William L. Dewey

Prolonged reversal of morphine tolerance with no reversal of dependence by protein kinase C inhibitors.

The expression of a high level of morphine antinociceptive tolerance in mice involves both PKC and PKA.

Effects of mGlu1 and mGlu5 metabotropic glutamate antagonists to reverse morphine tolerance in mice.

PKC and PKA inhibitors reverse tolerance to morphine-induced hypothermia and supraspinal analgesia in mice.

Task specificity of cross-tolerance between Delta9-tetrahydrocannabinol and anandamide analogs in mice.

Alterations in brain Protein Kinase A activity and reversal of morphine tolerance by two fragments of native Protein Kinase A inhibitor peptide (PKI).

Chronic Delta9-tetrahydrocannabinol treatment produces antinociceptive tolerance in mice without altering protein kinase A activity in mouse brain and spinal cord.

Protein Kinase A activity is increased in mouse lumbar spinal cord but not brain following morphine antinociceptive tolerance for 15 days.

Protein kinase inhibitor peptide (PKI): a family of endogenous neuropeptides that modulate neuronal cAMP-dependent protein kinase function.

Pharmacological characterization of novel water-soluble cannabinoids.

Determination of the role of conventional, novel and atypical PKC isoforms in the expression of morphine tolerance in mice.

How important is protein kinase C in mu-opioid receptor desensitization and morphine tolerance?

PKC and PKA inhibitors reinstate morphine-induced behaviors in morphine tolerant mice.

Decrease in N-methyl-D-aspartic acid receptor-NR2B subunit levels by intrathecal short-hairpin RNA blocks group I metabotropic glutamate receptor-mediated hyperalgesia.

Synthesis and pharmacological evaluation of phenylethynyl[1,2,4]methyltriazines as analogues of 3-methyl-6-(phenylethynyl)pyridine.

Evidence for an important role of protein phosphatases in the mechanism of morphine tolerance.

mGluR5 antagonists that block calcium mobilization in vitro also reverse (S)-3,5-DHPG-induced hyperalgesia and morphine antinociceptive tolerance in vivo.

Local production of O2- by NAD(P)H oxidase in the sarcoplasmic reticulum of coronary arterial myocytes: cADPR-mediated Ca2+ regulation.

Pre-treatment with a PKC or PKA inhibitor prevents the development of morphine tolerance but not physical dependence in mice.

Morphine tolerance in the mouse ileum and colon.

Formation and function of ceramide-enriched membrane platforms with CD38 during M1-receptor stimulation in bovine coronary arterial myocytes.

Design, synthesis, and biological evaluation of 6alpha- and 6beta-N-heterocyclic substituted naltrexamine derivatives as mu opioid receptor selective antagonists.

Chronic constriction injury reduces cannabinoid receptor 1 activity in the rostral anterior cingulate cortex of mice.

Role of CD38, a cyclic ADP-ribosylcyclase, in morphine antinociception and tolerance.

μ-opioid receptors: correlation of agonist efficacy for signalling with ability to activate internalization.

Chronic neuropathic pain in mice reduces μ-opioid receptor-mediated G-protein activity in the thalamus.

The role of β-arrestin2 in the mechanism of morphine tolerance in the mouse and guinea pig gastrointestinal tract.

Opioid-induced hypernociception is associated with hyperexcitability and altered tetrodotoxin-resistant Na+ channel function of dorsal root ganglia.

Differences in the characteristics of tolerance to μ-opioid receptor agonists in the colon from wild type and β-arrestin2 knockout mice.

Morphine efficacy is altered in conditional HIV-1 Tat transgenic mice.

6β-N-heterocyclic substituted naltrexamine derivative NAP as a potential lead to develop peripheral mu opioid receptor selective antagonists.

Production and actions of the anandamide metabolite prostamide E2 in the renal medulla.

Evidence for the putative cannabinoid receptor (GPR55)-mediated inhibitory effects on intestinal contractility in mice.

Characterization of 6α- and 6β-N-heterocyclic substituted naltrexamine derivatives as novel leads to development of mu opioid receptor selective antagonists.

Contribution of acid sphingomyelinase in the periaqueductal gray region to morphine-induced analgesia in mice.

Morphine decreases enteric neuron excitability via inhibition of sodium channels.

Design, synthesis, and biological evaluation of 17-cyclopropylmethyl-3,14β-dihydroxy-4,5α-epoxy-6β-[(4'-pyridyl)carboxamido]morphinan derivatives as peripheral selective μ opioid receptor Agents.

Electrophysiological characteristics of enteric neurons isolated from the immortomouse.

Ethanol reversal of cellular tolerance to morphine in rat locus coeruleus neurons.