Prolonged membrane potential depolarization in cingulate pyramidal cells after digit amputation in adult rats
<p>Abstract</p> <p>The anterior cingulate cortex (ACC) plays an important role in higher brain functions including learning, memory, and persistent pain. Long-term potentiation of excitatory synaptic transmission has been observed in the ACC after digit amputation, which might cont...
Saved in:
Main Authors: | , , , |
---|---|
Format: | Book |
Published: |
SAGE Publishing,
2005-08-01T00:00:00Z.
|
Subjects: | |
Online Access: | Connect to this object online. |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | <p>Abstract</p> <p>The anterior cingulate cortex (ACC) plays an important role in higher brain functions including learning, memory, and persistent pain. Long-term potentiation of excitatory synaptic transmission has been observed in the ACC after digit amputation, which might contribute to plastic changes associated with the phantom pain. Here we report a long-lasting membrane potential depolarization in ACC neurons of adult rats after digit amputation <it>in vivo</it>. Shortly after digit amputation of the hind paw, the membrane potential of intracellularly recorded ACC neurons quickly depolarized from ~-70 mV to ~-15 mV and then slowly repolarized. The duration of this amputation-induced depolarization was about 40 min. Intracellular staining revealed that these neurons were pyramidal neurons in the ACC. The depolarization is activity-dependent, since peripheral application of lidocaine significantly reduced it. Furthermore, the depolarization was significantly reduced by a NMDA receptor antagonist MK-801. Our results provide direct <it>in vivo </it>electrophysiological evidence that ACC pyramidal cells undergo rapid and prolonged depolarization after digit amputation, and the amputation-induced depolarization in ACC neurons might be associated with the synaptic mechanisms for phantom pain.</p> |
---|---|
Item Description: | 10.1186/1744-8069-1-23 1744-8069 |