Opioids stop breathing during overdose by silencing two small brain sites, with just 140 neurons in the breathing rhythm generator exerting the key effect.

Activation of mu-opioid receptors in the nucleus accumbens by their endogenous ligands promotes consumption of high-fat food in sated but not hungry rats, via enhancement of a neural signal that promotes cued approach behavior.

The discovery that opioid neuropeptide neuronal signaling controls feeding behavior in a genetically tractable invertebrate model may help unravel the mechanisms of appetite control in humans.

Pro-nociceptive and pro-inflammatory TRPM3 (transient receptor potential melastatin 3) channels, expressed in somatosensory neurons, are inhibited by activation of Gαi-coupled receptors, such as µ-opioid receptors, in vitro and in vivo.

Chemically distinct opioid ligands promote selective protein recruitment by opioid receptors in intact cells.

The structure-based design established a new approach to control pathway-selective activation of opioid receptors, resulting in new dual MOR/KOR G-protein biased agonist analgesics with attenuated liabilities.

Rats exposed to a single stressful event experience days-long constitutive activation of the kappa opioid receptor at inhibitory synapses in part of the brain’s reward system, which increases their drug-seeking behavior.

Exogenous opioid analgesia is mediated by MORs expressed in glutamatergic neurons, whereas endogenous opioid analgesia is mediated by MORs expressed in GABAergic neurons.

By differentially modulating the two major excitatory inputs to the striatum, mu- and delta-opioid receptors regulate the balance between thalamic and cortical inputs to the striatum.

A novel opioid formulation producing analgesia similar to conventional opioids without permeation of blood-brain or intestinal barriers, thus precluding sedation, constipation and respiratory depression.