It has been proposed that Ih contributes to SA in injured A-fibre dorsal root ganglion (DRG) neurons, mainly based on decreased SA frequency and tactile allodynia by application of the Ih blocker ZD72882,3. However, although Ih blockade is irreversible, the effects of ZD7288 on allodynia only lasted ~2 hrs, raising questions about the role of Ih in neuropathic pain. Our previous studies showed that compared to normal DRG neurons, Ih is reduced and harder to activate in 7 day L5 DRG neurons after L5 spinal nerve axotomy (SNA)1. In the present study we compared Ih and Ih kinetics in axotomised A-fibre neurons with and without SA 1 day and 7 days post axotomy (performed under 5% isoflurane in O2). This was to determine whether Ih might change selectively in neurons with SA, and thus contribute to the SA. We also examined the effects of ZD7288 on SA frequency during acute Ih blockade in vivo. Young female Wistar rats were anaesthetised (pentobarbital 80mg/kg i.p.) and hourly given muscle relaxant (pancuronium 0.5mg/kg i.v.), which was always accompanied by additional dosage of anesthetic (10mg/kg), a level that keeps the animals deeply anaesthetised in the absence of muscle relaxant. The animal was connected to a Small Animal Ventilator (Harvard Apparatus) at the same time as neuromuscular blocker was applied. Ih was recorded in vivo in A-fibre DRG neuronal soma in normal, day 1 and day 7 SNA rats by using discontinuous single electrode voltage clamp (dSEVC) technique (3M KCl, 40~80MΩ, 30°C). Ih at -100 mV was determined from the difference between instantaneous and steady state current. Ih density is Ih divided by cell capacitance. Action potentials (APs) were evoked by stimulating the dorsal root and neurons were classed as having C-, Aδ- or Aα/β conduction velocities (CVs). Animals were killed by overdose pentobarbital. Medians were compared by non-parametric Kruskall-Wallis or Mann-Whitney test. We found: 1) 27% and 10% of axotomised A-fibre neurons fired spontaneously 1 day and 7 day after SNA, respectively. All SA neurons had Aa/b CVs, with significantly faster CVs than non-SA Aa/b-neurons; 2) Ih in axotomised A-fibre DRG neurons was unchanged 1 day after SNA, but was significantly reduced at 7 days. The percentage of Ih reduction was even greater in SA (75%) than non-SA neurons (39%); 3) although, as I showed previously, Ih kinetics were slower 7 days after axotomy1, they did not differ between SA and non-SA neurons; 4) in neurons with SA 7 days after axotomy, intravenous application of ZD7288 blocked Ih in 8 mins with no obvious change of SF frequency at the same time. To summarise: 7 days after axotomy Ih was even more greatly reduced in A-fibre DRG neurons with, than without, SA, and SA frequency was not affected by blockade of Ih. We therefore conclude that Ih is unlikely to be a main cause of SA in axotomised A-fibre DRG neurons.