Intracellular potentials of inexcitable cells in epileptogenic cortex undergoing fibrillary gliosis after a local injury Academic Article Article uri icon

Overview

MeSH Major

  • Cell- and Tissue-Based Therapy
  • Spinal Cord Injuries

abstract

  • Intracellular recordings were obtained from 238 cells in the motor cortex of the cat 1-6 weeks after a cold injury was produced. Reactive astrocytes were the predominant cell in the gliotic upper layers of the cortex 2-3 weeks after injury when edema and inflammatory exudate had subsided. Chromatolysed and normal neurons were present in the deeper layers of the cortex. The electrocorticogram of cold-injured cortex exhibited surface negative paroxysmal discharges which developed 18-24 h after injury. The discharges occurred at intervals of 800-2200 msec in pentobarbital-anesthetized animals. Neurons were identified by means of spike and postsynaptic responses to intracellular, thalamic and cortical surface stimulation. Neurons in the lower portions of the lesion had membrane potentials as large as -70 mV. Areas of gliosis studied later than 2 weeks after injury contained electrically and synaptically inexcitable cells that had very stable resting membrane potentials as large as -92 mV. In most inexcitable cells surface stimulation of the cortex evoked slow depolarization, of up to 30 mV, rising to a maximum in 4-5 sec. Depolarization evoked by cortical stimulation was followed, in some inexcitable cells, by a slow hyperpolarizing potential with a maximum amplitude of 11 mV and with a duration of up to 85 sec. Some inexcitable cells with high membrane potentials exhibited rhythmic slow depolarizations which followed the paroxysmal discharges of the electrocorticogram. It is suggested that the inexcitable cells with high membrane potentials were reactive astrocytes. Mechanisms which might generate slow potential shifts in these cells are discussed. © 1971.

publication date

  • May 7, 1971

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1016/0006-8993(71)90654-8

PubMed ID

  • 5113518

Additional Document Info

start page

  • 181

end page

  • 201

volume

  • 28

number

  • 2