NMDA receptor-independent synaptic plasticity in the central amygdala in the rat model of neuropathic pain

Ryo Ikeda, Yukari Takahashi, Kazuhide Inoue, Fusao Kato

Research output: Contribution to journalArticlepeer-review

192 Citations (Scopus)


Neurons in the latero-capsular part of the central nucleus of the amygdala (CeA), a region now called the "nociceptive amygdala", receive predominantly nociceptive information from the dorsal horn through afferent pathways relayed at the nucleus parabrachialis (PB). Excitatory synaptic transmission between the PB afferents and these neurons is reported to become potentiated within a few hours of the establishment of arthritic or visceral pain, making it a possible mechanism linking chronic pain and unpleasant negative emotional experiences. However, it remains unknown whether such synaptic potentiation is consolidated or becomes adaptively extinct in the longer-lasting form of chronic pain, such as neuropathic pain, an as yet serious and frequent type of pain of important clinical concern. To address this issue, we recorded postsynaptic currents in CeA neurons evoked by PB tract stimulation in acute brain slices from young rats with neuropathic pain, as evaluated by tactile allodynic responses, following unilateral spinal nerve ligature made 1 week earlier. CeA neurons contralateral to the nerve ligation showed significantly larger-amplitude postsynaptic currents than those in the ipsilateral CeA and sham- and non-operated groups. The degree of synaptic potentiation, as compared between two sides, was positively correlated to that of tactile allodynia responses. In addition, blockade of NMDA receptors did not affect this potentiation. We conclude that potentiation of the PB-CeA synapse is consolidated in long-lasting neuropathic pain but that this potentiation results from a molecular mechanism distinct from that in arthritic and visceral pain.

Original languageEnglish
Pages (from-to)161-172
Number of pages12
Issue number1-2
Publication statusPublished - Jan 2007
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology
  • Anesthesiology and Pain Medicine


Dive into the research topics of 'NMDA receptor-independent synaptic plasticity in the central amygdala in the rat model of neuropathic pain'. Together they form a unique fingerprint.

Cite this