Inflammatory pain reduces correlated activity in the dorsal column nuclei

Abstract

Persistent pain can result in sensitization of neurons in the spinal cord dorsal horn and produce physiological changes in sites such as the thalamus, that receive projections from the dorsal horn. Although the dorsal column nuclei receive both primary afferent input and projections from the dorsal horn, their participation in persistent pain states is relatively unexplored, perhaps because they play a limited role in acute, cutaneous nociception. We have used a model of inflammatory pain to examine the physiological properties of dorsal column nucleus neurons during persistent pain. We used this model in order to minimize direct damage to large myelinated primary afferents that project directly to the dorsal column nuclei. Inflammation was produced by injection of complete Freund’s adjuvant into one hindpaw in rats, and neurons in the gracile nucleus were recorded 2–8 days later. Inflammation resulted in increased responsiveness to nociceptive (pinch) stimulation and increased incidence of afterdischarge firing 2–3 days after injection. Spontaneous activity was increased 6–8 days after injection. Inflammation decreased the strength of correlated firing in neuron pairs that shared common inputs, but did not affect the strength of monosynaptic interactions between neurons. These results suggest that the dorsal column nuclei can participate in persistent pain processes. Based on their anatomical connections, the dorsal column nuclei may contribute to thalamic changes during persistent pain as well as to supraspinal centers that modulate pain transmission in the spinal cord.