Paroxysmal afterpotentials and role of calcium-dependent potassium conductivity in neuronal activity of strychninized neocortex.

Reactions of cortical suprasylvian gyrus neurons were investigated intracellularly after supracortical strychnine application in immobilized and anaesthetized cats. It was shown that paroxysmal depolarizing shifts of membrane potential could be accompanied by de- and hyperpolarizing afterpotentials. When passing from epileptiform to normal physiological activity, short afterhyperpolarizations, 300-500 ms in duration, were converted into inhibitory postsynaptic potentials which were also accompanied by a decrease in membrane potential. When the frequency of paroxysmal discharge was less than 1 s, prolonged (1-2 s) afterhyperpolarizations were observed; at a higher frequency their summation led to tonic hyperpolarization of the membrane. The ictal discharges were accompanied by postictal hyperpolarizations of up to 30 s duration. The intracellular injection of EGTA blocking Ca2(+)-dependent potassium conductivity eliminated prolonged after- and postictal hyperpolarizations and produced depolarizing afterpotentials and a gradual depolarization of cell membranes. Our results indicate that the development of short hyperpolarizing afterpotentials could be determined by the inhibitory synaptic effects. The activation of Ca2(+)-dependent potassium conductivity caused by the development of prolonged afterhyperpolarizations and postictal polarizations, as well as maintained tonic hyperpolarization of cell membranes. Obviously, the depolarizing afterpotentials are of a non-synaptic origin and can be induced by inward calcium current.