Plasticity and in Spinal Dorsal Horn Neuron and Neuropathic Pain : An Analysis by Patch Clamp Recordings

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The actions of neurotransmitters and modulators have well been investigated in superficial spinal dorsal horn neurons, but little is known about those in deep dorsal horn neurons. Our previous studies suggested that SP, CGRP and somatostatin play important roles in synaptic transmission to deep dorsal horn neurons. In this study, responses of SP and mENK to deep dorsal horn neurons were examined by the blind patch clamp technique used freshly sliced spinal cord of the rat (3-4weeks). About 60% of deep dorsal horn neurons in the deep lamina (III-V) showed the slow inward currents more than 5 pA by the bath application of SP (1 μM) for 1 min. These currents are considered to be evoked though G protein-Coupled SP receptors on the patched cells. Some of the recorded neurons enhanced the number and the peak amplitude of spontaneous EPSCs and/or IPSCs by the application SP. On the other hand, about 60% of the deep dorsal horn neurons showed the slow outward currents more than 5 pA by the bath application of mENK (5 μM), DAMGO (mu-receptor agonist. 1 μM), or DADLE (delta-receptor agonist; 1 μM) for 1 min. These currents are also considered to be evoked though G protein-coupled mu/delta-receptors on the patched cells. The responsive neurons to mENK always displayed the outward current by DAMGO, DADLE, or both. The amplitude of outward current was not suppressed by the repetitive application of mENK. Most of deep dorsal horn neurons with the slow inward currents by SP showed the slow outward currents by enkephalin, DAMGO, or DADLE, and vice versa. The present study suggests that about 60% of deep dorsal horn neurons receive both excitatory inputs though the NK1 receptors and inhibitory inputs though the mu-/delta-receptors.