Pain reduction by focal electrical stimulation of the brain: An anatomical and behavioral analysis

Mayer, David J.; Liebeskind, John C.

doi:10.1016/0006-8993(74)90534-4

Cited by 684 publications

(128 citation statements)

References 33 publications

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“…Alpha-2 adrenoceptor agonists have analgesic properties when given parenterally, epidurally or intrathecally. Descending noradrenergic antinociceptive systems originating in the brainstem contribute to pain control by suppressing the spinal centripetal transmission of nociceptive impulses [141,142]. These pathways are activated by stimulation of the locus coeruleus [143] and dorsal raphe nucleus [144] and analgesia may be mediated by noradrenaline release [145].…”

Section: Analgesiamentioning

confidence: 99%

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

Khan¹,

Ferguson²,

Jones³

1999

Anaesthesia

606

423

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SummaryClonidine has proved to be a clinically useful adjunct in clinical anaesthetic practice as well as in chronic pain therapy because it has both anaesthetic and analgesic-sparing activity. The more selective alpha-2 adrenoceptor agonists, dexmedetomidine and mivazerol, may also have a role in providing haemodynamic stability in patients who are at risk of peri-operative ischaemia. The side-effects of hypotension and bradycardia have limited the routine use of alpha-2 adrenoceptor agonists. Investigations into the molecular pharmacology of alpha-2 adrenoceptors have elucidated their role in the control of wakefulness, blood pressure and antinociception. We discuss the pharmacology of alpha-2 adrenoceptors and their therapeutic role in this review.

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Section: Analgesiamentioning

confidence: 99%

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

Khan¹,

Ferguson²,

Jones³

1999

Anaesthesia

606

423

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show abstract

“…A study by Mayer and Liebeskind (1974) showed that direct stimulation of the PAG eliminated responsiveness to various noxious stimuli such as electric shock, tissue destructive pinch, and radiant heat applied to the tail. In a later study, a significant reduction in the pain response to formalin injection with PAG stimulation was also observed (Dennis et al, 1980).…”

Section: Periaqueductal Greymentioning

confidence: 99%

Stress-induced analgesia

Butler

Finn

2009

Progress in Neurobiology

560

420

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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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“…Thus, it would be interesting to investigate whether sucrose has the same analgesic effects as saccharin and whether these effects would still be present when an experimental model based on a different mechanism mediating pain is used. In the present study we investigated the tail-flick response to noxious heat, which is probably a spinal reflex (10,11). The use of different models for measuring pain is important because the analgesic effects of saccharin and sucrose could be due to one or more mechanisms.…”

mentioning

confidence: 99%

Sucrose ingestion causes opioid analgesia

Segato

Castro-Souza

Segato

et al. 1997

Braz J Med Biol Res

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The intake of saccharin solutions for relatively long periods of time causes analgesia in rats, as measured in the hot-plate test, an experimental procedure involving supraspinal components. In order to investigate the effects of sweet substance intake on pain modulation using a different model, male albino Wistar rats weighing 180-200 g received either tap water or sucrose solutions (250 g/l) for 1 day or 14 days as their only source of liquid. Each rat consumed an average of 15.6 g sucrose/ day. Their tail withdrawal latencies in the tail-flick test (probably a spinal reflex) were measured immediately before and after this treatment. An analgesia index was calculated from the withdrawal latencies before and after treatment. The indexes (mean ± SEM, N = 12) for the groups receiving tap water for 1 day or 14 days, and sucrose solution for 1 day or 14 days were 0.09 ± 0.04, 0.10 ± 0.05, 0.15 ± 0.08 and 0.49 ± 0.07, respectively. One-way ANOVA indicated a significant difference (F (3, 47) = 9.521, P<0.001) and the Tukey multiple comparison test (P<0.05) showed that the analgesia index of the 14-day sucrose-treated animals differed from all other groups. Naloxone-treated rats (N = 7) receiving sucrose exhibited an analgesia index of 0.20 ± 0.10 while rats receiving only sucrose (N = 7) had an index of 0.68 ± 0.11 (t = 0.254, 10 degrees of freedom, P<0.03). This result indicates that the analgesic effect of sucrose depends on the time during which the solution is consumed and extends the analgesic effects of sweet substance intake, such as saccharin, to a model other than the hot-plate test, with similar results. Endogenous opioids may be involved in the central regulation of the sweet substance-produced analgesia.

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Pain reduction by focal electrical stimulation of the brain: An anatomical and behavioral analysis

Cited by 684 publications

References 33 publications

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

Stress-induced analgesia

Sucrose ingestion causes opioid analgesia

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