EFFECTS OF SECTION OF THE CORPUS CALLOSUM ON DECOMPRESSION HYPOXIA AND ON PENTYLENETETRAZOL (METRAZOL) CONVULSIONS

Electroencephalographic studies were carried out in white rats with chronically implanted electrodes located on the skull over the frontal areas of the brain, with the animals suspended in a sling in a decompression chamber. Exposed to simulated elevated altitude at weekly intervals 4 to 6 months after section of the corpus callosum 26 animals revealed a greater sensitivity to hypoxia than 22 controls. This was shown by a lower threshold of convulsibility and by a longer duration of the convulsions. Under the experimental conditions employed the electrocortical activity in control animals consisted of 1.5–3 c/s and 4–6 c/s waves of up to 40-μv amplitude with 11–14 c/s waves superimposed. In the corpus-callotomized rats the activity was somewhat slower and of a higher amplitude, this being more apparent [Formula: see text] months after the operation than at the time of the decompression experiments. Decompression of both groups of animals resulted in characteristic EEG changes culminating in the appearance of hypoxic preconvulsive potentials of high voltage (60–180 μv) and slow frequency (1.5–3 c/s) which were first grouped in paroxysms of about 3 to 5 seconds' duration, later becoming continuous. When decompression was continued, this activity was followed by convulsive discharges, all of the manifestations being more pronounced and recurring at lower altitudes in the corpus-callotomized animals than in the controls. An analysis of the wave patterns in 28 sacrifice experiments with transection of the spinal cord and curarization of the animals showed that the observed EEG activity did not depend on motor components.The EEG patterns during the excitatory stages of hypoxia or asphyxia resembled closely certain phases of pentylenetetrazol-induced activity; however, at the height of the convulsive EEG pattern induced by pentylenetetrazol, periods of asphyxia disorganized the spike activity caused by this agent and markedly depressed the EEG.

EFFECTS OF SECTION OF THE CORPUS CALLOSUM ON DECOMPRESSION HYPOXIA AND ON PENTYLENETETRAZOL (METRAZOL) CONVULSIONS

Electroencephalographic studies were carried out in white rats with chronically implanted electrodes located on the skull over the frontal areas of the brain, with the animals suspended in a sling in a decompression chamber. Exposed to simulated elevated altitude at weekly intervals 4 to 6 months after section of the corpus callosum 26 animals revealed a greater sensitivity to hypoxia than 22 controls. This was shown by a lower threshold of convulsibility and by a longer duration of the convulsions. Under the experimental conditions employed the electrocortical activity in control animals consisted of 1.5–3 c/s and 4–6 c/s waves of up to 40-μv amplitude with 11–14 c/s waves superimposed. In the corpus-callotomized rats the activity was somewhat slower and of a higher amplitude, this being more apparent [Formula: see text] months after the operation than at the time of the decompression experiments. Decompression of both groups of animals resulted in characteristic EEG changes culminating in the appearance of hypoxic preconvulsive potentials of high voltage (60–180 μv) and slow frequency (1.5–3 c/s) which were first grouped in paroxysms of about 3 to 5 seconds' duration, later becoming continuous. When decompression was continued, this activity was followed by convulsive discharges, all of the manifestations being more pronounced and recurring at lower altitudes in the corpus-callotomized animals than in the controls. An analysis of the wave patterns in 28 sacrifice experiments with transection of the spinal cord and curarization of the animals showed that the observed EEG activity did not depend on motor components.The EEG patterns during the excitatory stages of hypoxia or asphyxia resembled closely certain phases of pentylenetetrazol-induced activity; however, at the height of the convulsive EEG pattern induced by pentylenetetrazol, periods of asphyxia disorganized the spike activity caused by this agent and markedly depressed the EEG.