Effect of Electrical Stimulation of the Central Amygdaloid Nucleus on the Nociceptive Neuron of the Cortex (SI) in the Cat.

Kawarada, Kei; Kamata, Kenichi; Matsumoto, Norio

doi:10.2170/jjphysiol.46.485

Cited by 5 publications

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“…The previous study has confirmed that brief electrical stimulation applied to the CeA evokes antinociception in the rat and cat. 54 Consequently we postulate that disinhibition in GABA CeA (caused by decreased level of D2 receptor) may facilitate analgesic (pain relief) and anxiolytic effects in incised mice. It seemed that analgesia might be mediated by decreased D2 receptor expressing and activation of CeA inhibitory neurons in the CeA in our study.…”

Section: Discussionmentioning

confidence: 97%

Dopamine receptor D2, but not D1, mediates the reward circuit from the ventral tegmental area to the central amygdala, which is involved in pain relief

et al. 2022

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Pain involves both sensory and affective dimensions. The amygdala is a key player in linking nociceptive stimuli to negative emotional behaviors or affective states. Relief of pain is rewarding and activates brain reward circuits. Whether the reward circuit from the ventral tegmental area (VTA) to the central amygdala (CeA) is involved in pain relief remains unexplored. Using a model of experimental postsurgical pain, we found that pain relief elicited conditioned place preference (CPP), activated CeA-projecting dopaminergic cells in the VTA, and decreased dopaminergic D2 receptor expression in the CeA. Activation of the VTA–CeA neural pathway using optogenetic approaches relieved incisional pain. Administration of a D2 receptor agonist reversed the pain relief elicited by light-induced activation of the VTA-CeA pathway. These findings indicate that the VTA-CeA circuit is involved in pain relief in mice via dopamine receptor D2 in the CeA.

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Section: Discussionmentioning

confidence: 97%

Dopamine receptor D2, but not D1, mediates the reward circuit from the ventral tegmental area to the central amygdala, which is involved in pain relief

et al. 2022

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“…An early study in guinea pigs showed that electrical stimulation of the amygdala may be algesic or analgesic, depending on the subregion stimulated (Lico et al, 1974). More recently, studies showed that electrical stimulation of the amygdala resulted in a reduction in nociception induced by formalin in rats (Mena et al, 1995) and a reduction in nociception during tooth pulp stimulation in cats (Kawarada et al, 1996). Electrical stimulation of the amygdala has also been demonstrated to enhance the startle reflex to an acoustic tone in rats (Rosen and Davis, 1990).…”

Section: Amygdalamentioning

confidence: 99%

Stress-Induced Analgesia

Tricklebank¹,

Curzon²

2013

Encyclopedia of Pain

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Abbreviations: SIA, stress-induced analgesia; FCA, fear-conditioned analgesia; GABA, Ȗ-aminobutyric acid; HA, high analgesia; LA, low analgesia; fMRI, functional magnetic resonance imaging; DNIC, diffuse noxious inhibitory control; PAG, periaqueductal grey; RVM, rostroventral medulla; 5-HT, 5-hydroxytryptamine; CB 1 , cannabinoid type 1; CB 2 , cannabinoid type 2; NMDA, N-methyl-D-aspartic acid; AMPA, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; mGluR, metabotropic glutamate receptor; NK1, neurokinin 1; SP, substance P; 2-AG, 2-arachidonoylglycerol; FAAH, fatty acid amide hydrolase; MGL, monoacylglycerol lipase; HPA, hypothalamo-pituitary-adrenal; ACTH, adrenocorticotropic hormone 3 ABSTRACT For over 30 years, scientists have been investigating the phenomenon of pain suppression upon exposure to unconditioned or conditioned stressful stimuli, commonly known as stress-induced analgesia. These studies have revealed that individual sensitivity to stressinduced analgesia can vary greatly and that this sensitivity is coupled to many different phenotypes including the degree of opioid sensitivity and startle response. Furthermore, stress-induced analgesia sensitivity can vary a great deal depending on age, gender, and prior experience to stressful, painful, or other environmental stimuli. Stress-induced analgesia is mediated by activation of the descending inhibitory pain pathway.Pharmacological and neurochemical studies have demonstrated involvement of a large number of neurotransmitters and neuropeptides. In particular, there are key roles for the HQGRJHQRXV RSLRLG PRQRDPLQH FDQQDELQRLG Ȗ-aminobutyric acid and glutamate systems. The study of stress-induced analgesia has enhanced our understanding of the fundamental physiology of pain and stress and has been a useful approach for uncovering new therapeutic targets for the treatment of pain and stress-related disorders.4

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“…The present report is the first to offer electrophysiological evidence that the amygdala exerts profound inhibition on nociception. A brief preliminary report of these findings has been presented previously [10].…”

mentioning

confidence: 91%

Effects of Conditioning Stimulation of the Central Amygdaloid Nucleus on Tooth Pulp-Driven Neurons in the Cat Somatosensory Cortex(SI).

Kawarada

Kamata²,

Matsumoto³

1999

JJP

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The sensation we call pain, like other sensations, can be modulated by exposure to a stressful situation such as a fight or athletic competition. It has been suggested that stress is a physiologic trigger of the intrinsic pain inhibitory system. This phenomenon has been termed as stress-induced analgesia (SIA) (see Amit and Galina [1] for review) or fear-induced analgesia [2]. Actually, acupuncture and transcutaneous electrical nerve stimulation, which might be considered stressful, have been used for analgesia as a clinical procedure [1]. However, the neuronal mechanism and anatomical substrates involved in SIA have remained unclear.It has been demonstrated that the central amygdaloid nucleus (ACE) has an integrative role for coordinating an organism's autonomic, endocrine, and behavioral responses to various stressful stimuli, and that electrical stimulation of the ACE can mimic several of the stress-like responses (see Glavin et al. [3] for review). Lesions of the ACE have been found to block cardiovascular, respiratory, and behavioral parameters of responses to stressors [4,5]. Intracere- Japanese Journal of Physiology, 49, 485-497, 1999 Key words: central amygdaloid nucleus, stress-induced antinociception, somatosensory cortex, tooth pulp-driven neuron, H 1 receptor. Abstract:To study the limbic control of nociception, we examined the effect of conditioning stimulation of the central amygdaloid nucleus (ACE) on tooth pulp-driven (TPD) neurons in the first somatosensory cortex (SI). Cats were anesthetized with N 2 O-O 2 (2 : 1) and 0.5% halothane, and immobilized with tubocurarine chloride. The tooth pulp test stimulus was applied by a single rectangular pulse (0.5 ms in duration and 3-5 times the threshold intensity for the jaw-opening reflex). Conditioning stimuli to the ACE consisted of trains of 33 pulses (300 A) delivered at 330 Hz at intervals of 8-10 s. In 35 out of 61 of the slow (S)-type TPD neurons with latencies of more than 20 ms, conditioning stimulation in the ACE, especially in the medial division, markedly reduced the firing response to the pulpal stimulation. The inhibition of the firing rate in the S-type neurons was 74% of the control. In these S-type neurons, the neurons that were inhibited had significantly longer latencies compared to the noninhibited neurons (45.0Ϯ17.6 ms, nϭ32 vs. 34.8Ϯ10.5 ms, nϭ26). In contrast, the ACE conditioning stimulation affected only one out of 18 fast-type TPD neurons with latencies of less than 20 ms. In addition, ACE stimulation had no effect on the spontaneous discharges of either S-type or F-type neurons. The ACE inhibitory effect on S-type neurons was not diminished by naloxone administration (1 mg/kg, I.V.), while the blockade of histamine H 1 -receptor by diphenhydramine hydrochloride (0.5 mg/kg, I.V.) partially reversed the inhibitory effect. These results suggest that the ACE inhibits ascending nociceptive information to the SI and that this inhibition is mediated in part by histamine (H 1 ) receptors. It seems likely that the antinociceptive ...

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Effect of Electrical Stimulation of the Central Amygdaloid Nucleus on the Nociceptive Neuron of the Cortex (SI) in the Cat.

Cited by 5 publications

References 0 publications

Dopamine receptor D2, but not D1, mediates the reward circuit from the ventral tegmental area to the central amygdala, which is involved in pain relief

Dopamine receptor D2, but not D1, mediates the reward circuit from the ventral tegmental area to the central amygdala, which is involved in pain relief

Stress-Induced Analgesia

Effects of Conditioning Stimulation of the Central Amygdaloid Nucleus on Tooth Pulp-Driven Neurons in the Cat Somatosensory Cortex(SI).

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