Brief increases in [Ca2+]i can result in prolonged
changes in neuronal properties. A Ca2+-dependent modulation
of the hyperpolarization-activated cation current (Ih) controls
the slow recurrence of synchronized thalamocortical activity. Here we show
that the persistent activation of Ih is initiated by rapidly
increased [Ca2+]i and subsequent production of cAMP.
The modulation is maintained via a facilitated interaction of cAMP with open
(voltage-gated) h-channels, inducing prolonged activation of I
h that may outlast the presence of increased free [Ca2+]
i and [cAMP]i. This persistent Ih activation
may control the presence and periodicity of both normal and abnormal synchronized
thalamocortical rhythms.
