Ba(2+), applied by micro-iontophoresis, excites most cortical neurones that are excitable by ACh; other neurones tend to be depressed.2. The discharges evoked by Ba(2+) resemble those evoked by ACh, but they have an even slower time course and are characterized by firing in high frequency bursts.3. The excitatory action of Ba(2+), unlike that of ACh, is not abolished by muscarine antagonists; but it can be prevented with dinitrophenol.4. The depolarizing effect of Ba(2+) is associated with a rise in membrane resistance and it has a reversal level 24 mV more negative than the resting potential.5. These observations suggest that, as in other tissues, Ba(2+) reduced the K(+) conductance by a direct action on the cell membrane. Some diminution in Na(+) inactivation is indicated by the repetitive firing at high frequency.6. TEA has a predominantly depressant effect on all neurones tested. Like Ba(2+), it often increases greatly the duration of spikes, but there is no regular change in resting membrane resistance and no tendency to repetitive firing. TEA probably reduces only the delayed K(+) current.7. Even in large doses neither Ba(2+) nor TEA interferes with the conductance increase that generates the typical prolonged IPSPs recorded in cortical neurones.
No takes yet. Share an insight, caveat, or question.
Krnjević et al. (1971) studied this question.
Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context: