Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Deletion of guanine nucleotide binding protein alpha z subunit in mice induces a gene dose dependent tolerance to morphine.

Neuropharmacology - 1 May 2004

Leck K J, Bartlett S E, Smith M T, Megirian D, Holgate J, Powell K L, Matthaei K I, Hendry I A

Abstract excerpt

The mechanism underlying the development of tolerance to morphine is still incompletely understood. Morphine binds to opioid receptors, which in turn activates downstream second messenger cascades through heterotrimeric guanine nucleotide binding proteins (G proteins). In this paper, we show that G(z), a member of the inhibitory G protein family, plays an important role in mediating the analgesic and lethality...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Dose-Response Relationship, Drug
Share to Drug Tolerance

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to GTP-Binding Protein alpha Subunits

Share to GTP-Binding Proteins

Share to Morphine

Share to Pain Threshold

Share to Protein Subunits

Share to Second Messenger Systems

Source

Identifiers

PMID: 15033343
DOI: 10.1016/j.neuropharm.2003.11.024

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Deletion of guanine nucleotide binding protein alpha z subunit in mice induces a gene dose dependent tolerance to morphine.PMID 15033343Read ↗

Differential control of opioid antinociception to thermal stimuli in a knock-in mouse expressing regulator of G-protein signaling-insensitive Gαo protein.Semantic proximity Read ↗

Mice deficient in the alpha subunit of G(z) show changes in pre-pulse inhibition, anxiety and responses to 5-HT(1A) receptor stimulation, which are strongly dependent on the genetic background.Semantic proximity Read ↗

Comparison of G-protein activation in the brain by mu-, delta-, and kappa-opioid receptor agonists in mu-opioid receptor knockout mice.Semantic proximity Read ↗

Mu-opioid receptor desensitization by beta-arrestin-2 determines morphine tolerance but not dependence.Semantic proximity Read ↗

mu Opioid receptor knockout in mice: effects on ligand-induced analgesia and morphine lethality.Semantic proximity Read ↗

The mu-opioid receptor gene-dose dependent reductions in G-protein activation in the pons/medulla and antinociception induced by endomorphins in mu-opioid receptor knockout mice.Semantic proximity Read ↗

Galanin protects against behavioral and neurochemical correlates of opiate reward.Semantic proximity Read ↗

Brain region specific actions of regulator of G protein signaling 4 oppose morphine reward and dependence but promote analgesia.Semantic proximity Read ↗

Impaired olfactory behavior in mice deficient in the alpha subunit of G(o).Semantic proximity Read ↗

Ethanol tolerance and withdrawal responses in GABA(A) receptor alpha 6 subunit null allele mice and in inbred C57BL/6J and strain 129/SvJ mice.Semantic proximity Read ↗

Spinal or supraspinal phosphorylation deficiency at the MOR C-terminus does not affect morphine tolerance in vivo.Semantic proximity Read ↗

Mice lacking the long splice variant of the gamma 2 subunit of the GABA(A) receptor are more sensitive to benzodiazepines.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.