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J Physiol. 2001 May 1;532(Pt 3):823-33.

Potentiation of sensory responses in the anterior cingulate cortex following digit amputation in the anaesthetised rat.

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Department of Anesthesiology, Washington University Pain Center, Washington University School of Medicine, St Louis, MO 63110, USA.


The anterior cingulate cortex (ACC) is important for processing different types of information, including sensory inputs. In the present study on anaesthetised rats, we recorded in vivo sensory responses of the ACC to peripheral electrical shocks. Peripheral electrical stimulation at high intensities sufficient to activate nociceptive sensory fibres elicited EPSPs within the ACC. Digit amputation caused long-lasting potentiation of ACC responses to peripheral electrical stimulation. Evoked field EPSPs remained enhanced for at least 120 min after the amputation. Because electrical shocks were delivered to the normal hindpaw, it is likely that plastic changes occur centrally in the spinal cord or the supraspinal structures following amputation. We also recorded field EPSPs of the ACC in response to focal cortical stimulation within the ACC. Like the sensory responses, field EPSPs produced by focal cortical stimulation within the ACC were potentiated after digit amputation, suggesting that long-lasting changes occurred locally within the ACC. Local blockade of peripheral activity by QX-314 at the amputated hindpaw 120 min after amputation did not significantly affect sensory responses induced within the ACC. Thus, peripheral ongoing inputs do not play an important role in maintaining potentiation within the ACC. Two pulses of hindpaw stimulation caused paired-pulse depression in the ACC. Local stimulation within the ACC also caused depression of sensory responses to hindpaw stimulation, suggesting that the population of synapses activated by local stimulation may overlap with that activated by peripheral hindpaw stimulation. Our results suggest that rapid enhancement of sensory responses can be observed in the ACC after amputation and that enhanced neuronal responses to subsequent somatosensory stimuli may contribute to phantom-limb pain.

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