Serotonin in the striatum

Neurones fire action potentials at different rates. One way to modulate the firing rate is via the after-hyperpolarisation, which brings the membrane potential to a value away from threshold potential. Two recent reports describe modulation of the after-hyperpolarisation in striatal cholinergic neurones (Goldberg and Wilson 2005; Blomeley and Bracci, 2005). These neurones are spontaneously active in the brain slice, and they are a suitable candidate for the tonically-active neurones observed in vivo. These neurones become silent (i.e. do not fire action potentials) during the execution of movement.
Cholinergic neurones shows two types of after-hyperpolarisation. A medium-duration after-hyperpolarisation (mAHP), and a slow after-hyperpolarisation (sAHP). The mAHP is caused by an apamin-sensitive calcium activated potassium channel. This is a small conductance K channel, also found in other preparations. The sAHP is caused by an apamin-insensitive channel that needs to be identified. Golberg and Wilson (2005) show that Ca that enters through N-type calcium channels (Ca_v2.2, blocked by ω-conotoxin GVIA) activates the mAHP. On the other hand, Calcium that enters through L-type calcium channels (Ca_v1 blocked by dihydropyridine) activates the sAHP. The obvious hypothesis here is that there might be a specific molecular association between the Calcium and calcium-activated K channels.
The work by Blomeley and Bracci (2005) also investigates the striatal cholinergic interneurones to shows that both component of the after-hyperpolarisation (mAHP, and sAHP) were reduced by serotonin. This is quite strange, because serotonin is not a neurotransmitter commonly associated with the striatum. The authors point out that such a modulation probably was lost and therefore unnoticed in whole cell recordings that wash out the intracellular content. They use the perforated-patch technique instead, that preserves the modulation. The receptor that mediates this modulation is the 5-HT2 subtype. The modulation by serotonin occurs directly, and not via an interneurone. The author used TTX, that block voltage-dependent Na-channels (and therefore transmitter release), to show that the modulation still present. A problem that needs to be solved is whether serotonin modulates the after-hyperpolarisation at the level of the potassium channels or at the level of the calcium channel.
It will be interesting to see a study showing the role of serotonin in vivo. What would then be the role of serotonin on striatal function, such as reward-based learning?