Stress-induced analgesia: Neural and hormonal determinants

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

doi:10.1016/0149-7634(80)90028-7

Cited by 345 publications

(90 citation statements)

References 124 publications

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“…The effects ofTyr-MIF-I are also similar to those of naloxone after warm-water swimming, a form of analgesia shown to be opiate-mediated (Bodnar et al, 1980;O'Connor & Chipkin, 1984). This once again demonstrates the ability of Tyr-MIF-I to affect behaviour in the same functional manner as the antiopiate naloxone.…”

Section: Discussionsupporting

confidence: 55%

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Tyr‐MIF‐1 attenuates antinociceptive responses induced by three models of stress‐analgesia

Galina

Kastin

1987

British J Pharmacology

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Tyr‐MIF‐1 (Tyr‐Pro‐Leu‐Gly‐NH2), a biologically active brain peptide, has previously been shown to antagonize the analgesia induced by morphine. In this report experiments are described in which mice were tested on the hot‐plate in three models of antinociception—shock, novel environment, and warm‐water swim—after the administration of various doses of Tyr‐MIF‐1 without any exogenous opiates. The peptide reduced the antinociception produced by all three methods of inducing endogenous antinociception. These results add further support for the existence of peptides like Tyr‐MIF‐1 that act as opiate antagonists.

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Section: Discussionsupporting

confidence: 55%

“…Warm-water swimming, the third stressor we used, induces an opiate form of antinociception (Bodnar et al, 1980;O'Connor & Chipkin, 1984 (10 x 25cm). …”

Section: Introductionmentioning

confidence: 99%

Tyr‐MIF‐1 attenuates antinociceptive responses induced by three models of stress‐analgesia

Galina

Kastin

1987

British J Pharmacology

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“…Analgesia induced by a mild stressor, such as a brief swim in lukewarm water, was described as mediated by the endogenous opioid system (Terman et al, 1986;Mogil et al, 1996). Alternatively, non-opioid pain inhibitory pathways are activated by more intense stress and involve neurotransmitter systems such as serotonin (Bodnar et al, 1980;Snow et al, 1982), glutamate (Marek et al, 1992), histamine (Hough et al, 1985;Robertson et al, 1988), and endocannabinoids (Hohmann et al, 2005). Interestingly, a collateral inhibition between opioid and non-opioid mechanisms was demonstrated, with both pathways being mutually antagonistic (Bodnar, 1990).…”

Section: Introductionmentioning

confidence: 99%

Dissociation of Analgesic and Hormonal Responses to Forced Swim Stress Using Opioid Receptor Knockout Mice

Contet

Gavériaux‐Ruff

Matifas

et al. 2005

Neuropsychopharmacol

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Exposure to stress triggers hormonal and behavioral responses. It has been shown that the endogenous opioid system plays a role in some physiological reactions to stress. The opioid system was described to mediate analgesia induced by mild stressors and to modulate the activation of the hypothalamic-pituitary-adrenal axis. Our study assessed the contribution of opioid receptors in stress-induced analgesia and adrenocorticotropic hormone (ACTH) and corticosterone release by a genetic approach. We performed a parallel analysis of mice deficient in mu, delta, or kappa opioid receptors, as well as of triple opioid receptor knockout mice, following exposure to a mild stress (3-min swim at 321C). In wild-type mice, stress elicited an increase in jumping latency on the hot plate, which was influenced by gender and genetic background. This analgesic response was reversed both by naloxone and by the triple mutation, and decreased in mu and delta opioid receptor knockout females. In wild-type females, stress also delayed front-and hindpaw behaviors in the hot plate test and increased tail-flick latency in the tail immersion test. Opioid receptor deletion however did not affect these stress responses. In addition, stress produced an increase in ACTH and corticosterone plasma levels. This endocrine response remained unchanged in all mutant strains. Therefore our data indicate that, under our stress conditions, the endogenous opioid system is recruited to produce some analgesia whereas it does not influence hypothalamic-pituitary-adrenal axis activity. This implies that brain circuits mediating analgesic and hormonal responses to stress can be dissociated.

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“…In particular, the principle function of receptors is to mediate responses to endogenous hormones and neurotransmitters, and drugs produce their effects in vivo in part by competing with these endogenous ligands. An example in the study of opioid antinociception would be that some stressors are thought to promote the release of endogenous, high efficacy opioids [12,13], and effects of exogenously administered drugs in stressed animals will be superimposed on a baseline of endogenous opioid effects. A competitive interaction between a drug and an endogenous ligand can be modeled using occupation theory [7,8], according to the equation:…”

Section: Tone Due To Endogenous Ligandsmentioning

confidence: 99%

Some implications of receptor theory for in vivo assessment of agonists, antagonists and inverse agonists

Negus

2006

Biochemical Pharmacology

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Drug effects can be classified into three major phenotypes: agonist, antagonist and inverse agonist. Agonist and inverse agonist effects are associated with receptor activation and inactivation, respectively, whereas antagonism implies that a drug produces no effect when administered alone but blocks the effects of agonists and inverse agonists. Attention has only recently begun to focus on the theoretical and clinical implications of inverse agonists, and studies of inverse agonism have also stimulated revisions in receptor theory. This commentary addresses two specific issues related to the application of receptor theory to studies of inverse agonists in vivo. First, principles of receptor theory suggest that increasing drug doses produce a graded pharmacological stimulus that is transduced by receptor-containing tissue into a biological response. However, assays vary in their ability to detect those responses, and any given assay provides only a narrow window on the full range of underlying drug effects. Consequently, in vivo assessment of inverse agonists will benefit from development of assays sensitive to graded inverse agonist effects. Second, detection of inverse agonist effects requires some preexisting level of receptor activity (or tone). This tone can result from at least two sources: (a) endogenous ligands for the receptor, or (b) constitutive receptor activity. Strategies for discriminating these two sources of tone will also contribute to the in vivo assessment of inverse agonist effects. Studies with intermediate efficacy ligands may be especially helpful in this regard, because their effects are differentially influenced by endogenous agonist tone versus constitutive receptor tone. KeywordsInverse agonist; Agonist; Antagonist; Receptor theory; In vivo; Constitutive activityThe terms "agonist", "antagonist", and most recently, "inverse agonist" have evolved to describe different profiles of drug effects. By convention, an agonist is considered to be a drug that activates receptors to produce a measurable effect in some assay. A full agonist produces a maximal effect under a given set of conditions, whereas a partial agonist produces a detectable but submaximal effect. Conversely, an inverse agonist produces an effect opposite to that of an agonist, and inverse agonists can also be "full" or "partial". An antagonist produces no effect on its own but blocks the effects of both agonists and inverse agonists. In the first study to demonstrate inverse agonist activity at a G-protein-coupled receptor (the delta opioid receptor), the delta opioid [D-Ala-2 -D-Leu-5 ]enkephalin increased GTPase activity in membranes from a cell line that expresses delta receptors (i.e. an agonist effect), whereas ICI174864 reduced GTPase activity below basal levels (i.e. an inverse agonist effect), and the effects of both drugs were blocked by MR2266 (an antagonist effect) [1].

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Stress-induced analgesia: Neural and hormonal determinants

Cited by 345 publications

References 124 publications

Tyr‐MIF‐1 attenuates antinociceptive responses induced by three models of stress‐analgesia

Tyr‐MIF‐1 attenuates antinociceptive responses induced by three models of stress‐analgesia

Dissociation of Analgesic and Hormonal Responses to Forced Swim Stress Using Opioid Receptor Knockout Mice

Some implications of receptor theory for in vivo assessment of agonists, antagonists and inverse agonists

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