Microinjection of arginine vasopressin into the central nucleus of amygdala suppressed nociceptive jaw opening reflex in freely moving rats

doi:10.1016/S0361-9230(01)00493-2

Brain Research Bulletin

Volume 55, Issue 1, 1 May 2001, Pages 117-121

https://doi.org/10.1016/S0361-9230(01)00493-2 Get rights and content

Abstract

This study was performed to examine the antinociceptive effect after microinjection of arginine vasopressin (AVP) into the central nucleus of amygdala. We recorded the jaw opening reflex in freely moving rats. After injection of 0.2 or 0.4 nM AVP into the central nucleus of amygdala, digastric electromyogram (dEMG) was suppressed to 55 ± 5% or 88 ± 3 of the control. Artificial cerebrospinal fluid had no effects on the basal dEMG activity. V₁ vasopressin receptor antagonist blocked the suppressive effect produced by microinjection of 0.4 nM AVP from 53 ± 3 to 81 ± 3% of the control. However, V₂ vasopressin receptor antagonist did not affect changes in dEMG. We observed dEMG activity after intracerebroventricular injection of naloxone, methysergide, or phentolamine. All drugs did not affect the basal dEMG activity at our dose. Naloxone blocked the suppressive effect of 0.4 nM AVP from 42 ± 4 to 79 ± 5% of the control. Methysergide also inhibited the suppression of dEMG from 44 ± 3 to 83 ± 6% of the control. However, phentolamine, an α-adrenergic receptor antagonist, did not affect the suppression of dEMG. These results indicate AVP in the central nucleus of amygdala has potent analgesic effects in the orofacial area. The antinociception of central AVP seems to be mediated by opioid and serotonergic pathways.

Introduction

The neuropeptide, arginine-vasopressin (AVP), is synthesized and transported from the supraoptic (SON) and paraventricular (PVN) nucleus of the hypothalamus and acts as a peripheral hormone to control the body fluid balance. AVP is released synaptically in the lateral septum, hippocampus, amygdala, habenula and several other brain structures [10] and involved in the memory process [22], cardiovascular regulation [30], thermoregulation [6] and motor behavior [33]. The several data suggest that the central AVP is also involved in the processing of pain transmission. AVP-containing fibers are found in several brain sites important as a pain modulator area [27]. Actually, antinociception was produced by intrathecal [34] intracerebroventricular [8], or systemic [34] administration of AVP. Noxious stimuli can increase synthesis of AVP in the hypothalamus [15] and its release into the plasma [28]. These results indicate that the central AVP released by stress seems to be involved in the regulation of the processing nociceptive information.

Amygdala has been shown in both human and animal studies as an important region regulating emotional response, such as anxiety or fear 18, 36. It has been also demonstrated that amygdala has a critical role on the conditional hypoalgesia with formalin tests [25] and tail-flick test 16, 26. Recent studies conducted in our laboratory 4, 5 have shown that microinjection of carbachol, cholinergic agonist, and glutamate, excitatory amino acid, suppressed nociceptive jaw opening reflex in freely moving rats. These results suggest that the amygdala seems to be involved in the pain modulation of the orofacial area.

A number of previous studies have shown that the central nucleus of amygdala has specific target regions for AVP to exert its physiological actions. Autoradiographic studies showed a specific AVP binding in the amygdala 9, 13. AVP-sensitive and AVP-containing neurons were found in the amygdala [12]. These data suggest that the central AVP may be involved in amygdala-related functions through the vasopressinergic neuron. Much work, however, has been done to elucidate the mechanism of analgesic action of the central AVP in the amygdala, but limited data is available concerning mechanisms of antinociceptive action of AVP in the orofacial area.

This study was designed to investigate the antinociceptive effect of AVP on the central nucleus of amygdala. To achieve this purpose, we monitored nociceptive jaw opening reflex after administration of AVP into the central nucleus of amygdala in freely moving rats. We also investigated the mechanisms of antinociception produced by microinjection of AVP into the central nucleus of amygdala.

Section snippets

Materials and methods

Experiments were carried out in 35 male Sprague-Dawley rats weighing 350–400 g and surgical procedures were performed under pentobarbital sodium (40 mg/kg, intraperitoneal). All procedures involving the use of animals were approved by Institutional Care and Use Committee of School of Dentistry, Kyungpook National University and carried out in accordance with the ethics guideline for investigation of experimental pain in conscious animals of IASP. Anesthetized rats were mounted on a stereotaxic

Results

The present study showed that administration of AVP into the central nucleus of amygdala suppressed dEMG in response to noxious electrical stimulation of the incisor (Fig. 1). aCSF had no effects on the dEMG respond to noxious electrical stimulation of the incisor. After injection of 0.2 or 0.4 nM AVP into the central nucleus of amygdala, dEMG was suppressed to 55 ± 5 or 88 ± 3% of the control, respectively. The suppression of dEMG produced by 0.4 nM AVP was maintained for 30 min and recovered

Discussion

The amygdala is a complex structure in the limbic system and one of the nuclei to control the regulating emotional response such as anxiety or fear 18, 36. There was strong evidence for the role of amygdala on antinociceptive response. The amygdaloid complex contains high levels of opiate receptors and enkephalin, which produce antinociception in the central nervous system [23] and has direct afferent connections with the periaqueductal gray (PAG), nucleus raphe magus (NRM), and locus coeruleus

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Microinjection of arginine vasopressin into the central nucleus of amygdala suppressed nociceptive jaw opening reflex in freely moving rats

Abstract

Introduction

Section snippets

Materials and methods

Results

Discussion

Neurosci. Lett.

Prog. Neuropsychopharmacol. Biol. Psychiatry

Brain Res. Bull.

Neurosci. Lett.

Neurosci. Res.

Brain Res.

Brain Res.

Brain Res.

Brain Res.

Pain

Neuroscience

Brain Res.

Peptides

Brain Res.

Brain Res.

Nucleus tractus solitarius-induced suppression of the jaw opening reflex and a possible interrelationship between antinociceptive and cardiovascular responses

J. Oral Biol.

Intracisternal antidepressants suppressed the nociceptive jaw opening reflex in freely moving rats

Kor. J. Physiol. Pharmacol.

Microinjection of glutamate into the amygdala modulates nociceptive and cardiovascular response in freely moving rats

Kor. J. Physiol. Pharmacol.