The cellular mechanisms of spike-frequency adaptation during prolonged disc
harges and of the slow afterhyperpolarization (AHP) that follows, as occur
in vivo with contrast adaptation, were investigated with intracellular reco
rdings of cortical neurons in slices of ferret primary visual cortex. Intra
cellular injection of 2 Hz sinusoidal or constant currents for 20 sec resul
ted in a slow (tau = 1-10 sec) spike-frequency adaptation, the degree of wh
ich varied widely among neurons. Reducing either [Ca2+](o) or [Na+](o) redu
ced the rate of spike-frequency adaptation. After the prolonged discharge w
as a slow (12-75 sec) AHP that was associated with an increase in membrane
conductance and a rightward shift in the discharge frequency versus injecte
d current relationship. The reversal potential of the slow AHP was sensitiv
e to changes in [K+](o), indicating that it was mediated by a K+ current. B
lockade of transmembrane Ca2+ conductances did not reduce the slow AHP. In
contrast, reductions of [Na+](o) reduced the slow AHP, even in the presence
of pronounced Ca2+ spikes. We suggest that the activation of Na+-activated
and Ca2+-activated K+ currents plays an important role in prolonged spike-
frequency adaptation and therefore may contribute to contrast adaptation an
d other forms of adaptation in the visual system in vivo.