PubMed Health⌕ Search

Biomedical subjects

M Wüster

Publications and source records attributed to M Wüster.

At least 37 records · Page 2Linked to original sources
PubMed1981

Selective localization of different types of opiate receptors in hippocampus as revealed by in vitro autoradiography.

The visualization of opiate binding sites within the hippocampus of the rat has been achieved by means of an in vitro autoradiography. In line with the concept of multiple opiate receptors, different opioid agonists revealed a particular distribution pattern. Whereas the selective delta-receptor agonist [3H]D-Ala2,D-Leu5-enkephalin specifically labelled binding sites in the CA2 area, [3H]etorphine grains displayed a uniform dense distribution throughout the pyramidal cell layers from CA1 to CA4.

Animals↗
PubMed1981

A selective distribution pattern of different opiate receptors in certain areas of rat brain as revealed by in vitro autoradiography.

A differential localization of binding sites in the rat brain for [3H]D-Ala2,Leu5-enkephalin ([3H]DADL) and [3H]etorphine ([3H]Eto) was been demonstrated by an in vitro autoradiography technique. Labeling with [3H]DADL was found predominantly in septum and paraventricular nuclei of hypothalamus, whereas [3H]Eto labeling was primarily observed in the periaqueductal gray and several thalamic nuclei. The distinctive patterns of labeling by the two ligands in certain central nervous system structures suggests the existence of specific neuronal pathways which are preferentially labeled with either [3H]DADL or [3H]Eto.

Animals↗
PubMed1981

Naloxone reduces abdominal muscle tone in mice and rats.

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.

Abdominal Muscles↗
PubMed1981

Differentiation of opiate receptors in the brain by the selective development of tolerance.

The selective development to either the delta-opiate receptor agonist D-Ala2,D-Leu5-enkephalin (DADL) or the mu-agonist sufentanyl (SUF) has been studied in the central nervous system of rats by use of osmotic minipumps for chronic administration of the drugs. The opiate-sensitive parameters analgesia and catatonia were investigated. Chronic intracerebroventricular infusion of DADL for 7 days produced a 15-fold shift in that for catatonia. In these rats, the potency of SUF in inducing analgesia and catatonia did not differ between DADL-treated animals and saline-infused controls. Similarly, chronic infusion of SUF resulted in tolerance towards SUF for both analgesia and catatonia. In these animals, DADL displayed a similar degree of tolerance w.r.t. its ability to evoke analgesia, whilst no tolerance could be detected for DADL-induced catatonia. The data indicate that prolonged stimulation of specific opiate receptors in the brain by selective agonists may bring about the selective development of tolerance for particular receptors. The data conflict with the notion that mu-receptors specifically mediate analgesia and delta-receptors catatonia.

Animals↗
PubMed1981

Pharmacological characterization of the epsilon-opiate receptor.

The epsilon-opiate receptor of the electrically stimulated rat vas deferens has been characterized by means of beta-endorphin, its fragments and derivatives thereof, as well as by its tolerance development. The data provide evidence for the uniqueness of the epsilon-receptor as compared to mu- and delta-receptors of the guinea-pig ileum and the mouse vas deferens, respectively. It appears that an activation of the epsilon-receptor requires at least the beta-endorphin sequence 1-21, which sharply contrasts with the relatively high sensitivity of mu- and delta-receptors to much shorter fragments of this opioid peptide. Furthermore, after chronic exposure of rats to etorphine, the isolated vas deferens shows a dramatic loss of sensitivity to mu-receptor agonists, but only a moderate decrease in sensitivity to beta-endorphin. The presented data contribute to the characterization of a distinct novel type of opiate receptor, the epsilon-receptor.

Animals↗
PubMed1981

Functional opiate receptors in the guinea-pig ileum: their differentiation by means of selective tolerance development.

A differentiation of multiple opiate receptors in the electrically stimulated longitudinal muscle-myenteric plexus preparation of the guinea-pig ileum is described employing the technique of tolerance development of selective opiate receptors. Apparently, mu- and kappa-opiate receptors are clearly differentiated in this tissue, since highly tolerant mu-receptors (80-fold) coexist with kappa-receptors of almost normal sensitivity and vice versa. Attempts to demonstrate delta-receptors failed, as there was complete cross-tolerance between mu- and delta-agonists. It is proposed that delta-agonists bring about their action via mu-receptors in this preparation. Although mu- and kappa-receptors have been demonstrated, neither of them appear to represent a uniform population.

Animals↗
PubMed1980

Opiate activity and receptor selectivity of dynorphin1-13 and related peptides.

Experiments on the mouse vas deferens preparation obtained from animals chronically pretreated with selective opioid agonists have revealed the existence of opiate receptors with a high degree of preference for dynorphin1-13, alpha-neoendorphin1-8 and the eta-agonist MR 2034. Modification of the dynorphin sequence, by introduction of D-alanine into position 2, resulted in a complete loss of dynorphin-like agonistic activity on the tolerant mouse vas deferens. None of the dynorphin-related peptides tested displayed a pronounced opiate-like antinociception when administered intracerebroventricularly into rats.

Animals↗
PubMed1980

Interaction of amphetamine and naloxone in feeding behavior in guinea pigs.

Chronic naloxone treatment of schedule-fed guinea pigs caused an initial anorexia followed by a resumption of food and water intake, despite the continued presence of the narcotic antagonist. During this state of chronic naloxone treatment, amphetamine exerted a similar degree of anorexia to that in animals not pretreated with naloxone. In contrast, amphetamine tolerant guinea pigs exhibited supersensitivity to naloxone with respect to feeding behavior. Since chronic amphetamine exposure results in an increased level of beta-endorphin in the hypothalamus it is suggested that an enhanced endorphinergic activity compensates for the effect of amphetamine on feeding mechanisms.

Amphetamine↗
PubMed1980

Inquiry into endorphinergic feedback mechanisms during the development of opiate tolerance/dependence.

Met-enkephalin and beta-endorphin levels were determined in the pituitary and brain of rats after treatment for several weeks with either agonists of high receptor affinity, such as levorphanol and etorphine, or with the narcotic antagnoist naloxone. Long-term activation of opiate receptors failed to change the endorphin levels in restricted areas of brain and pituitary, although a high degree of tolerance/dependence is apparent in those animals. Chronic blockade of opiate receptors by naloxone also fails to affect endorphin levels in the pituitary, but selectively increases metenkephalin levels in the striatum. The present data do not support the notion of negative feedback mechanisms to regulate endorphingergic functions during the development of opiate tolerance/dependence.

Animals↗
PubMed1980

Acute and chronic ethanol treatment changes endorphin levels in brain and pituitary.

Acute ethanol administration increased methionine-enkephalin (met-enkephalin) and beta-endorphin levels in distinct areas of the rat brain, whereas chronically supplied ethanol caused a depression of met-enkephalin and beta-endorphin levels in most of the brain areas investigated. The beta-endorphin content of the intermediate/posterior lobe of the pituitary of rats and guinea pigs decreased by 70%. Withdrawal of ethanol resulted in a complete recovery of endorphin levels in brain and pituitary within two weeks. Whether the observed alterations in endorphin concentrations are causally related to the primary mechanisms underlying alcohol dependence is uncertain, since no obvious signs of physical dependence were observed in treated animals.

Alcoholism↗
PubMed1980

Differential effects of potassium on the potency of different opioids in the mouse vas deferens.

The effect of potassium on the potency of different opioids to inhibit electrically evoked twitches of the mouse vas deferens has been studied. In general, opioids lose activity as the concentration of potassium increases. Distinct differences, however, were observed between specific opiate receptor agonists. Least sensitive to the effect of potassium proved mu- and delta-opiate receptor agonists, showing only a 2-fold increase in the concentration required to cause a half-maximal inhibition at 14 mM K+. In contrast, the supposed dynorphin receptor/kappa-receptor agonists exhibited at this concentration up to an 8-fold loss of potency. Dynorphin1-13 was found to be intermediate with a 5-fold loss of inhibitory activity. These data suggest a modulatory action of potassium for dynorphin- and kappa-receptors.

Animals↗
PubMed1980

Diazepam-induced release of opioid activity in the rat brain.

Acute intravenous injection of diazepam (2.5 mg/kg) in rats resulted in a moderate (2-fold) increase in pain threshold, as measured by the 'vocalization test'. This effect was not antagonized by naloxone (10 mg/kg, i.p.). However, pretreatment of the animals with the enzyme-inhibitor, bacitracin (50 micrograms, i.c.v.), dramatically enhanced the diazepam-induced antinociception. This increased effect was partially antagonized by naloxone, indicating an opioid-mediated mechanism as involved and further supports the hypothesis that benzodiazepine application may release opioid peptides in restricted areas of the CNS.

Analgesics↗