Abstract
The anterior cingulate cortex (ACC) modulates emotional responses to pain. Whereas,
the caudal ACC (cACC) promotes expression of pain affect, the rostral ACC (rACC) contributes
to its suppression. Both subdivisions receive glutamatergic innervation, and the present
study evaluated the contribution of N-methyl-d-aspartic acid (NMDA) receptors within these subdivisions to rats’ expression of pain
affect. Vocalizations that follow a brief noxious tail shock (vocalization afterdischarges,
VAD) are a validated rodent model of pain affect. The threshold current for eliciting
VAD was increased in a dose-dependent manner by injecting NMDA into the rACC, but
performance (latency, amplitude, and duration) at threshold was not altered. Alternately,
the threshold current for eliciting VAD was not altered following injection of NMDA
into the cACC, but its amplitude and duration at threshold were increased in a dose-dependent
manner. These effects were limited to Cg1 of the rACC and cACC, and blocked by pretreatment
of the ACC with the NMDA receptor antagonist d-2-amino-5-phosphonovalerate. These findings demonstrate that NMDA receptor agonism
within the cACC and rACC either increases or decreases emotional responses to noxious
stimulation, respectively.
Perspective
NMDA receptor activation of the rostral and caudal ACC respectively inhibited or enhanced
rats’ emotional response to pain. These findings mirror those obtained from human
neuroimaging studies; thereby, supporting the use of this model system in evaluating
the contribution of ACC to pain affect.
Key words
Abbreviations:
rACC (rostral anterior cingulate cortex), cACC (caudal anterior cingulate cortex), VAD (vocalization afterdischarge), VDS (vocalizations during shock), SMR (spinal motor reflex), NMDA (N-methyl-d-aspartate), AP-5 (d-2-amino-5-phosphonovalerate)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: June 12, 2019
Accepted:
June 2,
2019
Received in revised form:
May 22,
2019
Received:
April 5,
2017
Footnotes
This work was supported by the National Institutes of Health grant R01 NS045720.
Conflict of Interest: Authors report no conflicts of interest.
Identification
Copyright
© 2019 by United States Association for the Study of Pain, Inc.