Opioids inhibit GABA release ; this decreases the amount of inhibition and allows them to fire spontaneously.

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, 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.

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

** 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 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 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.

These receptors, which exist in a variety of areas in the body, inhibit firing of neurons that would otherwise be stimulated to do so by nociceptors.

The earliest PALs were little more than locks introduced into the control and firing systems of a nuclear weapon, that would inhibit either the detonation, or the removal of safety features of the weapon.

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.

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 ).

He has made a long study of visual inhibition, the process whereby a neuron firing in response to one group of retinal cells can inhibit the firing of another neuron ; this allows perception of relative contrast.

Unlike many other anticonvulsants, primidone works via interactions with voltage-gated sodium channels which inhibit high-frequency repetitive firing of action potentials.

The central analgesia system is mediated by 3 major components: the periaquaductal grey matter, the nucleus raphe magnus and the nociception inhibitory neurons within the dorsal horns of the spinal cord, which act to inhibit nociception-transmitting neurons also located in the spinal dorsal horn.

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.

Neurons send excitatory fibers to neurons in the thalamus and also from collateral to them ones via the thalamic reticular nucleus that inhibit these thalamus neurons or ones adjacent to them.

Neurotoxin activity can be characterized by the ability to inhibit neuron control over ion concentrations across the cell membrane, or communication between neurons across a synapse.

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

There is also some evidence for postsynaptic receptors on sympathetic neurons allowing the parasympathetic nervous system to inhibit sympathetic effects.

Dopaminergic neurons of the arcuate also inhibit the release of gonadotropin-releasing hormone, explaining in part why lactating ( or otherwise hyperprolactinemic ) women experience oligomenorrhea or amenorrhea ( infrequency or absence of menses ).

Photoreceptors that are part of the receptive fields of more than one ganglion cell are able to excite or inhibit postsynaptic neurons because they release the neurotransmitter glutamate at their synapses, which can act to depolarize or to hyperpolarize a cell, depending on the ion channels it opens.

There, they synapse with interneurons, which, in turn, excite or inhibit alpha motor neurons to the muscles of the contralateral limb.

These neurons activate descending pathways that synapse in the spinal cord and inhibit nociceptive cells in the dorsal horn.

Other brainstem sites, such as the parabrachial nucleus, the dorsal raphe, locus coeruleus, and the medullary reticular formation also mediate pain relief and use many different neurotransmitters to either facilitate or inhibit activity of the neurons in the dorsal horn.

Organophosphates inhibit an enzyme called acetylcholinesterase, causing a build up of acetylcholine, excessive stimulation of all types of cholinergic neurons, and a wide range of symptoms.

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.

They are primarily active during Non-rapid eye movement sleep, and inhibit other neurons that are involved in wakefulness.

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.

As an example, norepinephrine released from sympathetic neurons may interact with alpha-2A and alpha-2C receptors to inhibit neurally released norepinephrine.

Similarly, acetylcholine released from parasympathetic neurons may interact with muscarinic-2 and muscarinic-4 receptors to inhibit neurally released acetylcholine.