IK1 channels do not contribute to the slow afterhyperpolarization in pyramidal neurons

Neurons carry signals in the form of electrical impulses called action potentials. These nerve impulses result from ions flowing through proteins called ion channels in the neuron’s membrane, and they determine how the neuron communicates with neighboring neurons. The number of action potentials a neuron can produce can vary over a wide range. In the brain, a particular kind of ion channel limits the number of action potentials that many neurons produce via a negative feedback mechanism. That is to say, nerve impulses activate this ion channel and the activated channel then makes the neuron less able to send further nerve impulses for a while.The activity of this ion channel increases with age and it may be responsible for some forms of age-related decline in cognitive abilities. However, the exact identity of the ion channel responsible was unclear. Recent research has suggested the ion channel in question was a protein called IK1. This conclusion was largely based on how this ion channel responded to drugs in the laboratory. Wang, Materos-Aparico et al. sought to verify this conclusion and, in contrast with the previous reports, found that the IK1 ion channel did not respond to these drugs in the same way when it was in neurons in the brains of mice. In further experiments, mice that had been engineered to lack the IK1 ion channel still showed the characteristic negative feedback that regulates the firing of action potentials. Thus, Wang, Materos-Aparico et al. found no evidence to support the previous conclusion, and instead conclude that the exact identity of this important ion channel in the brain has yet to be defined.