• nerve injury;
  • neuropathic pain;
  • neuropeptides;
  • nociception;
  • patch-clamp;
  • sensory neuron


We examined the effect of galanin (10−15–10−7 m) on dispersed, mainly small-sized dorsal root ganglion (DRG) neurons in adult rats using whole-cell patch-clamp. Galanin and AR-M1896, a selective galanin type 2 receptor (GalR2) agonist, both significantly increased the number of action potentials in response to current pulses in 77% of the neurons, indicating an increase in excitability. Galanin also caused a rise in input resistance, decreased the holding current for −60 mV and depolarized the resting potential. In addition, Ca2+ currents elicited by voltage steps were significantly increased by both galanin and AR-M1896 in nearly 70% of the cells. This enhancement was observed in 30% of the neurons in the presence of nimodipine or ω-conotoxin, but in each case ≈ 60% less than without blocking either N- or L-type Ca2+ channels, indicating modulation of both types of Ca2+ channels. The percentage of small- and medium-sized neurons expressing GalR2 mRNA in DRGs in situ was similar to that showing increased excitability and Ca2+ current after galanin application, i.e. ≈ 70–80% of the neurons. The findings suggest that GalR2 has a role in controlling both the excitability, probably by inhibition of GIRK or leak K+ channels, and Ca2+ entry in a large population of presumably nociceptive neurons. The combination of the two effects, which possibly arise from separate biochemical pathways, would increase excitability and enhance intracellular Ca2+ signalling which would enhance sensory transmission. These mechanisms involving GalR2 receptors may underlie the pronociceptive effects of galanin described in the literature.