Figure 2.

The hyperpolarization was mediated by SK-type Ca²⁺-activated K⁺ channels. The depolarization had characteristics consistent with activation of a nonspecific cationic current. (A) ACPD puffs (60 ms) triggered Ca²⁺ waves (not shown) and a hyperpolarization and depolarization while this rat cell was held in current clamp at different membrane potentials. At depolarized potentials, both the hyperpolarization and the depolarization increased in magnitude. At hyperpolarized potentials, the hyperpolarization and depolarization both became smaller. Only the hyperpolarization reversed. (B) Ca²⁺ waves and a hyperpolarization were triggered by ACPD puffs onto rat neurons at different membrane potentials. Hyperpolarization magnitude increased with depolarization in all cells tested and reversed (−82.5 ± 1.0 mV) in all cells for which Ca²⁺ waves were triggered at potentials more negative than −80 mV. (C) Ca²⁺ waves and a depolarization were triggered by ACPD puffs onto rat neurons at different membrane potentials. Depolarization magnitude increased with depolarization and decreased with hyperpolarization in all cells tested but did not apparently reverse. (D) ACPD puffs (100 ms) onto this ferret neuron triggered Ca²⁺ waves with standard recording ACSF and following addition of the SK-type Ca²⁺-activated K⁺ channel antagonist, apamin (100 nM). In control recording ACSF, puffs of ACPD triggered a brief membrane hyperpolarization followed by a sustained membrane depolarization. Following application of apamin, the depolarization persisted, but the hyperpolarization was no longer detectable. (E) Ca²⁺ waves and a depolarization were triggered by puffs of ACPD (50–100 ms) onto this rat neuron in normal recording ACSF (100 ms puff) and following addition of the broad-spectrum K⁺ channel antagonist, TEA (10 mM; 50 ms puff). The depolarization was not inhibited by TEA exposure.