The role of endorphins in stress: Evidence and speculations

Amir, Shimon; Brown, Zavie W.; Amit, Zalman

doi:10.1016/0149-7634(80)90027-5

Cited by 348 publications

(66 citation statements)

References 202 publications

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“…Furthermore, the amygdala, which is thought to participate in some forms of stress-induced analgesia (Bellgowan and Helmstetter, 1996), may send some SP-containing afferents to the PAG (Gray and Magnuson, 1992). In addition, restraint stress not only produces SP release in brain areas that include the PAG (Bannon et al, 1983;Rosen et al, 1992;Culman and Unger, 1995;Hahn and Bannon, 1999), it also produces an opioid-dependent analgesia (Amir et al, 1980) and modifies PAG tissue SP content (Rosen et al, 1992). SP in the dorsal raphe is also known to modulate flight behavior in response and unconditioned fear stimulus (Mongeau et al, 1998).…”

Section: Conditions That May Engage Sp Neurotransmission In the Pag Amentioning

confidence: 98%

Cellular basis for the effects of substance P in the periaqueductal gray and dorsal raphe nucleus

Commons

Valentino

2002

J of Comparative Neurology

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Substance P (SP) is known to act at supraspinal sites to influence pain sensitivity as well as to promote anxiety. The effects of SP could be mediated in part by actions in the periaqueductal gray (PAG) and the dorsal raphe nucleus (DRN), adjoining mesencephalic cell groups that are strategically positioned to influence both nociception and mood. Previous studies have indicated that SP regulates both enkephalin and serotonin neurotransmission in these brain regions. To determine the mechanism underlying the effects of SP in the PAG and DRN, the distribution of the principal receptor for SP, the neurokinin 1 (NK1) receptor, was examined with respect to other neurotransmitter markers. PAG neurons that had NK1 receptor immunolabeling were interdigitated with and received contacts from enkephalin-containing neurons. However, only a few (16/144; 11%) neurons with NK1 receptor also contained enkephalin immunoreactivity after colchicine treatment. In the DRN, dendrites containing NK1 receptor were selectively distributed in the dorsomedial subdivision. The majority (132/137; 96%) of these dendrites did not contain immunoreactivity for the serotonin-synthesizing enzyme tryptophan hydroxylase. In contrast, neuronal profiles with NK1 receptor in both the PAG and the DRN often contained immunolabeling for glutamate. Light and electron microscopic examination revealed that 48-65% of cell bodies and dendrites with NK1 receptor were dually immunolabeled for glutamate. These data suggest that SP directly acts primarily on glutamatergic neurons in the PAG and DRN. To a lesser extent, enkephalin-containing neurons may be targeted. Through these actions, it may subsequently influence activity of larger populations of neurons containing enkephalin as well as serotonin. This circuitry could contribute to, as well as coordinate, effects of SP on pain perception and mood.

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Section: Conditions That May Engage Sp Neurotransmission In the Pag Amentioning

confidence: 98%

Cellular basis for the effects of substance P in the periaqueductal gray and dorsal raphe nucleus

Commons

Valentino

2002

J of Comparative Neurology

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“…The two POMC-related endocrine-neurohumoral systems (opioid and ACTH-corticosteroid) interact in their physiopharmacologic activity (Amir et al 1980, Pieretti et al 1994, and clear-cut separation between the effects modulated by either systems is hardly possible. However, for the first time we could demonstrate the importance of either systems for the triggering of various specific signs and symptoms of an experimental type-2 diabetes model (Loizzo et al 2012).…”

Section: Enduring Improved Efficiency Of the Cns And The Visual Systemmentioning

confidence: 99%

Enhanced brain performance in mice following postnatal stress

Loizzo

Spampinato

Campana

et al. 2012

Journal of Endocrinology

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The double postnatal stress model (brief maternal separation plus sham injection daily applied from birth to weaning) induces metabolic alterations similar to type 2 diabetes in young-adult male mice. We verify whether 1) the stress also induces brain metabolic-functional alterations connected to diabetes and 2) different alterations are modulated selectively by two stress-damaged endogenous systems (opioid-and/or ACTH-corticosteroid-linked). Here, diabetes-like metabolic plus neurophysiologicneurometabolic parameters are studied in adult mice following postnatal stress and drug treatment. Surprisingly, together with 'classic' diabetes-like alterations, the stress model induces in young-adult mice significantly enhanced brain neurometabolic-neurophysiologic performances, consisting of decreased latency to flash-visual evoked potentials (Kw8%); increased level (Cw40%) and reduced latency (Kw30%) of NAD(P)H autofluorescence postsynaptic signals following electric stimuli; enhanced passive avoidance learning (Cw135% latency); and enhanced brain-derived neurotrophic factor level (Cw70%). Postnatal treatment with the opioid receptor antagonist naloxone prevents some alterations, moreover the treatment with antisense (AS; AS vs proopiomelanocortin mRNA) draws all parameters to control levels, thus showing that some alterations are bound to endogenous opioid-system hyper-functioning, while others depend on ACTHcorticosterone system hyper-functioning. Our stress model induces diabetes-like metabolic alterations coupled to enhanced brain neurometabolic-neurophysiologic performances. Taken all together, these findings are compatible with an 'enduring acute-stress' reaction, which puts mice in favorable survival situations vs controls. However, prolonged hormonal-metabolic imbalances are expected to also produce diabetes-like complications at later ages in stressed mice.

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“…P-Endorphin and other natural and synthetic opioids are involved in a series of functions, such as pain, nerve cell excitability and epilepsy, immunomodulation, stress and others. Analgesia induced by opioids and opioid peptides is a well known phenomenon (Millan, 1986) and the role of endorphins in stress has also been studied (Amir et al, 1980). Furthermore, in animals, opioids may have pro-and anticonvulsant effects (Ramabadran & Bansinath, 1990).…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone‐induced selective inhibition of the central μ opioid receptor: functional in vivo and in vitro evidence in rodents

Pieretti

Giannuario

Domenici

et al. 1994

British J Pharmacology

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U50,488. 3 In experiments performed in an in vitro model of cerebral excitability in the rat hippocampal slice, dexamethasone strongly prevented both the increase of the duration of the field potential recorded in CAl, and the appearance and number of additional population spikes induced by A receptor agonists. 4 In both models pretreatment with cycloheximide, a protein synthesis inhibitor, prevented the antagonism by dexamethasone of responses to the 1i opioid agonists. 5 Our data indicate that in the rodent brain there is an important functional interaction between the corticosteroid and the opioid systems at least at the receptor level, while 6 and K receptors are modulated in different ways.

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The role of endorphins in stress: Evidence and speculations

Cited by 348 publications

References 202 publications

Cellular basis for the effects of substance P in the periaqueductal gray and dorsal raphe nucleus

Cellular basis for the effects of substance P in the periaqueductal gray and dorsal raphe nucleus

Enhanced brain performance in mice following postnatal stress

Dexamethasone‐induced selective inhibition of the central μ opioid receptor: functional in vivo and in vitro evidence in rodents

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