Disease relevance of morphine

• RESULTS: Morphine significantly reduced the intensity of brush-induced allodynia but had no effect on other evoked pains (i.e., static mechanical and thermal allodynia/hyperalgesia) [1].
• Studies in mice have shown that beta-arrestin-2 plays an important role in the development of morphine-induced tolerance, constipation, and respiratory depression [2].
• STUDY DESIGN: Morphine was infused for 2 to 4 days (140 microg/kg over 1 hour followed by 20 microg/kg/h) to 31 ventilator-treated newborn infants (gestational age, 24 to 41 weeks; birth weight, 765 to 4,015 g) [3].
• Proceedings: Morphine hyperthermia, prostaglandin synthetase inhibitors and naloxone [4].
• CONCLUSION: Morphine-augmented cholescintigraphy optimizes the diagnosis of acute cholecystitis in patients with the suggestive, but not pathognomonic, cholescintigraphic pattern at 1 hr of gallbladder nonvisualization with a pericholecystic rim sign, regardless of its intensity [5].

Psychiatry related information on morphine

• In rats, NTX reduces morphine-induced impulsive choice bias; however, nothing is known about the drug's effect on discrete aspects of impulsive behavior in humans, such as decision-making and inhibitory control [6].
• The locomotor activity (LMA) effects of morphine (MRP) and (+/-)-ethylketocyclazocine (EKC) were studied in two inbred mouse strains, C57B1/6J (C57) and DBA/2J (DBA) [7].
• RESULTS: Morphine microinjections in NST provoked a dose-dependent enhancement of all the polygraphic and behavioral manifestations of slow wave sleep [8].
• We found that previously extinguished morphine (3 mg/kg, i.p.) CPP was markedly reinstated by a priming injection of morphine (2 mg/kg, i.p.) or an acute environmental stressor (forced swim for 10 min), but not by the stress induced by a 24-h food deprivation [9].
• Both 20 mg HYD/1000 mg ACET and MOR impaired psychomotor performance [10].

High impact information on morphine

• BACKGROUND: Morphine analysis of hair is used in forensic toxicology to study the addiction history of heroin addicts [11].
• BACKGROUND & AIMS: Morphine increases residual lower esophageal sphincter (LES) pressure during swallow-induced LES relaxation to levels shown experimentally to prevent reflux [12].
• Comment on "Human White Blood Cells Synthesize Morphine: CYP2D6 Modulation" [13].
• Short-term morphine treatment inhibited PKA activity and then decreased the phosphorylation of Na+,K+-ATPase, leading to increase in enzyme activity [14].
• Modulation of fear-potentiated startle and vocalizations in juvenile rhesus monkeys by morphine, diazepam, and buspirone [15].

Chemical compound and disease context of morphine

• 4 Morphine (5 x 10(-6) M) as well as the opioid peptides D-Ala2, N-Phe4, Met-(0)-01 (FK 33-824; 9 x 10(-7) M), D-Met2-Pro5 enkephalin (3 x 10(-7) M) and D-Ala2-D-Leu5-enkephalin (5 x 10(-6) M) inhibited the magnitude of the noncholinergic contracture but did not alter contractile responses to exogenous substance P (4 x 10(-11) M--4 x 10(-10) M) [16].
• In diabetic rats, lacosamide attenuated cold (10, 30 mg/kg, i.p.), warm (3, 10, 30 mg/kg, i.p.) and mechanical allodynia (30 mg/kg, i.p.). Streptozotocin-induced thermal and mechanical hyperalgesia were reduced by lacosamide at doses of 10 and 30 mg/kg, i.p. Morphine (3 mg/kg) showed similar efficacy on allodynia and hyperalgesia [17].
• BACKGROUND: A previous study showed a relation between pholcodine (PHO) consumption, prevalence of IgE-sensitization to PHO, morphine (MOR) and suxamethonium (SUX) and anaphylaxis to neuromuscular blocking agents (NMBA) [18].
• 6 Morphine, enkephalins, opiate antagonists and cyclic guanosine 3',5'-monophosphate have a peripheral analgesic effect in the prostaglandin hyperalgesia test [19].
• 3. To determine whether these effects were operative in the brain, rats received an injection of either morphine 50 micrograms/kg or its diluent (control) into the lateral cerebral ventricle intracerebroventricularly (i.c.v.). Morphine significantly increased (P < 0.05) the threshold for the development of arrhythmias [20].

Biological context of morphine

• CONCLUSIONS: Morphine should be used with caution in prematurely born infants because of its low clearance, which correlates with gestational age [3].
• 1. Morphine (10(-8)-10(-5) M) did not change the membrane potential, membrane resistance and electrical threshold required to produce the action potential of smooth muscle cells of guinea-pig ileum or mouse vas deferens [21].
• The induction of sister chromatid exchange (SCE) by opium pipe scrapings (sukhteh, Su) and the pyrolysis products of opium (Op) and of its major alkaloids, morphine (Mo), have been compared with that of cigarette smoke condensate (CSC) [22].
• Chronic (5 days) morphine (10-100 mg/kg), SNC-80 (10 mg/kg), or U50488H (10 mg/kg) was associated with the induction of tachyphylaxis to the acute effects [23].
• The stimulating activity of MN and MAM is attributed to the hydrophilic interaction of the proton donor-acceptor type with the polar regions of the luciferase located outside the binding pocket of the active site [24].

Anatomical context of morphine

• DAMGO induced arrestin-2 translocation to the plasma membrane and considerable MOR1 internalization, whereas morphine did not induce arrestin-2 translocation and induced very little MOR1 internalization [25].
• 2. Morphine (10(-8)-10(-7) M) markedly suppressed the amplitude of excitatory junction potential (e.j.p.) of ileum or that of vas deferens [21].
• We show here that a glial modulator propentofylline (PPF) dramatically diminished the activation of astrocytes induced by drugs of abuse, such as methamphetamine (METH) and morphine (MRP) [26].
• Acute treatments with high doses of sufentanil and morphine (mu-agonists), SNC-80 (delta-agonist), and U50488H (kappa-agonist) induced significant decreases (30-60%) in FADD immunodensity in the cerebral cortex, through specific opioid receptor mechanisms (effects antagonized by naloxone, naltrindole, or nor-binaltorphimine) [23].
• Equipotent antinociceptive doses, as determined by a tail-flick response, for centrally administered (periaqueductal gray) morphine (M) and D-Ala2, D-Leu5 enkephalin (DADLE) were established as 5 micrograms and 19 micrograms, respectively [27].

Associations of morphine with other chemical compounds

• Morphine and DAMGO enhanced MOR1 phosphorylation over basal [25].
• The PKC inhibitor bisindolylmaleimide 1 (GF109203X) inhibited MOR1 phosphorylation under basal conditions and in the presence of morphine, but it did not inhibit DAMGO-induced phosphorylation [25].
• These results indicate that the NR2B-containing NMDA receptors in the NAc and the dorsal hippocampus play a significant role in mediating the reinstatement of rewarding responses to morphine [9].
• 1 Morphine, methadone, levorphanol, pethidine, etonitazene and related morphine-like alkaloids produced an increase in the electrically-evoked muscular contraction of the rat vas deferens [28].
• The effect of l-stepholidine (SPD), a novel alkaloid extract of the Chinese herb Stephania with partial dopamine D1 receptor agonistic and D2 receptor antagonistic dual actions, on morphine conditioned place preference (CPP) was studied [29].

Gene context of morphine

• Culture supernatants were assayed by ELISA for CCL2 protein. beta-funaltrexamine (beta-FNA) was used to block mu-opioid receptor (MOR)s. RESULTS: Morphine upregulated CCL2 mRNA and protein in neuronal cultures in a concentration- and time-dependent fashion, but had no effect on CCL2 production in astrocyte or microglial cell cultures [30].
• Both MOR and M6G increased the concentration of IGF binding protein-1 (IGFBP-1) in plasma and liver 2 h after injection [31].
• We speculate that differential affinities of MOR and M6G to the different opiate receptor subtypes might be responsible for their distinct effects on GH/IGF-I system [31].
• F9202, F9204, and Mor could significantly increase CREB phosphorylation from 2.88 to 3.59 folds over control levels after 30-min exposure [32].
• CONCLUSION: Mor, F9202, and F9204, which could induce psychological dependence affected via the micro-opioid receptor, stimulated intracellular signal pathways involving Ca2+/calmodulin-dependent protein kinases (CCDPK) and protein kinase C (PKC) pathways, which in turn initiated CREB phosphorylation [32].

Analytical, diagnostic and therapeutic context of morphine

• Chronic (28 day) subcutaneous infusion of clomipramine (CMI) via an Alzet minipump attenuated both central M-and DADLE-induced analgesia by day 15; attenuation persisted for the duration of the infusion (day 29) [27].
• On the other hand, intra-nucleus accumbens (N.Acc.) administration of astrocyte-conditioned medium (ACM) aggravated the development of rewarding effects induced by METH and MRP via the Janus kinase/signal transducers and activators of transcription (Jak/STAT) pathway, which modulates astrogliosis and/or astrogliogenesis [26].
• Sites of action of morphine involved in the development of physical dependence in rats. II. Morphine withdrawal precipitated by application of morphine antagonists into restricted parts of the ventricular system and by microinjection into various brain areas [33].
• 4. Morphine (0.13-8 muM) inhibited the contractions of the cat nictitating membrane caused by electrical stimulation [34].
• Dexketoprofen-induced antinociception in animal models of acute pain: Synergy with morphine and paracetamol [35].

References