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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several observations have led to the hypothesis that endogenous opioids may modulate the growth and development of the brain. In the present study, we have examined the effect of morphine on the incorporation of [3H]thymidine into the DNA of neonatal rat brains in vivo and in vitro. We have found that morphine, when administered to one-day-old rats, inhibited [3H]thymidine incorporation into brain DNA in a long-lasting, naloxone-reversible manner. Morphine inhibited DNA synthesis in animals one and 4 days of age but not in older animals. This effect was tissue-specific, and did not appear to be due simply to respiratory depression or decreased availability of precursor to the brain. Naloxone, when administered acutely, or naltrexone, chronically, had no effect on [3H]thymidine incorporation, indicating that endogenous opioids do not tonically depress DNA synthesis. When neonatal brain tissue was incubated with morphine in vitro. [3H]thymidine incorporation values were not different from controls. These data indicate that the effect of morphine on DNA synthesis in vivo may be an indirect one, rather than a direct action on proliferating cells.
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PMID:Effects of morphine on DNA synthesis in neonatal rat brain. 381 16

Morphine 20 mg and pethidine 50 mg were accidentally injected intrathecally in a patient who had received large doses of opioids epidurally for cancer pain and who had shown tolerance to their effects. The well established tolerance to spinal opioids did not protect the patient against a moderate degree of respiratory depression. Morphine concentrations 6.5 hours after the morphine injection were 103,500 ng/ml and 52 ng/ml in cerebrospinal fluid and serum, respectively.
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PMID:Respiratory depression after intrathecal opioids. Report of a patient receiving long-term epidural opioid therapy. 382 91

Tritium-labeled morphine was injected into the lumbar (L4-5) subarachnoid space of three baboons. The animals were sacrificed 3, 6, and 24 hr thereafter. Morphine concentrations were measured at five predetermined positions within the spinal cord, medulla oblongata, and frontal lobes of the brain by scintillation-count assay. The results revealed that morphine ascends in the subarachnoid space and is absorbed into the spinal cord and medulla oblongata in a time-dependent fashion. Ventilation was most depressed and maximal concentrations of morphine were detected in the medulla six hours after injection. Delayed respiratory depression, occasionally reported after intraspinal morphine injection, may therefore be caused as a result of the affinity of morphine for binding sites, possibly opiate receptors, situated within the vital respiratory and cardiovascular neuronal complexes of the medulla.
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PMID:Morphine concentration in brain and spinal cord after subarachnoid morphine injection in baboons. 383 37

Twenty-one unmedicated, sequentially admitted psychiatric patients of either sex and four male healthy volunteers were given an intravenous injection of 2.5 mg morphine. Blood samples were drawn immediately before and at 30-minute intervals for 3 hours after the injection and assayed for cortisol. Morphine suppressed cortisol secretion. Early resumption of cortisol secretion (escape) was more frequent in patients with a diagnosis of major depressive disorder and with abnormal dexamethasone suppression test results. The sensitivity of this infusion paradigm for the diagnosis of major depressive disorder was 40%, and the specificity was 82%. The implications of these findings for the pathophysiology of depression are discussed.
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PMID:Cortisol escape from morphine suppression. 386 50

The possible role of the nucleus accumbens (ACB) and, in some experiments, the septum mediale (SM) in mediating alterations in locomotor activity, produced by various opioids, was evaluated in the rat, the drug being injected either into the left central part of the ACB or into the left SM. Morphine, predominantly acting at the mu-type receptors, given in larger doses (13 or 40 nmol into the ACB) produced depression of locomotor activity and catalepsy, whereas 2.5 nmol were ineffective. Co-administration of naloxone into the ACB suppressed the effects of morphine. D-ala2, D-leu5-enkephalin (DADL), a preferential delta-type receptor agonist, produced a biphasic effect on locomotor activity, namely an inhibition of it and a catalepsy, followed by a locomotor activation. This effect was observed after 4 or 13 nmol; 1 nmol produced a delayed locomotor activation without any previous inhibition, whereas 0.4 or 0.1 nmol were ineffective. Equimolar doses of naloxone, when co-administered with DADL, only partially antagonized these effects of DADL. In contrast, co-administration of a small dose of DADL and an excess dose of naloxone into the ACB produced an immediate increase in locomotor activity. Injections of a predominant kappa type receptor agonist, MR 2033-Cl, were ineffective. Injection of DADL, either alone or combined with naloxone into the SM (1 nmol) produced an immediate stimulation of locomotor activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Locomotor activity of rats after injection of various opioids into the nucleus accumbens and the septum mediale. 391 Oct 70

A prospective study of the effect and side-effects of epidural morphine for pain relief in 1085 patients after thoracic, abdominal, urologic, or orthopaedic surgery was performed. Morphine chloride was diluted in saline or bupivacaine and administered through an epidural catheter placed at a segmental level appropriate for the type of surgery. The initial dose was 4 or 6 mg morphine and supplementary doses were given when needed to obtain complete freedom from pain during deep breathing or nursing care. The total dose of epidural morphine from end of surgery until the next morning varied from 4 to 18 mg. 97% of hip arthroplasty patients, 91% of prostatectomy patients and thoracotomy patients, 90% of patients after major lower extremity surgery and 88% of patients after laparotomy were completely satisfied with the postoperative course. For hip arthroplasty and major extremity surgery, an initial dose of 4 mg of epidural morphine was as effective as 6 mg. After prostatectomy, laparotomy, and thoracotomy, an initial dose of 6 mg gave significantly better effect than 4 mg. Pruritus occurred in 11%, nausea or vomiting in 34%, and respiratory depression in 0.9% of the total patient population. Urinary retention occurred in 42% of patients not having urinary catheters in place. Postoperative nausea or vomiting was more frequent in women than in men (P less than 0.001). There was a higher incidence of nausea or vomiting in men experiencing pain than in men who were completely pain-free after abdominal surgery (P less than 0.001). Respiratory depression was rare and occurred as a gradually decreasing respiratory rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidural morphine for postoperative pain: experience with 1085 patients. 397 21

A morphine infusion paradigm was used to investigate opioid mechanisms in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis in depression. The subjects were unmedicated psychiatric inpatients and healthy volunteers. Morphine suppressed cortisol secretion. Early resumption of cortisol secretion was associated with a diagnosis of major depression and abnormal dexamethasone suppression test results. Our data suggest that the hyperactivity of the HPA axis observed in depression is abnormally resistant to opioid inhibition as well as glucocorticoid feedback.
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PMID:Opioid regulation of hypothalamic-pituitary-adrenal function in depression. 397 56

Twenty-two unmedicated inpatients with major depression and 18 healthy volunteers of either sex were given an intravenous injection of 5 mg morphine. Blood samples were drawn immediately before and at intervals for 3 hrs after the injection and assayed for prolactin. Morphine stimulated prolactin secretion. The prolactin response of females was significantly greater than the response of male subjects. There were no significant differences in the prolactin response to morphine between depressed and healthy subjects. The implications of these findings for the hypothesized role of the opioid system in the pathophysiology of depression are discussed.
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PMID:Prolactin response to morphine in depression. 397 63

Contrary to previous reports of morphine's depression of locus coeruleus (LC) unit activity in anesthetized animals, acute administration of morphine (0.5, 2.0 or 4.0 mg/kg, i.p.) did not decrease the unit activity of noradrenergic neurons in the area of the LC of freely moving cats. In fact at the higher doses examined (2.0 and 4.0 mg/kg) morphine significantly increased unit activity. Naloxone (1 mg/kg, i.p.) administration reversed the increase in unit activity produced by morphine. When these same studies were conducted in cats first anesthetized with chloral hydrate, morphine produced a significant decrease in unit activity in a naloxone-reversible manner. These results suggest that previous reports of systemic morphine's depression of LC unit activity may be at least partially attributable to an interaction with anesthesia. Morphine's multiplicity of actions upon the LC is discussed.
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PMID:Locus coeruleus unit activity in freely moving cats is increased following systemic morphine administration. 404 75

The effect of morphine on the cutaneo-adrenal nerve reflex was studied in rats anesthetized with urethane-chloralose. Morphine (1 mg/kg, i.v.) significantly depressed the reflex increase in adrenal nerve activity induced by noxious lower chest pinching. Morphine (10 mg/kg, i.v.) significantly inhibited the reflex decrease in adrenal nerve activity induced by innocuous lower chest and hindlimb brushing, as well as the response induced by noxious lower chest pinching. Reversal by naloxone of the morphine-induced depression of the cutaneo-adrenal nerve reflexes indicates that the opioid receptor is associated with these effects of morphine.
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PMID:Effect of morphine on the adrenal sympathetic reflex elicited by mechanical stimulation of the skin in rats. 406 57


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