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Previously, we have reported that apoptosis of cerebellar granular neurons induced by incubation in 5 mm K⁺ and serum‐free medium (LK‐S) was associated with an increase in the delayed rectifier K⁺ current (I_K). Here, we show that I_K associated with apoptotic neurons is mainly encoded by a Kv2.1 subunit. Silencing Kv2.1 expression by small interfering RNA reduces I_K and increases neuron viability. Forskolin is able to decrease the I_K amplitude recording from neurons of both the LK‐S and control group, and prevents apoptosis of granule cells that are induced by LK‐S. Dibutyryl cAMP mimicks the effect of forskolin on the modulation of I_K and, accordingly, the inhibitor of protein kinase A, H‐89, aborts the neuron‐protective effect induced by forskolin. Whereas the expression of Kv2.1 was silenced by Kv2.1 small interfering RNA, the inhibition of forskolin on the current amplitude was significantly reduced …