Korean J Physiol Pharmacol.
2001 Jun;5(3):213-221.
Dual effect of dynorphin A on single-unit spike potentials in rat trigeminal nucleus
- Affiliations
-
- 1Department of Physiology, School of Medicine, Kyungpook National University, Daegu, South Korea. jaespark@knu.ac.kr
Abstract
- The amygdala is known as a site for inducing analgesia, but its
action on the trigeminal nucleus has not been known well. Little
information is available on the effect of dynorphin on NMDA
receptor-mediated electrophysiological events in the trigeminal nucleus.
The purpose of this study was to investigate the changes in the single
neuron spikes at the trigeminal nucleus caused by the amygdala and the
action of dynorphin on the trigeminal nucleus. In the present study,
extracellular single unit recordings were made in the dorsal horn of the
medulla (trigeminal nucleus caudalis) and the effects of
microiontophoretically applied compounds were examined. When (D-Ala2,
N-Me-Phe4, Glys5-ol)enkephalin (DAMGO, 10-25 mM), a mu-opioid receptor
agonist, was infused into the amygdala, the number of NMDA-evoked spikes
at the trigeminal nucleus decreased. However, the application of naloxone
into the trigeminal nucleus while DAMGO being infused into the amygdala
increased the number of spikes. Low dose (1 mM) of dynorphin in the
trigeminal nucleus produced a significant decrease in NMDA-evoked spikes
of the trigeminal nucleus but the NMDA-evoked responses were facilitated
by a high dose (5 mM) of dynorphin. After the kappa receptors were
blocked with naloxone, dynorphin induced hyperalgesia. After the NMDA
receptors were blocked with AP5, dynorphin induced analgesia. In
conclusion
, dynorphin A exerted dose-dependent dual effects (increased &
decreased spike activity) on NMDA-evoked spikes in the trigeminal
nucleus. The inhibitory effect of the dynorphin at a low concentration
was due to the activation of kappa receptors and the excitatory effect at
a high concentration was due to activation of NMDA receptors in the
trigeminal neurons.