Analgesia induced by cold-water stress: Attenuation following hypophysectomy

Bodnar, Richard J.; Glusman, Murray; Brutus, Martin; Spiaggia, Angela; Kelly, Dennis D.

doi:10.1016/0031-9384(79)90122-7

Cited by 129 publications

(30 citation statements)

References 38 publications

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“…The HPA axis has also been shown to play a role in the mediation of SIA (Filaretov et al, 1996) -a concept that was briefly discussed in section 4.1.5. The first study to investigate the role of the HPA axis in SIA showed that hypophysectomized rats did not express cold-water swim SIA (Bodnar et al, 1979). In another study, rats which had received chronic treatment of metyrapone, a drug known to increase levels of ACTH, expressed potentiated SIA in the tail flick and hot plate tests following cold-water swim (Mousa et al, 1981).…”

Section: The Role Of the Hypothalamo-pituitary-adrenal Axis In Siamentioning

confidence: 99%

“…Hemorrhagic shock (Helmstetter and Fanselow, 1987) (Fukuda et al, 2001) Radiant heat Footshocks (US) (Akil et al, 1976;Madden et al, 1977) Re-exposure to context associated with footshocks (CS) (Chance et al, 1978;Hayes et al, 1978) Continuous cold swim (US) (Bodnar et al, 1978a;Bodnar et al, 1978b) Intermittent cold swim (US) (Bodnar et al, 1979) Intraperitoneal injection of hypertonic saline (US) (Wright and Lincoln, 1985) Food restriction (US) (Wideman et al, 1996) Nitroglycerin Restraint stress (US) (Costa et al, 2005) Mouse Formalin/Formic acid Footshocks (US) (Chesher and Chan, 1977) Radiant heat Elevated plus maze (US) (Lee and Rodgers, 1990) Exposure to predators (US) (Kavaliers, 1988) Social isolation (US) (Puglisi-Allegra and Oliverio, 1983) Defeat experience (US) (Rodgers and Randall, 1987) Predator odor (US) (Kavaliers et al, 1997) Tail pinch Communication box (US) (Takahashi et al, 1987) Insect bites Social learning of fear to biting insects (CS) (Kavaliers et al, 2001) Attack by intruders Social conflict (US) …”

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confidence: 99%

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Stress-induced analgesia

Butler

Finn

2009

Progress in Neurobiology

543

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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Section: The Role Of the Hypothalamo-pituitary-adrenal Axis In Siamentioning

confidence: 99%

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confidence: 99%

Stress-induced analgesia

Butler

Finn

2009

Progress in Neurobiology

543

420

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“…Second, although the opiate antagonist naloxone elimi nates opiate analgesia at low doses [17], it only partially attenuates cold-water swim analgesia at high doses [6]. Third, removal of the pituitary gland in rats attenuates cold-water swim analgesia [2] while potentiating the anal gesic response to morphine [5]. It seems plausible that the deficit in cold-water swim analgesia induced by MSG may be caused by damage to the medial-basal hypothalamus which in turn might interrupt the appropriate neural or hormonal signals from the brain to the pituitary respon sible for the formation of the analgesic response to coldwater swims.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Monosodium Glutamate

Bodnar¹,

Abrams²,

Zimmerman³

et al. 1980

Neuroendocrinology

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Neonatal administration of monosodium glutamate (MSG) produces neurotoxic degeneration of the retina and medial-basal hypothalamus, including the arcuate nucleus. Since this hypothalamic area contains the only neuronal cell bodies in brain which contain adrenocorticotrophic hormone (ACTH) and β-lipotropin (β-LPH) and β-endorphin, destruction of these cells by MSG may interfere with pain responses mediated by nerve fibers arising from these perikarya. The present study examined whether MSG-treated rats, as compared to Iittermate controls, exhibited concomitant changes in the immunocytochemical distribution of ACTH and β-LPH, and their reactivity to several analgesia-inducing manipulations. Although MSG-treated rats did not differ from control rats in their baseline reactivity to electric shock, they displayed an inability to exhibit analgesia following acute exposure to cold-water swim stress. In addition, MSG-treated rats showed an attenuated analgesic response following morphine administration. However, the analgesia elicited by either abrupt food deprivation, or the glucoprivic stress of 2-deoxy-Z)-glucose, was unaffected by neonatal MSG treatment. Concomitant with these selective analgesic deficits, MSG-treated rats displayed a marked immunocytochemical reduction in ACTH/β-LPH perikarya and terminals in brain, but not pituitary. These data indicate that multiple pain-inhibitory systems exist, and that some rely upon an intact medial-basal hypothalamus to produce analgesia.

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“…tolerance to morphine [1,2,4,7,13,21]; on the other hand, hypophysectomy abolishes stress-induced analgesia [6,14] while enhancing morphine-induced analgesia [11,18]. The present study addresses two related questions -whether pi tuitary levels of immunoreactive cor relate with the analgesic responses elicited by prolonged foot-shock, and whether corticosteroids may have a differ ential effect on prolonged foot-shock analgesia and mor phine-induced analgesia, given their postulated critical role in opioid mediated forms of stress-indiced analgesia [16].…”

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Prolonged Foot-Shock Induced Analgesia: Glucocorticoids and Non-Pituitary Opioids Are Involved

1983

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In rats, the analgesic response induced by prolonged intermittent foot-shock is abolished by naloxone or adrenalectomy, and is restored in adrenalectomized animals by the administration of dexamethasone or corticosterone, but not deoxycorticosterone. Levels of immunoreactive β-endorphin in the anterior pituitary are significantly elevated by adrenalectomy alone, and further by dexamethasone and corticosterone; in contrast, immunoreactive β-endorphin levels in the neuro-intermediate lobe are raised by deoxycorticosterone. These findings suggest that analgesic responses produced by prolonged intermittent foot-shock involve both the pituitary-adrenal axis and endogenous, non-pituitary opioids.

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Analgesia induced by cold-water stress: Attenuation following hypophysectomy

Cited by 129 publications

References 38 publications

Stress-induced analgesia

Stress-induced analgesia

Neonatal Monosodium Glutamate

Prolonged Foot-Shock Induced Analgesia: Glucocorticoids and Non-Pituitary Opioids Are Involved

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