Figure 1

Experimental paradigm. a. Schematic representation of the experimental setting to record from single antidromically identified lamina I projection neurons. Cells were recorded from control animals and animals that received a chronic constriction injury of the sciatic nerve. b. Confirmation of recording from lamina I projection neuron. Top: extracellular single unit recordings from a lamina I neuron showing one-for-one following of a train of antidromic stimuli (lower traces mark the stimulus; 1 mA, 200 μs duration; up to 500 Hz) delivered from the electrode positioned in the lateral parabrachial nucleus. Conduction distance was 100 mm. bottom: collision of the first of 4 antidromic action potentials (25 Hz) with an orthodromic action potential (*) occurring within the critical interval. The arrow points to the position where the first antidromic action potential would have occurred in absence of the orthodromic action potential (as in the trace on the left). c. Graph showing results of nociceptive reflexes to mechanical stimuli of the rats included in the current study. Peripheral nerve injury (N = 12) caused a significant reduction of the withdrawal threshold to mechanical stimulation of the hind paw. Nerve injured animals were taken between 16 and 24 days post-injury. Animals were anesthetized with pentobarbital or ketamine/xylazine and single unit extracellular recording was performed from lamina I projection neurons identified by antidromic stimulation from the parabrachial nucleus.