activated T-type Ca2 channels are widely expressed in various types of neurons.
Once deinactivated by hyperpolarization, T-type channels are ready to be activated by a
small depolarization near the resting membrane potential and, therefore, are optimal
for regulating the excitability and electroresponsiveness of neurons under physiological conditions
near resting states. Ca2 influx through T-type channels engenders low-threshold Ca2 spikes,
which in turn trigger a burst of action potentials. Low-threshold burst firing has been implicated in
the synchronization of the thalamocortical circuit during sleep and in absence seizures. It also has
been suggested that T-type channels play an important role in pain signal transmission, based on
their abundant expression in pain-processing pathways in peripheral and central neurons. In this
review, we will describe studies on the role of T-type Ca2 channels in the physiological as well as
pathological generation of brain rhythms in sleep, absence epilepsy, and pain signal transmission.
Recent advances in studies of T-type channels in the control of cognition will also be briefly