1. The mechanism underlying a large slow inward tail current was studi
ed in serotonergic dorsal raphe (DR) neurones. The tail current is mos
t easily observed under conditions of suppressed K+ channel outward cu
rrents and follows the activation of a calcium current. This current m
ay underlie a slow after-depolarizing potential (ADP) which follows ac
tion potentials observed in acutely isolated DR neurones. 2. The after
-hyperpolarizing potential (AHP) following action potentials which sho
uld reverse at E(K) (the reversal potential for potassium) becomes an
ADP at less negative potentials than expected due to contamination by
the slow inward tail current. 3. DR neurones were acutely isolated enz
ymatically; the ADP in current clamp and the tail current underlying i
t in voltage clamp were studied using the patch clamp method. When the
external Ne was replaced with TEA or choline the slow inward tail cur
rent was completely abolished. Blocking K+ channels from the inside of
the cell membrane with 40 mm TEACl or large concentrations of interna
l Cs+ also blocked the slow inward tail current. 4. The tail current p
roved to be independent of calcium influx or intracellular calcium rel
ease as it was not affected by inorganic calcium channel blockers or c
affeine. 5. The tail grew exponentially upon lengthening the depolariz
ing test pulse and appeared to reverse close to 0 mV indicating that t
he current was carried by a non-selective cation conductance. Removal
of external Na+ and replacement with Li+ ions reversibly blocked the t
ail current by 77%. 6. The data rule out several mechanisms for the ge
neration of the current, namely: a calcium-activated chloride conducta
nce, a calcium-activated non-selective cation conductance, a Na+-Ca2exchange pump current or a sodium-activated K+ conductance. 7. The slo
w tail current may be explained by postulating an inward movement of N
a+ through a channel which is blocked by high concentrations of extern
al TEA and Li+ or internal Cs+ or 40 mm TEA.