Neurotransmitter Interactions and Early Convulsive Activity

2015 ◽  
pp. 217-225 ◽  
Author(s):  
C Kellogg
Keyword(s):  
Convulsive Activity

ACETYLCHOLINE AND CONVULSIVE ACTIVITY

1949 ◽  
Vol 12 (1) ◽  
pp. 17-27 ◽  
Author(s):  
J. Hyde ◽  
S. Beckett ◽  
E. Gellhorn
Keyword(s):  
Convulsive Activity

Experiments on the Prolongation of Induced Epileptiform Convulsions in the Cat

1952 ◽  
Vol 98 (412) ◽  
pp. 454-456 ◽  
Author(s):  
Hugo Ruf
Keyword(s):  
Electrical Activity ◽  
Intravenous Injection ◽  
Experimental Research ◽  
Electric Stimulation ◽  
List Type ◽  
Type Number ◽  
Convulsive Activity ◽  
Cortical Electrical Activity ◽  
Epileptiform Convulsions

THE present paper offers a brief summary of work which has been published in German journals dealing with the prolongation of induced convulsions. In the course of my experimental research the following phenomena were demonstrated:(1)Continuousconvulsionslastingup to oneand a half hours were produced by the administration of oxygen and adrenaline, preceded by the injection of phenyl-methyl-aminopropane.(2)Prolonged convulsions of 33 minutes were produced by the intravenous injection of 2 ml. of a io per cent. metrazol solution and continuous oxygen in suffiation.(3)Isolated continuous convulsive activity of the cerebellum was produced lasting 30 minutes after cessation of respiration and of all cortical electrical activity. This was achieved by continuous insuffiation of oxygen together with the injection of adrenaline and strychnine.(4)Activation of a prolonged convulsion up to 11 minutes, without further electric stimulation, was effected via the thalamus by the injection of adrenaline after administration of phenyl-methyl-aminopropane and continuous oxygen in sufflation.

Spinal Unit Activity During Synchronization of a Convulsive Type (Strychnine Tetanus)

1956 ◽  
Vol 186 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Carlo A. Terzuolo ◽  
Bo E. Gernandt
Keyword(s):  
Spinal Cord ◽  
Intravenous Injection ◽  
Unit Activity ◽  
Single Unit ◽  
Slow Waves ◽  
Single Unit Activity ◽  
Oscillatory Potential ◽  
Convulsive Activity ◽  
Decerebrate Cat ◽  
The Relationship

Single unit activity during convulsive synchronized discharge and the relationship between unit activity and slow ‘waves’ were studied in the spinal cord of the decerebrate cat after intravenous injection of strychnine. Steel needle microelectrodes were used. Units did discharge in burst (from 1 to 5 impulses) only in coincidence with the slow oscillatory potential (tetanic ‘waves’). The firing is confined to the rising phase of this potential. Changes in d.c. state related to a convulsive activity were also studied. A relationship was found between frequency of the tetanic rhythm and d.c. state of spinal structures. The mechanisms of synchronization and rhythmicity of the convulsive activity in a population of neurons are discussed in connection with the problem of interaction between units.

The influence of activation of the superior colliculi on convulsive activity during picrotoxin kindling

1993 ◽  
Vol 23 (6) ◽  
pp. 562-567 ◽  
Author(s):  
A. A. Shandra ◽  
L. S. Godlevskii ◽  
S. L. Vikhrestyuk ◽  
A. A. Oleinik
Keyword(s):  
Convulsive Activity ◽  
Superior Colliculi ◽  
Picrotoxin Kindling

Electrical and Vascular Concomitants of Spreading Depression

1957 ◽  
Vol 189 (1) ◽  
pp. 159-166 ◽  
Author(s):  
A. Van Harreveld ◽  
Sidney Ochs
Keyword(s):  
Spreading Depression ◽  
Potential Change ◽  
Vascular Changes ◽  
Convulsive Activity ◽  
Slow Potential ◽  
Narrow Region ◽  
Transport Of Ions ◽  
The Relationship ◽  
The Brain

Spreading depression is accompanied by a slow potential change, a drop in cortical conductivity and by vascular changes. The latter were investigated in histological preparations of cortex frozen while a spreading depression was in progress. In the cat and rabbit a broad wave of vasodilatation was observed. In the rabbit this appeared to be preceded by a narrow region of vasoconstriction. Spreading depression can be changed into spreading convulsive activity by administering CO2 in the respiratory air (7–12%). CO2 markedly decreased the drop in cortical conductivity but affected the magnitude of the slow potential change only moderately. It is postulated that both the conductivity drop during spreading depression and a similar drop observed after asphyxiation of the brain are caused by a transport of ions from the intercellular compartment into cortical cellular elements. The relationship between the slow potential change, conductivity drop, vascular changes and the changes in the electrocorticogram during spreading depression is discussed.

Kinetics of Drug Action in Disease States XV: Effect of Pregnancy on the Convulsive activity of Pentylenetetrazol in Rats

1985 ◽  
Vol 74 (11) ◽  
pp. 1233-1235 ◽  
Author(s):  
Iqbal M. Ramzan ◽  
Gerhard Levy
Keyword(s):  
Drug Action ◽  
Convulsive Activity ◽  
Disease States ◽  
Kinetics Of

Low convulsive activity of a new carbapenem antibiotic, DK-35C, as compared with existing congeners

Toxicology ◽  
1999 ◽  
Vol 138 (2) ◽  
pp. 59-67 ◽  
Author(s):  
Changbae Jin ◽  
Insook Jung ◽  
Hee-Jung Ku ◽  
Juwon Yook ◽  
Dong-Hyun Kim ◽  
...  
Keyword(s):  
Convulsive Activity ◽  
Carbapenem Antibiotic

Effect of humidity on hyperoxic toxicity

1993 ◽  
Vol 75 (5) ◽  
pp. 1980-1983 ◽  
Author(s):  
Y. Lin ◽  
D. Jamieson
Keyword(s):  
Relative Humidity ◽  
Hyperbaric Oxygen ◽  
Convulsive Activity ◽  
Normobaric Hyperoxia ◽  
Pulmonary Damage ◽  
Low Humidity ◽  
Hyperbaric Oxygen Exposure ◽  
Oxygen Poisoning ◽  
Rats And Mice ◽  
Time To Onset

Time to onset of hyperbaric oxygen-induced convulsions was measured in mice and rats exposed to hyperbaric oxygen (515–585 kPa) under conditions of low humidity (dry gas, < 10% relative humidity) or in a humidified environment (60% relative humidity). At all pressures tested, the duration of convulsive activity was markedly increased (P < 0.001), because of the earlier onset of severe generalized convulsions, in the groups of rodents exposed to the higher humidity. Pulmonary oxygen poisoning was determined by increases in lung wet and dry weights. Such pulmonary damage was also significantly (P < 0.001) increased in the humidified groups. Hyperoxic toxicity was also measured in rats and mice exposed to approximately 100% oxygen (normobaric hyperoxia) under conditions of 30 or 62% relative humidity. In contrast to the results obtained with hyperbaric oxygen exposure, there was slightly less toxicity in the rodents maintained at 62% compared with 30% humidity in normobaric hyperoxia.

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