Opioids inhibit the firing of neurons in the locus coeruleus.

Opioids work in the modulation of pleasure or pain relief by either blocking neurotransmitter release or by hyperpolarizing neurons by opening up a potassium channel which effectively temporarily blocks the neuron.

Opioids requiring Cytochrome P-450 activation ( e. g. codeine, dihydrocodeine ) should perhaps be used with an agent not chemically related to the SSRIs ; conversely, they may impact parts of the Liberation, Absorption, Distribution, Metabolism & Elimination profile for morphine, hydromorphone, oxymorphone & c the other way.

Opioids also may act on the gut indirectly through tonic gut spasms after inhibition of nitric oxide generation.

Opioids, while very effective analgesics, may have some unpleasant side-effects.

Opioids were used to treat major depression until the late 1950s.

* Opioids ' classical use besides pain relief is as an anti-diarrhoeal drug.

Opioids have agonist actions on the intestinal opioid receptors, which when activated cause constipation.

** Phenylpiperidine derivative Opioids: Meperidine / Pethidine, Tramadol, Methadone, Fentanyl, Dextropropoxyphene, Propoxyphene.

" Opioids: Past, Present and Future.

Opioids and opiate receptors occur naturally in crustaceans and, although at present no certain conclusion can be drawn, their presence indicates that lobsters may be able to experience pain.

Opioids may mediate their pain in the same way as in vertebrates.

Opioids include heroin ( diacetylmorphine, not used in medicine in most countries ), oxycodone, hydromorphone, hydrocodone ( Vicodin ), fentanyl, pethidine, tramadol and others.

Opioids can fragment sleep and decrease REM and stage 2 sleep.

Opioids such as morphine and heroin do not cause pupil dilation.

# Opioids, particularly methadone, are particularly effective treatments for the symptoms of severe RLS and do not have the negative side-effects ( augmentation and rebounding ) of dopamine agonists.

Opioids are efficacious analgesics in chronic malignant pain and modestly effective in nonmalignant pain management.

Opioids and anaesthetic drugs tend to depress ventilation, especially with regards to carbon dioxide response.

Opioids which have other neurotransmitter impacts such as tramadol, pethidine, & c. can also cause jerks, but unlike the above are not completely benign.

Opioids such as morphine are not used as the primary medicine since they are not effective sedative medications compared to benzodiazepines.

For more information on the palliative care use of sedatives and the safe use of opioids see Opioids.

Opioids are known to have strong antidepressive, anxiolytic and antipsychotic effects and thus opioid dependence often develops as a result of self medication.

In the mammalian cerebral cortex, a class of neurons called neurogliaform cells can inhibit other nearby cortical neurons by releasing the neurotransmitter GABA into the extracellular space.

In the classical sense, μ opioid receptors are presynaptic, and inhibit neurotransmitter release ; through this mechanism, they inhibit the release of the inhibitory neurotransmitter GABA, and disinhibit the dopamine pathways, causing more dopamine to be released.

The activated striatal neurons ( NAC neurons ) then project to the ventral pallidum where they inhibit the inhibitory GABA neurons.

This ability of GABA to inhibit neurotransmitter release from these preparations was not blocked by bicuculline, was not mimicked by isoguvacine, and was not dependent on Cl ¯, all of which are characteristic of the GABA < sub > A </ sub > receptor.

Neurotransmitters can inhibit impulse firing ( primarily done by γ-aminobutyric acid, or GABA ) or they can excite the neuron into firing ( primarily done by glutamate ).

Histamine H < sub > 3 </ sub > receptors are expressed in the central nervous system and to a lesser extent the peripheral nervous system, where they act as autoreceptors in presynaptic histaminergic neurons, and also control histamine turnover by feedback inhibition of histamine synthesis and release .< ref name =" pmid2172771 "> The H < sub > 3 </ sub > receptor has also been shown to presynaptically inhibit the release of a number of other neurotransmitters ( i. e. it acts as an inhibitory heteroreceptor ) including, but probably not limited to dopamine, GABA, acetylcholine, noradrenaline, and serotonin.

The VLPO neurons release the inhibitory neurotransmitters galanin and GABA to inhibit the monaminergic cell groups in the locus coeruleus, the raphe nucleus, and the tuberomammillary nucleus.

Medications that act on cell membrane ion channels, are GABA inhibitory neurotransmission, and also inhibit excitatory glutamate transmission have shown to be extremely effective in treating an array of child psychopathological disorders.

Norepinephrine-dopamine disinhibitors ( NDDIs ) act by antagonizing the serotonin 5-HT < sub > 2C </ sub > receptor, which normally acts to inhibit norepinephrine and dopamine release, thereby promoting outflow of these neurotransmitters.

Fas-induced apoptosis can be blocked by use of FLIPs ( FLICE-inhibitory proteins, which inhibit caspases-8 and-10 ), Bcl-2 ( which prevents cytochrome c release and the subsequent activation of caspase 9 ), and CrmA ( Cytokine response modifier A ).

To inhibit thyroid hormone release from the thyroid gland, sodium iodide, potassium iodide, and / or Lugol's solution can be given.

Long sequences of alternating glycine and alanine have been shown to inhibit substrate unfolding decreasing the efficiency of proteasomal degradation ; this results in the release of partially degraded byproducts, possibly due to the decoupling of the ATP hydrolysis and unfolding steps.

They suppress the release of cytokines and other inflammatory signals, and inhibit the production of reactive oxygen species.

Antihistamines ( or " histamine antagonists ") inhibit the release or action of histamine.

Many CB < sub > 1 </ sub > receptors are located on axon terminals, where they act to inhibit the release of various neurotransmitters.

Presynaptic receptors with an inhibitory potential are called autoreceptors and inhibit neurotransmitter synthesis and release.

Fentanyl binds μ-opioid G-protein-coupled receptors, which inhibit pain neurotransmitter release by decreasing intracellular Ca2 + levels.

Other drugs like octreotide ( somatostatin agonist ) and bromocriptine ( dopamine agonist ) can be used to block GH secretion because both somatostatin and dopamine negatively inhibit GHRH-mediated GH release from the anterior pituitary.

Antiandrogens can inhibit the release of the gonadotropic hormone, luteinizing hormone ( LH ), suppressing testosterone synthesis in the ovaries.

It travels across the median eminence to the anterior pituitary gland via the hypophyseal portal system where it stimulates the release of thyroid-stimulating hormone from cells called thyrotropes and excess levels inhibit dopamine which will then stimulate the release of prolactin which in turn decreases GnRH.

They are presynaptic neurotoxins that ( via sodium channels ) induce spontaneous, repetitive firing of action potentials in autonomic and motor neurons and inhibit neurally mediated transmitted release resulting in a surge of endogenous acetylcholine, noradrenaline and adrenaline.

The reason for this delay has not fully been elucidated, but it is believed to be due to many factors, including achieving steady-state levels of MAO inhibition and the resulting adaptations in mean neurotransmitter levels, the possibility of necessary desensitization of autoreceptors which normally inhibit the release of neurotransmitters like serotonin and dopamine, and also the upregulation of enzymes such as serotonin N-acetyltransferase.

On the contrary, however, the physiological effects of stress, often characterized by release of glucocorticoids such as cortisol, as well as activation of the sympathetic division of the autonomic nervous system, have been shown to inhibit the process of neurogenesis in primates.

Metabotropic receptors on the presynaptic membrane can inhibit or, more rarely, facilitate neurotransmitter release from the presynaptic neuron.

( The decreased calcium level slows the release of the neurotransmitter glutamate, which can either excite or inhibit the postsynaptic bipolar cells.

Also, when macula densa cells detect higher concentrations of Na and Cl they inhibit Nitric Oxide Synthetase ( decreasing renin release ) with an unknown pathway.

Projections from the raphe nuclei also terminate in the dorsal horn of spinal gray matter where they regulate the release of enkephalins, which inhibit pain sensation.