Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In pontine slices of the rat brain, the frequency of spontaneous action potentials of locus coeruleus (LC) neurones was recorded extracellularly. Noradrenaline 0.1-100 mumol/l, UK 14,304 0.01-100 nmol/l, [Met5]-enkephalin 1-10,000 nmol/l and [D-Ala2,D-Leu5]enkephalin 0.1-1,000 nmol/l, all depressed the firing rate. Rauwolscine 1 mumol/l antagonized the effects of both noradrenaline and UK 14,304, but potentiated the effects of [Met5]enkephalin and [D-Ala2, D-Leu5]enkephalin. Idazoxan 1 mumol/l acted in a similar manner. Prazosin 1 mumol/l did not change the effects of either noradrenaline or [Met5]enkephalin. Naloxone 0.1 mumol/l antagonized both [Met5]enkephalin and [D-Ala2, D-Leu5]enkephalin, but failed to alter the effects of either noradrenaline or UK 14,304. Rauwolscine, idazoxan and prazosin, all 1 mumol/l, as well as naloxone 0.1 mumol/l, did not influence the firing rate when given alone. Desipramine 1 mumol/l inhibited the discharge of action potentials in a rauwolscine-antagonizable manner. Noradrenaline 10 mumol/l produced the same depression of firing, both in the presence of noradrenaline 1 mumol/l and [Met5]enkephalin 0.03 mumol/l. Likewise, the effect of [Met5]enkephalin 0.3 mumol/l was the same, irrespective of whether it was added to a medium containing [Met5]enkephalin 0.03 mumol/l or noradrenaline 1 mumol/l. The spontaneous activity of LC neurones is inhibited by somatic alpha 2-adrenoceptors and opioid mu-receptors. We suggest that the two receptors interact with each other at a site located between themselves and not in the subsequent common signal transduction system.
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PMID:Blockade of alpha 2-adrenoceptors increases opioid mu-receptor-mediated inhibition of the firing rate of rat locus coeruleus neurones. 198 56

Morphine and its major metabolites, morphine-3-glucuronide and morphine-6-glucuronide, were given intracerebroventricularly (i.c.v.) to rats. The antinociceptive effects were assessed in the tail-flick and hot-plate tests as well as the writhing test. Ventilatory effects were studied in halothane-anaesthetized rats. Based on calculated ED50 values, morphine-6-glucuronide was approximately 200 times more potent that morphine itself in the tail-flick and hot-plate tests. In the writhing test the difference in ED50 was approximately 9-fold. Morphine and morphine-6-glucuronide administered i.c.v. induced dose-related decreases in minute ventilation in the dose range 2.7 x 10(-9)-1.3 x 10(-7) mol. The dose-response curve for minute ventilation was steeper for morphine-6-glucuronide than for morphine. Morphine-6-glucuronide was approximately 10 times more potent than morphine in depressing minute ventilation. Morphine-6-glucuronide reduced both tidal volume and respiratory frequency, while morphine reduced only the tidal volume. Morphine-3-glucuronide, in contrast, increased both tidal volume and respiratory frequency, causing an increase in minute ventilation. Apnoea was elicited after the highest doses of morphine-6-glucuronide but not of morphine. The potency difference for depression of minute ventilation between morphine-6-glucuronide and morphine corresponded well to the difference in the writhing test but not to the potency difference in the tail-flick or hot-plate tests. The ventilatory depression induced by morphine and morphine-6-glucuronide was readily reversed by naloxone, while the hyperventilation caused by morphine-3-glucuronide was slightly potentiated by the opioid antagonist. Naloxone pretreatment completely blocked the ventilatory depression induced by morphine-6-glucuronide. These results show that the potent ventilatory depression induced by morphine-6-glucuronide is related to its antinociceptive effects in rats. Furthermore, the fact that morphine-3-glucuronide stimulated ventilation and that morphine had a more shallow ventilatory dose-response curve compared to morphine-6-glucuronide may indicate that morphine-3-glucuronide is a functional antagonist of the depressive effects of morphine and morphine-6-glucuronide on ventilation.
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PMID:Antinociceptive and ventilatory effects of the morphine metabolites: morphine-6-glucuronide and morphine-3-glucuronide. 205 Jan 92

1. The antidepressant trazodone and its main metabolite m-chlorophenylpiperazine (mCPP) were investigated for their analgesic properties and their sensitivity to a threshold dose of morphine in acetic acid abdominal constriction and hot plate tests. 2. The drugs elicited hypoalgesic effects at about the same doses in the two analgesic assays. 3. Naloxone (2 mg/kg i.p.) prevented the hypoalgesia of trazodone but not of mCPP in the hot plate test. The opiate antagonist did not affect the responses of both drugs to the writhing test. 4. Subanalgesic doses of the two drugs increased the sensitivity to morphine in both assays. The results further support the suggested role played by opioid and 5-HT systems on depression.
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PMID:Antinociceptive effects of trazodone and m-chlorophenylpiperazine (mCPP) in mice: interaction with morphine. 205 Feb 81

Spring-born crossbred ewe lambs were raised in a natural photoperiod and saline (N = 6) or naloxone (1 mg/kg) in saline (N = 6) was injected (i.m.) every 2 h for 6 h at 5, 10 and 15 weeks of age and for 8 h at 20, 25 and 30 weeks of age. Blood samples were taken every 12 min during treatment periods. Naloxone had no effect on time to first oestrus (controls 235 +/- 6 days, naloxone 242 +/- 7 days). Mean serum LH concentrations and LH pulse frequency were elevated by naloxone in ewe lambs at 20, 25, and 30 weeks of age (P less than 0.05). The only FSH response to naloxone was a depression of mean serum concentrations at 30 weeks of age (P less than 0.05). LH pulse amplitude was elevated at 5 weeks of age in all ewe lambs and declined thereafter to a nadir at 30 weeks of age in control, but not in naloxone-treated animals (P less than 0.05). LH pulse frequency was elevated at 10 weeks of age in control ewe lambs and in all animals at 30 weeks of age (P less than 0.05). FSH pulse frequency declined from 5 weeks of age in control ewe lambs (P less than 0.05), with very few pulses noted in 25- and 30-week-old animals. We conclude that (1) opioidergic suppression of LH, but not FSH, secretion developed at 20 weeks of age in the growing ewe lambs used in the present study, with no obvious change in suppression before the onset of first oestrus: (2) pulsatile FSH secretion occurred in the young ewe lamb but was lost as the lamb matured: (3) attainment of sexual maturity was preceded by an elevation in LH pulse frequency.
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PMID:Effect of naloxone on gonadotrophin secretion at various stages of development in the ewe lamb. 211 30

Naloxone (Narcan), a semisynthetic opioid antagonist, has approved therapeutic use for the treatment of opioid-induced central nervous system depression. With the implementation of epidural and intrathecal opioid analgesia, naloxone has been used for the treatment of side effects associated with these methods of analgesia. Consequently, there has been greater utility of naloxone for postoperative orthopaedic, noncritical patients. Naloxone was thought to be devoid of any intrinsic activity and, therefore, thought to have few side effects. There have been several reports of cardiovascular complications associated with naloxone administration that have disputed this view. Since use of naloxone is increasing in orthopaedic nursing practice, orthopaedic nurses need to understand the potential complications associated with its use.
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PMID:Naloxone: a word of caution. 216 31

In the present study, it was observed that ohmefentanyl (OMF) affected microiontophoretically applied spontaneous discharges of respiration related units (RRUs) in the nucleus ambigus of rats. Of 96 RRUS recorded, 48 units were depressed following OMF application, 14 units increased in discharges, 14 units increased and then decreased, 9 units decreased and then increased. The remaining 11 units were not influenced. Naloxone administered iontophoretically not only blocked OMF-induced depression in 11 out of 15 units, but blocked OMF-induced facilitation in 5 out of 6 units. U-50488 administered microiontophoretically antagonized OMF-induced depression in 9 out of 13 units. Duration of the depression produced by OMF was much longer than that of the facilitation. The result suggests that the subtype of opiate receptors mediating the depression seen to be different from that responsible for the facilitation.
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PMID:[Effects of microiontophoretically applied OMF on spontaneous discharges of respiration related units (RRUs) in the region of nucleus ambigus of rat]. 217 47

Locomotor activity was studied in the rabbit following injections of morphine, ethylketocyclazocine and N-allylnormetazocine. All three drugs produced only depression of activity. The opioid antagonist naloxone antagonized the effects of both morphine and ethylketocyclazocine. Naloxone (0.1 mg/kg) did not antagonize the effects of N-allylnormetazocine. Naloxone alone depressed locomotor activity at doses above 0.3 mg/kg. This effect of naloxone was partially antagonized by 0.1 mg/kg ethylketocyclazocine, but not by 0.1 mg/kg morphine. The GABA agonist muscimol (0.1 and 1.0 mg/kg) also did not antagonize the effect of naloxone on locomotor activity. Finally, amphetamine did not produce a great deal of locomotor activation in the rabbit, which may indicate that increasing activity in the rabbit by drug intervention may be inherently difficult. These results indicate that the opioids have effects in the rabbit that are clearly different from those observed in rodents, where morphine and N-allylnormetazocine have been reported to produce locomotor activation, and naloxone typically has little effect. In addition, the effects of the opioids on locomotor activity were clearly distinguishable from their effects on learning in the rabbit. While morphine and ethylketocyclazocine were approximately equipotent in depressing locomotor activity, morphine is much less potent than ethylketocyclazocine in retarding acquisition of the classically conditioned nictitating membrane response in the rabbit.
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PMID:Effects of morphine, ethylketocyclazocine, N-allylnormetazocine and naloxone on locomotor activity in the rabbit. 219 Feb 57

The respiratory control center receives afferent stimuli from mechanical and neuromechanical sources. Information from both these sources, combined with voluntary and involuntary CNS control, effects stimulation of the respiratory muscles. In the infant, insufficiency of one or more of these elements of the respiratory control center is associated with considerable morbidity and mortality. Pharmacologic manipulation may provide a means of intervention. The xanthine derivative theophylline has been successfully used in the treatment of bronchopulmonary dysplasia and apnea in the infant. Naloxone, an endorphin antagonist, is widely used for the reversal of narcotic-induced respiratory depression but has not been shown to be clinically effective for either severely or moderately asphyxiated infants. Although doxapram has not been extensively studied and lacks an oral preparation, it is a potentially viable therapy in the treatment of refractory apnea and congenital hypoventilation syndromes. Almitrine's success in adults with chronic obstructive pulmonary disease has not been duplicated in infants with similar respiratory impairments. Progesterone and prostaglandin, although proved to influence respiratory activity, should be regarded as very experimental therapeutic modalities.
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PMID:Pharmacologic manipulation of the respiratory control center in the infant. 219 44

Persons with chronic mountain sickness (CMS) hypoventilate and are more hypoxemic than normal individuals, but the cause of the hypoventilation is unclear. Studies of 14 patients with CMS and 11 healthy age-matched control subjects residing in Lhasa, Tibet, China (3,658 m) were conducted to test the hypothesis that hypoventilation, blunted hypoxic ventilatory responsiveness (HVR), and hypoxic ventilatory depression of CMS were due to increased endogenous opioid production. Patients with CMS compared with control subjects exhibited hypoventilation (end-tidal carbon dioxide pressure [PETCO2] = 36.6 +/- 1.0 versus 31.5 +/- 0.5 mm Hg, p less than 0.05), lower tidal volume (VT = 0.54 +/- 0.02 versus 0.61 +/- 0.02 ml BTPS, p less than 0.05), blunted HVR (shape parameter A = 17 +/- 8 versus 114 +/- 22 mm Hg/L BTPS/min, p less than 0.05), and a depressant effect of ambient hypoxia on ventilation (delta PETCO2 with acute hyperoxia = -3.5 +/- 0.5 versus -1.0 +/- 0.6 mm Hg, p less than 0.05). Reduced forced expiratory volume in 1 s to vital capacity ratios (FEV1/VC) and a higher proportion of cigarette smokers in the group of patients with CMS compared with control subjects suggested that at least some patients with CMS had mild airway obstructive lung disease. Naloxone infusion (0.14 mg/kg) to six patients with CMS did not change resting VT, PETCO2, HVR, or SaO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased ventilation and hypoxic ventilatory responsiveness are not reversed by naloxone in Lhasa residents with chronic mountain sickness. 225 47

The gastroenterology nurse must be familiar with the use of Narcan. Narcan is frequently administered in the endoscopy suite after the procedure for the reversal of narcotic depression induced by pre-procedure intravenous sedation. Knowledge of Narcan will allow the nurse to safely administer the medication as well as adequately assess the patient's response to it.
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PMID:Narcan (naloxone HCl). 228 24


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