Korean J Physiol Pharmacol.
1998 Dec;2(6):687-693.
Microinjection of glutamate into the amygdala modulates nociceptive and cardiovascular response in freely moving rats
- Affiliations
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- 1Department of Oral Physiology, School of Medicine, Kyungpook Dentistry National University, Taegu 700-422, Korea.
- 2Department of Physiology, School National of Medicine, Kyungpook University, Taegu 700-422, Korea.
Abstract
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This study was performed to examine the mean arterial pressure and
nociceptive jaw opening reflex after microinjection of glutamate into
the amygdala in freely moving rats, and to investigate the mechanisms
of antinociceptive action of amygdala. Animals were anesthetized with
pentobarbital sodium (40 mg/kg, ip). A stainless steel guide cannula
(26 gauge) was implanted in the amygdala and lateral ventricle.
Stimulating and recording electrodes were implanted into each of 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. After 48 hours of recovery from surgery,
mean arterial pressure and digastric electromyogram (dEMG) were
monitored in freely moving rats. Electrical shocks (200 musec duration,
0.5~2 mA intensity) were delivered at 0.5 Hz to the dental pulp
every 2 minutes. After injection of 0.35 M glutamate into the amygdala,
mean arterial pressure was increased by 8+/-2 mmHg and dEMG was
suppressed to 71+/-5% of the control. Injection of 0.7 M glutamate
elevated mean arterial pressure by 25+/-5 mmHg and suppressed dEMG to
20+/-7% of the control. The suppression of dEMG were maintained for 30
minutes. Naloxone, an opioid receptor antagonist, inhibited the
suppression of dEMG elicited by amygdaloid injection of glutamate from
28+/-4 to 68+/-5% of the control. Methysergide, a serotonin receptor
antagonist, also inhibited the suppression of dEMG from 33+/-5 to 79+/-4%
of the control. However, phentolamine, an alpha-adrenergic receptor
antagonist, did not affect the suppression of dEMG. These results
suggest that the amygdala can modulate both cardiovascular and
nociceptive responses and that the antinociception of amygdala seems to
be attributed to an augmentation of descending inhibitory influences on
nociceptive pathways via serotonergic and opioid pathways.