Referenced in: none

Automatically associated channels: Cav1.3

Title: 5-HT and dopamine modulates CaV1.3 calcium channels involved in postinhibitory rebound in the spinal network for locomotion in lamprey.

Authors: Di Wang, Sten Grillner, Peter Wallén

Journal, date & volume: J. Neurophysiol., 2011 Mar , 105, 1212-24

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21228305

Abstract
Postinhibitory rebound (PIR) can play a significant role for producing stable rhythmic motor patterns, like locomotion, by contributing to burst initiation following the phase of inhibition, and PIR may also be a target for modulatory systems acting on the network. The current aim was to explore the PIR in one type of interneuron in the lamprey locomotor network and its dependence on low voltage-activated (LVA) calcium channels, as well as its modulation by 5-HT and dopamine. PIR responses in commissural interneurons, mediating reciprocal inhibition and left-right alternation in the network, were significantly larger than in motoneurons. The L-type calcium channel antagonist nimodipine reduced PIR amplitude by ∼ 50%, whereas the L-channel agonist BAY K 8644 enhanced PIR amplitude, suggesting that LVA calcium channels of the L-subtype (Ca(V)1.3) participate in the PIR response. The remainder of the response was blocked by nickel, indicating that T-type (Ca(V)3) LVA calcium channels also contribute. No evidence was obtained for the involvement of a hyperpolarization-activated current. Furthermore, 5-HT, acting via 5-HT(1A) receptors, reduced PIR, as did dopamine, acting via D(2) receptors. Coapplication of nimodipine caused no further PIR reduction, indicating that these modulators target Ca(V)1.3 channels specifically. These results suggest that PIR may play a prominent role in the generation of alternating network activity and that the Ca(V)1.3 and Ca(V)3 subtypes of LVA calcium channels together underlie the PIR response. 5-HT and dopamine both target PIR via Ca(V)1.3 channels, which may contribute significantly to their modulatory influence on locomotor network activity.