Korean J Physiol Pharmacol.
1998 Jun;2(3):307-312.
Intracisternal antidepressants suppressed the nociceptive jaw opening
reflex in freely moving rats
- Affiliations
-
- 1Department of Oral Physiology, School of Dentistry, Kyungpook National University, Taegu 700-422, Korea.
Abstract
-
This study was performed to investigate the mechanism of central
analgesic effects of antidepressants. Thirty four male rats were
anesthetized with pentobarbital sodium (40 mg/kg, ip). A stainless
steel guide cannula and a PE tube (PE10) were implanted into the
lateral ventricle and cisterna magna area. Stimulating and recording
electrodes were implanted into the incisor pulp and anterior digastric
muscle. Electrodes were led subcutaneously to the miniature cranial
connector sealed on the top of the skull with acrylic resin. The jaw
opening reflex was used in freely moving rats, and antidepressants were
administered intracisternally in order to eliminate the effects of
anesthetic agents on the pain assessment and evaluate the importance of
the central action site of antidepressants. After 48 hours of recovery
from surgery, digastric electromyogram (dEMG) of freely moving rats was
recorded. Electrical shocks (200 musec duration, 0.5-2 mA intensity)
were delivered at 0.5 Hz to the dental pulp every 2 minute.
Intracisternal administration of 15 microgram imipramine suppressed dEMG
elicited by noxious electrical stimulation in the tooth pulp to 76+/-6%
of the control. Intracisternal administration of 30 jig desipramine,
nortriptyline, or imipramine suppressed dEMG remarkably to 48 +/- 2, 27
+/- 8, or 25 +/- 5% of the control, respectively. Naloxone, methysergide,
and phentolamine blocked the suppression of dEMG produced by
intracisternal antidepressants from 23+/-2 to 69+/-4%, from 32+/-5 to
80+/-9%, and from 24+/-6 to 77+/-5% of the control, respectively. These
results
indicate that antidepressants produce antinociception through
central mechanisms in the orofacial area. Antinociception of
intracisternal antidepressants seems to be mediated by an augmentation
of descending pain inhibitory influences on nociceptive pathways.