitive after‐discharge seems to arise by a process of intra‐neuronal potential difference leading to high‐frequency firing, a process postulated to play a role in epileptogenic focal firing. The capacity of DPH to suppress hyperpolarization of nerve endings subjected to high‐frequency stimulation probably accounts for DPH's efficacy in suppressing repetitive after‐discharges and its previously described capacity to suppress posttetanic potentiation in spinal cord monosynaptic pathways. RÉSUMÉ Les médicaments anticonvulsifsdiphénylhydantoïne (DPH)etdiphénylthiohydantoïne (DPTH) suppriment les post‐décharges répétitives qui se produisent dans les termi‐naisons du nerf soleus du chat. Puisque ces post‐décharges répétitives sont respon‐sables de presque toute la potentiation post‐tétanique (PPT) dans cette jonction neuro‐musculaire, DPH, DPTH et à un moindre degré certains autres médicaments anti‐convulsifs font diminuer la PPT. La post‐décharge répétitive semble se produire par une différence de potentiel intra‐neuronale qui est àľorigine ďune décharge de haute fréquence, un processus qui jouerait un rôle dans la décharge ďun foyer épileptogène. La capacityé de DPH de supprimer ľhyperpolarisation des terminaisons neuronales soumises à une stimulation à haute fréquence explique probablement ľefficacité de DPH de supprimer des post‐décharges répétitives et sa capacityé de supprimer la PPT dans le trajet monosynaptique spinal qui a déjàété décrite.

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The mechanism of after‐bursts in cerebral cortex

Cited by 55 publications

References 21 publications

Effect of Anodal Polarization on the Firing Pattern of Single Cortical Cells

Effect of Anodal Polarization on the Firing Pattern of Single Cortical Cells

ABNORMALITY OP PROTEIN DISTRIBUTION ON THE EPILEPTIC BRAIN and ITS SIGNIFICANCE

Effects of Anticonvulsant Drugs on Nerve Terminals

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