Journal of neurophysiology
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Pain can involuntarily capture attention and disrupt pain-unrelated cognitive activities. The brain mechanisms of these effects were explored by laser- and visual-evoked potentials. Consecutive nociceptive laser stimuli and visual stimuli were delivered in pairs. ⋯ The data confirm that nociceptive processing competes with pain-unrelated cognitive activities for attentional resources and that concomitant nociceptive events affect behavior by depressing attention allocation to ongoing cognitive processing. The laser-evoked potential magnitude reflected the engagement of attention to the novel nociceptive stimuli. We conclude that the laser-evoked potentials index the activity of a neural system involved in the detection of novel salient stimuli in order to focus attention and prioritize action to potentially damaging dangers.
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Tissue injury in early life can produce distinctive effects on pain processing, but little is known about the underlying neural mechanisms. Neonatal inflammation modulates excitatory synapses in spinal nociceptive circuits, but it is unclear whether this results directly from altered afferent input. Here we investigate excitatory and inhibitory synaptic transmission in the rat superficial dorsal horn following neonatal hindlimb surgical incision using in vitro patch-clamp recordings and test the effect of blocking peripheral nerve activity on the injury-evoked changes. ⋯ Prolonged blockade of primary afferent input from the time of injury was achieved by administration of bupivacaine hydroxide or tetrodotoxin to the sciatic nerve at P3. The increase in mEPSC frequency evoked by P3 incision was prevented by blocking sciatic nerve activity. These results demonstrate that increased afferent input associated with peripheral tissue injury selectively modulates excitatory synaptic drive onto developing spinal sensory neurons and that the enhanced glutamatergic signaling in the dorsal horn following neonatal surgical incision is activity dependent.