It has been suggested that I_h drives neuropathic pain (Chaplan et al. 2003) partly because rat isolated large diameter L5 DRG neuronal somata in vitro, showed increased I_h density and depolarised V_0.5 (half-activation potential) after L5 spinal nerve ligation. In this study we examined whether such changes occur in vivo in Aα/β-neurons after L5 spinal nerve axotomy (SNA). Young female Wistar rats were anaesthetised (pentobarbital 80mg/kg i.p.) and underwent neuromuscular blockade (pancuronium 0.5mg/kg i.v.). The muscle relaxant was giving hourly and always accompanied by additional dosage of anesthetic (10mg/kg), a level that in the absence of muscle relaxant keeps the animals deeply anaesthetised. The arterial blood pressure was monitored throughout the experiment. By using discontinuous single electrode voltage clamp (dSEVC) technique (3M KCl, 40~80MΩ, 30 deg), I_h was recorded in somata of L4-L6 DRG neurons in normal and in axotomised L5 DRG neurons 7 days after SNA. I_h at -100 mV was determined from the difference between instantaneous and steady state current. I_h density is I_h divided by the cell capacitance. Action potentials (APs) were evoked by stimulating the dorsal root with a bipolar electrode. Neurons were classed as having C-, Aδ- or Aα/β conduction velocities. Animals were killed by a pentobarbital overdose. Medians were compared by non-parametric Kruskall-Wallis or Mann-Whitney test. I_h was recorded from 98 neurons in normal rats (n=27), and 68 in SNA rats (n=13). I_h was identified on the basis of its activation properties, time-dependant rectification and reversal potential (V_rev) which were consistent with previous findings (Tu et al. 2004; Yao et al. 2003). Some properties of I_h did not change in axotomised Aα/β-fibre neurons. V_rev was similar (-30.3±1.0mV n=35 for normal, -31.1±2.0mV n=12 for axotomy). The slope of the I-V curve derived from tail currents was reduced (~0.09 nA/mV for normal, ~0.07 nA/mV for axotomy, p<0.05). However, after dividing the currents by cell capacitance this difference vanished (~0.82 ns/pF for normal, ~0.71 ns/pF for axotomy) suggesting a shrinkage of neurons after axotomy. Changes in I_h occurred in axotomised L5 Aα/β-fiber neurons compared with in normal neurons. Both I_h amplitude and density were significantly reduced (P<0.01) after axotomy. A higher proportion of axotomised neurons expressed I_h (100% n=68 for axotomy, 89% n=98 for normal; p<0.05, Chi2 test). V_0.5 for axotomised Aα/β-fibre neurons was shifted negatively from -84.1±0.8mV (n=36) to -87.4±1.5mV (n=27) (p<0.01). Our findings suggest that I_h is likely to be both harder to activate and smaller in axotomised Aα/β-fibre neurons. Therefore, I_h is an unlikely primary cause of increased excitability in axotomised Aα/β-fibre neuronal somata.