Rosette formation by human T and B lymphocytes in the presence of adrenergic and cholinergic drugs.

It was shown that adrenergic drugs, which increase the intracellular levels of cAMP, inhibit the rosette formation by T-lymphocytes, but stimulate the rosettes produced by B-lymphocytes. Cholinergic drugs, which increase the levels of cGMP, on the contrary, stimulate the formation of rosettes by T-lymphocytes but inhibit those produced by B-lymphocytes.     

Rosette formation by human T and B lymphocytes in the presence of adrenergic and cholinergic drugs

Summary It was shown that adrenergic drugs, which increase the intracellular levels of cAMP, inhibit the rosette formation by T-lymphocytes, but stimulate the rosettes produced by B-lymphocytes. Cholinergic drugs, which increase the levels of cGMP, on the contrary, stimulate the formation of rosettes by T-lymphocytes but inhibit those produced by B-lymphocytes.Acknowledgments. This investigation was supported by Grant from National Council for Scientific and Technological Development (CNPq), Rio de Janeiro, Brazil.     

Piroxicam-induced analgesia: Evidence for a central component which is not opioid mediated

Piroxicam is a nonsteroidal anti-inflammatory drug with a potent analgesic effect. In order to establish whether the analgesic action of Piroxicam has a central component, we studied the effect of the drug on the nociceptive orbicularis oculi reflexes evoked by electrical stimulation of the cornea and supraorbital nerve in healthy subjects. Piroxicam significantly suppressed the corneal reflex and R3 component of the blink reflex by 28% (p<0.05) and 50% (p<0.01), respectively. This effect was not reversed by the i.v. injection of naloxone. Beta-endorphin levels did not change. Piroxicam administration induces distinct inhibitory changes in nociceptive reflexes, which suggests that the analgesic action of the drug has a central component. The ineffectiveness of naloxone, and the lack of beta-endorphin changes, indicate that this central action is independent of the opioid system; other pain regulatory systems are probably involved.     

Piroxicam-induced analgesia: evidence for a central component which is not opioid mediated.

Piroxicam is a nonsteroidal anti-inflammatory drug with a potent analgesic effect. In order to establish whether the analgesic action of Piroxicam has a central component, we studied the effect of the drug on the nociceptive orbicularis oculi reflexes evoked by electrical stimulation of the cornea and supraorbital nerve in healthy subjects. Piroxicam significantly suppressed the corneal reflex and R3 component of the blink reflex by 28% (p < 0.05) and 50% (p < 0.01), respectively. This effect was not reversed by the i.v. injection of naloxone. Beta-endorphin levels did not change. Piroxicam administration induces distinct inhibitory changes in nociceptive reflexes, which suggests that the analgesic action of the drug has a central component. The ineffectiveness of naloxone, and the lack of beta-endorphin changes, indicate that this central action is independent of the opioid system; other pain regulatory systems are probably involved.     

Effect of the administration of (d-Ala)2methionine-enkephalin on the serotonin metabolism in rat brain

Summary The effect of cerebroventricular injection of [D-Alanine] methionine-enkephalin (DALA), a synthetic analog of met-enkephalin, on the serotonergic system of rat brain has been studied. This opioid peptide caused an increase in 5HT turnover which was particularly evident in the limbic forebrain. This effect was completely antagonized by naloxone pretreatment.Acknowledgments. Support received from Tecnofarmaci, Rome, is gratefully acknowledged.     

Hemmung von Morphin-Effekten durch synthetische Substanz P

Summary Synthetic Substance P and naloxone abolish the proconvulsive action of morphine on pentetrasol-induced seizures. It is suggested that Substance P could be a natural antagonist of morphine in the central nervous system.

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Am 20. März 1976 gestorben.     

Narcotic antagonism of seizures induced by a dopamine-derived tetrahydroisoquinoline alkaloid

This paper describes experiments designed to evaluate whether the narcotic antagonist naloxone significantly interferes with seizures induced by tetrahydroisoquinolines (TIQs). In these experiments we found that naloxone significantly reduced seizure scores induced by intra-cranially infusing mice with 50 micrograms of the dopamine-derived tetrahydroisoquinoline (TIQ) alkaloid, 6,7-dihydroxy TIQ. These findings support an opioid involvement in the actions of TIQs and may lead to further understanding of opioid-mediated novel excitatory receptors.     

Role of the Raphe Magnus nucleus in morphine analgesia : studies with intracerebral microinjections in the rat]

Microinjections of low concentration of morphine (5 micrograms) into the nucleus Raphé Magnus of the Rat produce a strong analgesia that can be reversed by systemic naloxone, an opiate antagonist. The administration of naloxone (5 micrograms) into the Raphé Magnus considerably reduces the effects of intravenous morphine. The effects of microinjections of morphine are strongly reduced by Cinanserin, suggesting a role for serotoninergic mechanisms in morphine analgesia.     

Identification of lymphocyte subpopulations by simultaneous E-rosette formation and unspecific acid esterase staining.

E-rosettes of human peripheral blood lymphocytes were stained by an unspecific acid esterase stain; 74.5% of the rosette forming cells were esterase positive, while only 30% of the non-rosette forming cells showed a reaction product.     

Identification of lymphocyte subpopulations by simultaneous E-rosette formation and unspecific acid esterase staining

Summary E-rosettes of human peripheral blood lymphocytes were stained by an unspecific acid esterase stain; 74.5% of the rosette forming cells were esterase positive, while only 30% of the non-rosette forming cells showed a reaction product.     

Narcotic antagonism of seizures induced by a dopamine-derived tetrahydroisoquinoline alkaloid

Summary This paper describes experiments designed to evaluate whether the narcotic antagonist naloxone significantly interferes with seizures induced by tetrahydroisoquinolines (TIQs). In these experiments we found that naloxone significantly reduced seizure scores induced by intra-cranially infusing mice with 50 g of the dopamine-derived tetrahydroisoquinoline (TIQ) alkaloid, 6,7-dihydroxy TIQ. These findings support an opioid involvement in the actions of TIQs and may lead to further understanding of opioid-mediated novel excitatory receptors.     

Naloxone reduces abdominal muscle tone in mice and rats

Summary The effect of naloxone on muscle tone was investigated in mice and rats at various times after administration. The naloxone effect was also tested in diazepam-pretreated animals. Naloxone was found to display muscle relaxant activity. This effect appeared to be additive to that of diazepam.     

Inhibitory effect of methionine- and leucine-enkephalin on contractions of the guinea-pig ileum elicited by PGE1

Summary Methionine-enkephalin and leucine-enkephalin (m-enk and l-enk) have been shown to antagonize contractions of the isolated guinea-pig intestine elicited by PGE₁. The inhibitory effect of these 2 pentapeptides is abolished by naloxone.     

Circling behavior induced by phencyclidine in mice and its inhibition by naloxone

Phencyclidine (PCP), when given to mice, induces general hyperactivity and rapid circling, similar to that caused by morphine. These effects are partially antagonized by naloxone.     

Stress by restraining potentiates morphine catalepsy in rats

Restraint-induced stress potentiated morphine catalepsy in rats. This potentiation was partially antagonized by pharmacologic treatments decreasing central serotonin, acetylcholine, prostaglandins and by naloxone. Selective increase in central dopamine also inhibited the potentiation.     

Ocular instillation of naloxone increases intraocular pressure in morphine-addicted patients: a possible test for detecting misuse of morphine

The effect of conjunctival instillation of naloxone on intraocular pressure has been examined in morphine-addicted patients as compared to non-addicted healthy volunteers. Morphine-addicted subjects showed a lower basal value of intraocular pressure as compared to the control volunteers. The instillation of naloxone caused a normalization of intraocular pressure to a level similar to that of control volunteers. This test seems to be a useful screening method for detecting morphine addiction.     

Ocular instillation of naloxone increases intraocular pressure in morphine-addicted patients: A possible test for detecting misuse of morphine

Summary The effect of conjunctival instillation of naloxone on intraocular pressure has been examined in morphine-addicted patients as compared to non-addicted healthy volunteers. Morphine-addicted subjects showed a lower basal value of intraocular pressure as compared to the control volunteers. The instillation of naloxone caused a normalization of intraocular pressure to a level similar to that of control volunteers. This test seems to be a useful screening method for detecting morphine addiction.     

Naloxone prevents the analgesic action of alpha-MSH in mice

alpha-MSH (0.1, 1, 10 micrograms) was administered intracerebroventricularly and its action on pain sensitivity was investigated by the hot-plate method in mice. alpha-MSH produced dose-dependent analgesia and this analgesic effect was prevented by naloxone (1 mg/kg, s.c.). It is possible that alpha-MSH may play a role in the mechanism of pain through endogeneous opioid systems.     

Direct evidence for pH-dependent Fc receptors on proximal enterocytes of suckling rat gut.

By means of an erythrocyte-antibody rosette technique, Fc receptors, functional at pH 6.0 but not at 7.2, were shown to be present on enterocytes isolated from duodenum and jejunum (but absent from ileum) of 12-20-day-old suckling rats.     

Stress by restraining potentiates morphine catalepsy in rats

Summary Restraint-induced stress potentiated morphine catalepsy in rats. This potentiation was partially antagonized by pharmacologic treatments decreasing central serotonin, acetylcholine, prostaglandins and by naloxone. Selective increase in central dopamine also inhibited the potentiation.Acknowledgments. SKB is an ECFMG Senior Faculty Fellow from the Department of Pharmacology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India. Partial research support by the Dakota State Aerie Fraternal Order of Eagles is gratefully acknowledged.