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At least 19 recordsLinked to original sources
PubMedDate not supplied

Studies on the mechanism of post-etorphine catalepsy. Modyfying effect of amphetamine, apomorphine and dihydroxy-phenylalanine (L-dopa) on etorphine-induced concentrations of dopamine and noradrenaline in the rat central nervous system.

Studies on the mechanism of post-etorphine catalepsy. Modyfying of amphetamine, apomorphine and dihydroxyphenyl-alanine (L-DOPA) on etorphine-induced concentrations of dopamine and noradrenaline in the rat central nervous system. Acta Physiol. Pol., 1979, 30 (2): 279--287. During stereotypy induced with amphetamine, apomorphine and 1-dihydroxyphenylalanine (L-DOPA) increased concentrations of dopamine (DA) and noradrenaline (NA) were found in the motor centres of the central nervous system (CNS). In post-etorphine catalepsy the concentrations of DA and NA were also increased in the frontal cortex, striopallidum, pons and cerebellum and in the lumbosacral spinal cord. However, these stereotypy-inducing agents used in premedication of post-etorphine catalepsy delayed significantly its onset and reduced its duration.

Amphetamine↗
PubMed1978

Subcellular distribution of etorphine in rat brain and evidence for in vitro stereospecific binding.

1 Control experiments were carried out by homogenizing rat brain at 0 degrees C with sucrose containing various concentrations of [3H]-etorphine. Subcellular fractionation of this homogenate showed that the distribution of the labelled drug amongst the primary fractions was dependent on the concentration of etorphine in the homogenate. 2 Rats were injected intravenously with 0.2 and 20 microgram/kg of [3H]-etorphine. The brains were homogenized and fractionated in sucrose containing 4.2 x 10(-5) M unlabelled etorphine in order to control redistribution artifacts. Different distribution profiles in the subcellular fractions were observed at these two dose levels. 3 Concurrent administration of either cyprenorphine or naloxone with intravenous etorphine, caused a shift of the labelled drug from the P3 fraction to the supernatant fraction. 4 The subcellular distribution of intravenously administered [3H]-etorphine was also studied by homogenizing brains in etorphine-free sucrose, and sucrose containing either levorphanol or dextrorphan. From these experiments it was concluded that the P3 microsomal fraction is a major site to which in vivo etorphine is stereospecifically bound in the rat brain.

Animals↗
PubMed1975

The specificity of binding of the narcotic agonist etorphine in synaptic membranes of rat brain in vivo.

When 3H-etorphine was administered to rats in a pharmacologically effective dose (0.75 mug/kg intracisternally), the labeled drug was concentrated in synaptic membrane fractions isolated from the brains of rats killed 10 min after etorphine injection. Pretreatment of the animals with the narcotic antagonists naloxone, diprenorphine or l-cyclorphan, blocked the pharmacological responses to etorphine and reduced 3H-etorphine binding in the membrane fractions. The differences between 3H-etorphine bound in synaptic membranes of rats treated with d-cyclorphan (inactive isomer) and l-cyclorphan (active antagonist) were in the same range as the reductions in etorphine binding in antagonist-treated rats, indicating that stereospecific and pharmacologically-specific binding sites in synaptic membranes in vivo were of the same magnitude: about 0.04 pmol/g brain.

Animals↗
PubMed1992

Involvement of supraspinal epsilon and mu opioid receptors in inhibition of the tail-flick response induced by etorphine in the mouse.

Etorphine, a potent opioid agonist, has been reported to bind to both mu and epsilon opioid receptors. The present studies were designed to determine what types of opioid receptors and neurotransmitters for descending pain control systems were involved in antinociception induced by etorphine in mice. Morphine, a typical mu opioid receptor agonist, and beta-endorphin, an epsilon opioid receptor agonist, were used for comparison. Antinociceptive response induced by etorphine (20 ng) given i.c.v was blocked by i.c.v administration of D-Phe-Cys-Tyr-D-Tyr-Orn-Thr-Pen-Thr-NH2 (CTOP, 25 ng) and beta-endorphin-(1-27) [beta-EP-(1-27)] (6 micrograms), but not ICI 174,864 (ICI, 5 micrograms) or norbinaltorphimine (N-BNI, 5 micrograms). The antinociception induced by i.c.v. etorphine was also antagonized by the i.c.v. pretreatment of beta-funaltrexamine (beta-FNA, 50 ng, 24 hr). Intracerebroventricular administration of beta-EP-(1-27) (3 micrograms) caused a further attenuation of the i.c.v. etorphine-induced antinociception in mice pretreated with beta-FNA. The antinociceptive response induced by morphine (2 micrograms) given i.c.v. was blocked by i.c.v. administration of CTOP (25 ng) or beta-FNA (50 ng), but not beta-EP-(1-27) (6 micrograms), ICI (5 micrograms) or N-BNI (5 micrograms). These results indicate that the antinociception induced by etorphine given i.c.v. is mediated by the stimulation of both mu and epsilon opioid receptors whereas the antinociception induced by morphine given i.c.v. is mediated by the stimulation of mu, but not epsilon opioid receptors at supraspinal sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗
PubMedDate not supplied

The effect of etorphine on dopamine and noradrenaline concentrations in different central nervous system structures in the rat.

The effect of etorphine on dopamine and noradrenaline concentrations in different central nervous system structures in the rat. Acta Physiol. Pol., 1977, 28 (6): 529-540. Intramuscular administration of etorphine in immobilizing doses (0.008 mg/kg) was followed by a rise in dopamine concentration in the examined motor structures of the central nervous system (striopallidum, pons, cerebellum, lumbosacral intumescence of the spinal cord). Only in the motor centres of the frontal cortex dropamine concentration was decreased. At the time etorphine decreased the concentration of noradrenaline in striopallidum and raised it in the other examined structures of the central nervous system. A correlation was found between the concentrations of both substances, especially in the frontal motor centres and striopallidum. Post etorphine accumulation of dopamine in the striopallidum (for 6.369 to 11.322 mcg/g of fresh tissue) with simultaneous inhibition of motor activity of the animals suggests that etorphine inhibits the release of dopamine from the presynaptic elements in the motor centres of the central nervous system in rats. This leads to a decreased dopamine action on its receptors. Some post etorphine behavioral changes (rigidity, spastic flexion, muscle tremor) support this hypothesis.

Animals↗
PubMed1979

Interaction of morphine, etorphine and enkephalins with dopamine-stimulated adenylate cyclase of monkey amygdala.

Adenylate cyclase activity (AC) of homogenates of monkey amygdaloid nucleus was approximately doubled in the presence of dopamine (10 micrometer). Morphine, etorphine, and several enkephalin analogs (met-enkephalin, D-ala2-met-enkephalin, and D-met2, pro5-enkephalinamide) were capable of inhibiting the stimulation of AC produced by dopamine (90-100% with etorphine or D-ala2-met-enkephalin). Unlike morphine and etorphine, the peptides exhibited bell-shaped dose-response curves for this inhibition with maximal effects at approximately 1 X 10(-7) M, but negligible effects at 1 X 10(-5) M. Under the conditions studied, only etorphine inhibited basal AC. Naloxone antagonized the inhibitory effects of each of the opioids tested, and dextrorphan, an inactive L-(+)-opiate, failed to inhibit the dopamine response. Together these data indicate that the effects were mediated via the classically described stereospecific opiate receptor. The relative order of potency (etorphine greater than enkephalins greater than morphine) was similar to that previously reported for the binding affinities of these drugs in rat brain homogenates. The influence of narcotic agents on dopamine stimulated AC was eliminated by either freezing the amygdaloid tissue or preincubating the homogenate at 4 degrees C; the dopamine responses, however, could still be elicited. The narcotic receptor interaction with the adenylate cyclase thus appears to be distinct from and more labile than that of the dopamine receptor. Gpp(NH)p-stimulated AC was not inhibited by morphine. It is postulated that the inhibition involves interaction of opiate receptors with catalytic units of dopamine-stimulated AC, but not with other cyclase species which may provide the major component of Gpp(NH)p-stimulated activity in amygdala.

Adenylyl Cyclases↗
PubMed1975

Etorphine in man. I. Subjective effects and suppression of morphine abstinence.

The effects of etorphine, a potent morphine-like drug, were qualitatively and quantitatively compared to those of morphine. In nondependent subjects, etorphine in doses of 0.025, 0.050, and 0.100 mg produced pupillary constriction and morphine-like subjective effects and euphoria. Etorphine was 500 times as potent as morphine, with a very rapid onset and short duration of action. In morphine-dependent subjects, etorphine suppressed abstinence but for a shorter period than morphine. These studies indicate that in man etorphine is a morphine-like drug with a high abuse potential.

Clinical Trials as Topic↗
PubMed1975

Development of a radioimmunoassay for etorphine (preliminary communication).

A radioimmunoassay for etorphine has been developed using antibodies raised in a rabbit against an etorphine-3-hemisuccinate-bovine serum albumin conjugate. Using tritiated etorphine as the label, the antiserum could be used at a final dilution of 1:4 and had an avidity of 1.8 times 10-9 L.M.-1. The sensitivity of the assay was 0.88 plus or minus 0.04 ng etorphine per ml of serum and there was no cross-reactivity with any of the six opiate alkaloids examined over the range 0-100 ng/ml.

Animals↗
PubMed1977

3H-etorphine levels in CNS of tolerant and non-tolerant rats.

Rats were rendered tolerant to etorphine by administering it daily for 5 days at doses of either 10 microgram/kg i.v. or 5 microgram/kg s.c..3H-etorphine was then injected to tolerant and non-tolerant rats; after 15 min their brain and spinal cord were removed for 3H-etorphine assay. Tolerant rats had lower 3H-etorphine levels in both tissues than control rats.

Animals↗
PubMedDate not supplied

The effects of etorphine, fentanyl and morphine on noradrenaline and dopamine concentrations in the striatum of rat.

The effects of etorphine, fentanyl and morphine on noradrenaline and dopamine concentrations in the striatum of rat. Acta Physiol. Pol. 1977, 28 (2): 107--112. Dopamine (DA) concentrations were determined after administration of etorphine (M 99--0.008 mg/kg), fentanyl (0.006 mg/kg) and very high doses of morphine (20.0 mg/kg). DA was chosen as a striatal neurotransmitter playing the main role in the extrapyramidal system. The concentrations of noradrenaline (NA) were determined for comparison. Etorphine in therapeutic doses and morphine in subtoxic doses increased the concentration of DA in striatal neurons. Since, under these conditions, the behavior of animals resembles the symptom complex characteristic of the so-called parkinsonian or postneuroleptic syndrome in which a deficiency of absence of DA has been found in striatum, it might be supposed that the cataleptic action of etorphine and morphine may be due to inhibition of presynaptic striatal structures, with consequent disturbances in DA release from its stores.

Animals↗
PubMed1978

Analgesic effect of etorphine in rats with selective depletions of brain monoamines.

The analgesic effect of etorphine was compared with that of morphine in rats with electrolytic lesions of the nucleus medianus raphe or injected intraventricularly with 6-hydroxydopamine. The effect of both compounds was markedly reduced in animals with raphe lesions, but not significantly modified in those receiving 6-hydroxydopamine. Etorphine and morphine significantly increased the forebrain levels of 5-hydroxyindolacetic acid when administered subcutaneously at doses of 5mg/kg and 2 microgram/kg, respectively. Neither drug significantly affected the forebrain levels of monoamines. It is concluded that, as for morphine the integrity of the serotoninergic system in the brain is important for the full analgesic effect of etorphine.

Analgesics↗
PubMed1976

Inspiration inhibiting effect of etorphine-derivatives.

The inspiration inhibiting vagal reflex as elicited in rabbits by tracheal occlusion in inspiratory position, is strongly increased by etorphine and its derivatives, the 19-isoamylderivative benig of outstanding activity.

Animals↗
PubMed1977

Etorphine and shuttle-box self-stimulation in the rat.

Rats were trained to turn rewarding electrical brain stimulation on and off by crossing back and forth in a shuttle-box. Moderate doses of the narcotic analgesic, etorphine, increased mean ON times while having little effect on OFF times. Tolerance did not develop to the reward enhancement action over five consecutive days of injections. This paradigm seems valuable for exploration of the reinforcing properties of narcotic drugs.

Animals↗
PubMed1977

The immobilization of wapiti with etorphine hydrochloride.

Data and observations on the use of Etorphine hydrochloride (M99) (in combination with Acepromazine) and its antagonist M50-50 for immobilization of captive elk (Cervus elaphus canadensis) are presented. The study period covers 3 years during which 8 adult elk were immobilized 52 times with M99. The average dose of M99 administered for each immobilization was 2.2 mg per 100 kg body weight. Reversal with M50-50 was effected by an average dose of 4.4 mg per 100 body weight. Induction averaged 5.9 minutes while reversal took an average of 4.6 minutes.

Acepromazine↗
PubMed1975

The capture and translocation of gemsbok Oryx gazella gazella in the Nambi Desert with the aid of fentanyl, etorphine and tranquillizers.

Twenty-three gemsbok in the Namib Desert were captured with combinations of fentanyl or etorphine hydrochloride, hyoscine hydrobromide and tranquilizers such as azaperone, SU - 9064, triflupromazine hydrochloride and acetylpromazine maleate. Fentanyl, a New immobilizing compound, proved to be a safe and effective immobilizing drug for capturing gemsbok. The gemsbok were chased on the interdune plains and darted from a Land Rover with the Palmer powder-charge Cap-Chur gun. A six-seater helicopter was used on a trial basis to dart a gemsbok, but it is suggested that a smaller, more manoeuvrable helicopter be used for further operations. All the gemsbok were transported under narcosis from the capture area to an enclosure. Chlorpromazine hydrochloride was injected into the captured gemsbok to sedate them in their new confined environment. Tranquillizers such as chlorpromazine hydrochloride, acetylpromazine maleate and a new tranquillizer SU - 9064 were used to sedate the animals during long distance transportation in crates. This prevented the animals from injuring themselves and damagin the crates. For the first time in South West Africa wild animals were transported by air. A journey by road which under normal circumstances would have taken over 40 hours, was completed in less than 9 hours by utilizing aerial transportation. There were no losses during transportation and only two gemsbok were injured during the translocation operation.

Acepromazine↗