Analgesia from rostral brain stem stimulation in the rat

Rhodes, Dell L.; Liebeskind, John C.

doi:10.1016/0006-8993(78)90362-1

“…An efferent anti-nociceptive projection of the meso-diencephalic junction to the spinal cord was also suggested to play a role during stimulation-produced analgesia (Peschanski and Mantyh, 1983). Rhodes and Liebeskind (1978) also demonstrated that stimulation of the pretectal region of the meso-diencephalic junction of the brainstem produced a potent analgesic effect in the tail-flick, pinch, and hot-plate tests. The hypothalamus can relay information to the PAG or the rostroventral medulla (RVM), both of which play a pivotal role in the modulation of nociception (Aimone et al, 1988;Behbehani et al, 1988;Cechetto and Saper, 1988).…”

Section: Brainstemmentioning

confidence: 96%

Stress-induced analgesia

Butler

¹

,

Finn

²

2009

Progress in Neurobiology

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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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“…In both hypothalamus and thalamus, electrical stimulation of regions near the midline causes analgesia (Rhodes & Liebeskind, 1978). So does stimulation of the substantia nigra, and this analgesia too MORPHINE AND 5-HT IN THE RAT 407 was shown to be abolished by methysergide or p-CPA (Sandberg & Segal, 1978).…”

mentioning

confidence: 99%

Mapping, in the rat central nervous system, of morphine‐induced changes in turnover of 5‐hydroxytryptamine.

Snelgar¹,

Vogt²

1981

The Journal of Physiology

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SUMMARY1. It is known that the full clinical effect of morphine is not seen if those neurones of the central nervous system which contain 5-hydroxytryptamine (5-HT) have been inactivated. Morphine increases 5-HT turnover in brain and cord, and the present work is an attempt at mapping the sites at which turnover is accelerated.2. The degree of interaction at various sites of the C.N.S. was measured by the increment in the content of 5-hydroxyindol-3-yl acetic acid (5-HIAA) elicited by morphine in rats pre-treated with probenecid. The effect was produced by as little as 3-5 mg morphine hydrochloride/kg; for the sake of convenience this dose was doubled in most experiments. Pre-treatment with probenecid was not necessary for the effect, but a minimum interval of 90 min between injection of morphine and analysis of the brain was essential.3. Morphine did not act indiscriminately on all 5-HT neurones, as seen by the fact that the increment in 5-HIAA formation was independent of the density of 5-HT neurones in the tissue. Nor was there any relation between basal 5-HT turnover of a region and the size of its response to morphine.4. Highly reactive sites were found in dorsal cord, medulla, superior colliculi, substantia nigra, thalamus, hypothalamus, amygdala and striatum. Cortical areas were less responsive, but with large differences among themselves. Hippocampus, central grey, olfactory bulb, cerebellum and white matter had lower or negligible increases in 5-HT turnover. There was no increase in the turnover of the (non-neural) 5-HT of the pineal gland.5. The relation of the reactive sites to their content in endogenous opioids and to the probable localization of the pharmacological actions of morphine is discussed.

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“…Direct stimulation of the posterior hypothalamus produced a potent analgesic effect in the tail flick, pinch, and hot plate tests in an early study conducted by Rhodes and Liebeskind (1978) suggesting a role of the hypothalamus in the descending inhibitory pain pathway.…”

Section: Hypothalamusmentioning

confidence: 97%

Stress-Induced Analgesia

Tricklebank¹,

Curzon²

2013

Encyclopedia of Pain

8

0

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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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Analgesia from rostral brain stem stimulation in the rat

Cited by 191 publications

References 35 publications

Stress-induced analgesia

Stress-induced analgesia

Mapping, in the rat central nervous system, of morphine‐induced changes in turnover of 5‐hydroxytryptamine.

Stress-Induced Analgesia

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