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{{BioPsy}}
  
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[[Image:Amphetamine-2D-skeletal.svg|thumb|right|200px|[[Amphetamine]], the prototypical releasing agent, which acts on norepinephrine and dopamine.]]
  
   
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A '''releasing agent''' ('''RA'''), or simply '''releaser''', is a [[drug]] that induces the [[synapse|release]] of a [[neurotransmitter]] from the [[synapse|presynaptic neuron]] into the [[synapse]], leading to an increase in the [[extracellular]] [[concentration]]s of the [[neurotransmitter]]. Many drugs use [[neurotransmitter]] [[synapse|release]] to exert their [[psychological]] and [[physiological]] effects, namely the [[amphetamine]]s and related [[chemical compound|compound]]s. The vast majority of currently known releasing agents work on the [[monoamine]] neurotransmitters [[serotonin]], [[norepinephrine]], and [[dopamine]].
 +
A '''releasing agent''' ('''RA'''), or simply '''releaser''', is a [[drug]] that induces the [[synapse|release]] of a [[neurotransmitter]] from the [[synapse|presynaptic neuron]] into the [[synapse]], leading to an increase in the [[extracellular]] [[concentration]]s of the [[neurotransmitter]]. Many drugs use [[neurotransmitter]] [[synapse|release]] to exert their [[psychological]] and [[physiological]] effects, namely the [[amphetamine]]s and related [[chemical compound|compounds]]. The vast majority of currently known releasing agents work on the [[monoamine]] neurotransmitters [[serotonin]], [[norepinephrine]], and [[dopamine]].
   
 
== Mechanism of action ==
  
== Mechanism of action ==
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== Neurotoxicity ==
  
== Neurotoxicity ==
   
−
A number of releasing agents, notably many of those derived from [[amphetamine]], have been found to be [[neurotoxic]] to [[serotonin]] and/or [[dopamine]] [[neurons]] via damage to [[axon]]s and [[dendrite]]s, [[enzyme]]s, [[mitochondria]], [[DNA]], [[membrane transport protein|plasmalemmal]] and [[vesicular transport protein|vesicular transporter]]s, and the [[cell membrane]], ultimately causing [[cell death]] or [[apoptosis]] as a result. Examples include amphetamine, [[methamphetamine]], [[methylenedioxymethamphetamine|MDMA]], [[fenfluramine]], and [[parachloroamphetamine|PCA]], among others. In contrast, [[piperazine]], [[indane|aminoindane]], and [[oxazoline]] releasing agents, as well as those from various other [[chemical family|chemical families]], are considered to be either fully non[[toxicity|toxic]], or significantly less [[toxicity|toxic]] in comparison.{{Citation needed|date=August 2010}}
 +
A number of releasing agents, notably many of those derived from [[amphetamine]], have been found to be [[neurotoxic]] to [[serotonin]] and/or [[dopamine]] [[neurons]] via damage to [[axon]]s and [[dendrite]]s, [[enzyme]]s, [[mitochondria]], [[DNA]], [[membrane transport protein|plasmalemmal]] and [[vesicular transport protein|vesicular transporters]], and the [[cell membrane]], ultimately causing [[cell death]] or [[apoptosis]] as a result. Examples include amphetamine, [[methamphetamine]], [[methylenedioxymethamphetamine|MDMA]], [[fenfluramine]], and [[parachloroamphetamine|PCA]], among others. In contrast, [[piperazine]], [[indane|aminoindane]], and [[oxazoline]] releasing agents, as well as those from various other [[chemical family|chemical families]], are considered to be either fully non[[toxicity|toxic]], or significantly less [[toxicity|toxic]] in comparison.{{Citation needed|date=August 2010}}
   
 
The neurotoxicity of some of these drugs is believed to be caused by [[oxidative stress]] induced by the generation of [[reactive oxygen species]] or [[free radical]]s, highly [[reactivity (chemistry)|reactive]] [[particle]]s that rip apart [[protein]]s and induce [[chain reaction]]s of destruction. The [[free radical]]s are thought to be generated as [[byproduct]]s when either the base [[chemical compound|compound]] or one or more of its [[metabolite]]s are broken down by the [[enzyme]]s [[monoamine oxidase]] (MAO-B) and/or [[cyclooxygenase]] (COX), among others, from within the presynaptic cell. [[Hyperthermia]] and simultaneous serotonin and dopamine release may play a major role in augmenting the damage as well.
  
The neurotoxicity of some of these drugs is believed to be caused by [[oxidative stress]] induced by the generation of [[reactive oxygen species]] or [[free radical]]s, highly [[reactivity (chemistry)|reactive]] [[particle]]s that rip apart [[protein]]s and induce [[chain reaction]]s of destruction. The [[free radical]]s are thought to be generated as [[byproduct]]s when either the base [[chemical compound|compound]] or one or more of its [[metabolite]]s are broken down by the [[enzyme]]s [[monoamine oxidase]] (MAO-B) and/or [[cyclooxygenase]] (COX), among others, from within the presynaptic cell. [[Hyperthermia]] and simultaneous serotonin and dopamine release may play a major role in augmenting the damage as well.
   
−
These observations are supported by the facts that [[antioxidant]]s such as [[ascorbic acid]], [[Monoamine oxidase inhibitor|MAO-B inhibitors]] like [[selegiline]], drugs that induce [[hypothermia]] such as [[5-HT2 receptor|5-HT<sub>2</sub>]], [[D2 receptor|D<sub>2</sub>]], [[β-adrenergic receptor|β-adrenergic]], and [[NMDA receptor|NMDA]] [[receptor (biochemistry)|receptor]] [[receptor antagonist|antagonist]]s, as well as [[GABAA receptor|GABA<sub>A</sub>]] and [[GABAB receptor|GABA<sub>B</sub>]] receptor [[agonist]]s, and [[serotonin reuptake inhibitor]]s and [[dopamine reuptake inhibitor]]s, respectively, are [[neuroprotective]], and can help reduce damage caused by neurotoxic releasing agents.
 +
These observations are supported by the facts that [[antioxidant]]s such as [[ascorbic acid]], [[Monoamine oxidase inhibitor|MAO-B inhibitors]] like [[selegiline]], drugs that induce [[hypothermia]] such as [[5-HT2 receptor|5-HT<sub>2</sub>]], [[D2 receptor|D<sub>2</sub>]], [[β-adrenergic receptor|β-adrenergic]], and [[NMDA receptor|NMDA]] [[receptor (biochemistry)|receptor]] [[receptor antagonist|antagonists]], as well as [[GABAA receptor|GABA<sub>A</sub>]] and [[GABAB receptor|GABA<sub>B</sub>]] receptor [[agonist]]s, and [[serotonin reuptake inhibitor]]s and [[dopamine reuptake inhibitor]]s, respectively, are [[neuroprotective]], and can help reduce damage caused by neurotoxic releasing agents.
   
 
== List of releasing agents ==
  
== List of releasing agents ==
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<div style="-moz-column-count:2; column-count:2; -webkit-column-count:2;">
  
<div style="-moz-column-count:2; column-count:2; -webkit-column-count:2;">
   
−
; [[Organic compound|Natural compound]]s
 +
; [[Organic compound|Natural compounds]]
 
* [[Cathine]] (found in ''[[Catha edulis]]'' (Khat))
  
* [[Cathine]] (found in ''[[Catha edulis]]'' (Khat))
 
* [[Cathinone]] (found in ''[[Catha edulis]]'' (Khat))
  
* [[Cathinone]] (found in ''[[Catha edulis]]'' (Khat))
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; [[Pharmaceutical drug]]s
  
; [[Pharmaceutical drug]]s
−
* [[Substituted amphetamine|Amphetamine]]s
 +
* [[Substituted amphetamine|Amphetamines]]
 
** [[Amphetamine]] (Adderall, Dexedrine; "Speed")
  
** [[Amphetamine]] (Adderall, Dexedrine; "Speed")
 
** [[Benzphetamine]] (Didrex)
  
** [[Benzphetamine]] (Didrex)
Line 132: Line 131:
 
* [[Tryptamine]]<ref name="pmid1570019"/>
  
* [[Tryptamine]]<ref name="pmid1570019"/>
 
* [[Tyramine]]<ref name="pmid2500604"/>
  
* [[Tyramine]]<ref name="pmid2500604"/>
−  
 
</div>
  
</div>
−  
 
== Comparison of binding profiles ==
  
== Comparison of binding profiles ==
   
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{| class="wikitable sortable"
  
{| class="wikitable sortable"
−
| ''' Compound ''' || '''[[Norepinephrine|NA]] (Release)''' || '''[[Dopamine|DA]] (Release)''' || '''[[Serotonin|5-HT]] (Release)'''
 +
| '''Compound ''' || '''[[Norepinephrine|NA]] (Release)''' || '''[[Dopamine|DA]] (Release)''' || '''[[Serotonin|5-HT]] (Release)'''
−
|-
 +
|-
−
| [[4-Fluoroamphetamine]] || 28 || 51.5 || 939
 +
| [[4-Fluoroamphetamine]] || 28 || 51.5 || 939
−
|-
 +
|-
−
| [[4-Methylamphetamine]] || 22.2 || 44.1 || 53.4
 +
| [[4-Methylamphetamine]] || 22.2 || 44.1 || 53.4
−
|-
 +
|-
−
| [[Aminorex]] || 26.4 || 49.4 || 193
 +
| [[Aminorex]] || 26.4 || 49.4 || 193
−
|-
 +
|-
−
| [[Amphetamine|(d)-Amphetamine]] || 7.07 || 24.8 || 1,765
 +
| [[Amphetamine|(d)-Amphetamine]] || 7.07 || 24.8 || 1,765
−
|-
 +
|-
−
| [[Benzylpiperazine]] || 62 || 175 || 6,050
 +
| [[Benzylpiperazine]] || 62 || 175 || 6,050
−
|-
 +
|-
−
| [[Cathine]] || 15.0 || 68.3 || -
 +
| [[Cathine]] || 15.0 || 68.3 || -
−
|-
 +
|-
−
| [[Cathinone|(l)-Cathinone]] || 12.4 || 18.5 || 2,366
 +
| [[Cathinone|(l)-Cathinone]] || 12.4 || 18.5 || 2,366
−
|-
 +
|-
−
| [[Chlorphentermine]] || - || 2,650 || 30.9
 +
| [[Chlorphentermine]] || - || 2,650 || 30.9
−
|-
 +
|-
−
| [[Ephedrine]] || 130.5 || 1,170 || -
 +
| [[Ephedrine]] || 130.5 || 1,170 || -
−
|-
 +
|-
−
| [[Fenfluramine]] || 739 || - || 79.3
 +
| [[Fenfluramine]] || 739 || - || 79.3
−
|-
 +
|-
−
| [[Methamphetamine|(d)-Methamphetamine]] || 12.3 || 24.5 || 736
 +
| [[Methamphetamine|(d)-Methamphetamine]] || 12.3 || 24.5 || 736
−
|-
 +
|-
−
| [[Levomethamphetamine|(l)-Methamphetamine]] || 28.5 || 416 || 4,640
 +
| [[Levomethamphetamine|(l)-Methamphetamine]] || 28.5 || 416 || 4,640
−
|-
 +
|-
−
| [[Methcathinone|(l)-Methcathinone]] || 13.1 || 14.8 || 1,772
 +
| [[Methcathinone|(l)-Methcathinone]] || 13.1 || 14.8 || 1,772
−
|-
 +
|-
−
| [[Methylenedioxyamphetamine|MDA]] || 108 || 190 || 160
 +
| [[Methylenedioxyamphetamine|MDA]] || 108 || 190 || 160
−
|-
 +
|-
−
| [[Methylenedioxymethamphetamine|MDMA]] || 110 || 278 || 72
 +
| [[Methylenedioxymethamphetamine|MDMA]] || 110 || 278 || 72
−
|-
 +
|-
−
| [[Naphthylaminopropane]] || 11.1 || 12.6 || 3.4
 +
| [[Naphthylaminopropane]] || 11.1 || 12.6 || 3.4
−
|-
 +
|-
−
| [[Norfenfluramine]] || 168 || 1,925 || 104
 +
| [[Norfenfluramine]] || 168 || 1,925 || 104
−
|-
 +
|-
−
| [[Phenmetrazine]] || 50.4 || 131 || 7,765
 +
| [[Phenmetrazine]] || 50.4 || 131 || 7,765
−
|-
 +
|-
−
| [[Phentermine]] || 39.4 || 262 || 3,511
 +
| [[Phentermine]] || 39.4 || 262 || 3,511
−
|-
 +
|-
−
| [[Phenylpropanolamine]] || 89.5 || 836.6 || -
 +
| [[Phenylpropanolamine]] || 89.5 || 836.6 || -
−
|-
 +
|-
−
| [[Pseudoephedrine]] || 2,158 || 5,556.6 || -
 +
| [[Pseudoephedrine]] || 2,158 || 5,556.6 || -
−
|-
 +
|-
−
| [[Tyramine]] || 40.6 || 119 || 2,775
 +
| [[Tyramine]] || 40.6 || 119 || 2,775
−
|-
  
 
|}
  
|}
   
−
The values above are expressed as [[dissociation constant|equilibrium dissociation constant]]s ([[Half maximal effective concentration|EC<sub>50</sub>]] ([[nanomolar|nM]])). Lower values correspond to higher binding at the site, or in other words, less is more. NE, DA, and 5-HT correspond to the abilities of the compounds to induce the release of [[norepinephrine]], [[dopamine]], and [[serotonin]], respectively. All compounds listed are [[racemic]] unless noted otherwise.
 +
The values above are expressed as [[dissociation constant|equilibrium dissociation constants]] ([[Half maximal effective concentration|EC<sub>50</sub>]] ([[nanomolar|nM]])). Lower values correspond to higher binding at the site, or in other words, less is more. NE, DA, and 5-HT correspond to the abilities of the compounds to induce the release of [[norepinephrine]], [[dopamine]], and [[serotonin]], respectively. All compounds listed are [[racemic]] unless noted otherwise.
   
 
== See also ==
  
== See also ==

Latest revision as of 16:28, 14 April 2015

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A releasing agent (RA), or simply releaser, is a drug that induces the release of a neurotransmitter from the presynaptic neuron into the synapse, leading to an increase in the extracellular concentrations of the neurotransmitter. Many drugs use neurotransmitter release to exert their psychological and physiological effects, namely the amphetamines and related compounds. The vast majority of currently known releasing agents work on the monoamine neurotransmitters serotonin, norepinephrine, and dopamine.

Mechanism of action

Releasing agents cause the release of monoamine neurotransmitters by a complex mechanism of action. First, they penetrate the presynaptic cell primarily by being taken up as a substrate by binding to the plasmalemmal transporter(s), including the dopamine transporter (DAT), norepinephrine transporter (NET), and/or serotonin transporter (SERT). Some, such as amphetamine and methamphetamine, can also diffuse directly across the cell membrane to varying degrees. Next, they inhibit the vesicular reuptake of the neurotransmitter by the vesicular monoamine transporter 2 (VMAT2)[1] (via binding or pH-gradient), and thus inhibit the repackaging of the neurotransmitter(s) from the cytoplasm into vesicles. Finally, releasing agents reverse the action of the plasmalemmal transporter(s) via a process known as phosphorylation, allowing the neurotransmitter(s) to flow out from the cytoplasm into the nerve terminal or synapse. This leads to an increase in the extracellular concentrations of dopamine, norepinephrine, and/or serotonin, and therefore an increase in overall monoaminergic neurotransmission.

Releasing agents also function as reuptake inhibitors to varying extents due to their competitive plasmalemmal transporter affinity and binding, and this property plays a role in their overall effects.

Neurotoxicity

A number of releasing agents, notably many of those derived from amphetamine, have been found to be neurotoxic to serotonin and/or dopamine neurons via damage to axons and dendrites, enzymes, mitochondria, DNA, plasmalemmal and vesicular transporters, and the cell membrane, ultimately causing cell death or apoptosis as a result. Examples include amphetamine, methamphetamine, MDMA, fenfluramine, and PCA, among others. In contrast, piperazine, aminoindane, and oxazoline releasing agents, as well as those from various other chemical families, are considered to be either fully nontoxic, or significantly less toxic in comparison.[citation needed]

The neurotoxicity of some of these drugs is believed to be caused by oxidative stress induced by the generation of reactive oxygen species or free radicals, highly reactive particles that rip apart proteins and induce chain reactions of destruction. The free radicals are thought to be generated as byproducts when either the base compound or one or more of its metabolites are broken down by the enzymes monoamine oxidase (MAO-B) and/or cyclooxygenase (COX), among others, from within the presynaptic cell. Hyperthermia and simultaneous serotonin and dopamine release may play a major role in augmenting the damage as well.

These observations are supported by the facts that antioxidants such as ascorbic acid, MAO-B inhibitors like selegiline, drugs that induce hypothermia such as 5-HT2, D2, β-adrenergic, and NMDA receptor antagonists, as well as GABAA and GABAB receptor agonists, and serotonin reuptake inhibitors and dopamine reuptake inhibitors, respectively, are neuroprotective, and can help reduce damage caused by neurotoxic releasing agents.

List of releasing agents

Natural compounds
Pharmaceutical drugs
Designer drugs
  • 4-Fluoroamphetamine (4-FA)[3]
  • 4-Fluoromethcathinone (4-FMC; Flephedrone)
  • 4-Methoxyphenylpiperazine (MeOPP; Paraperazine)[3]
  • 4-Methylaminorex (4-MAR; "Ice", "EU4EUH")
  • 4-Methylmethcathinone (4-MMC; Mephedrone)
  • 4-Methylthioamphetamine (4-MTA)
  • 5-Methoxyalphaethyltryptamine (5-MeO-AET)
  • 5-Methoxyalphamethyltryptamine (5-MeO-AMT)[3]
  • β-Keto-Methylbenzodioxolbutanamine (bk-MBDB; Butylone)
  • Benzodioxylbutanamine (BDB)[3]
  • Benzylpiperazine (BZP)[9]
  • meta-Chlorophenylpiperazine (mCPP)[3][10][11]
  • Methcathinone
  • Methylbenzodioxolbutanamine (MBDB)
  • Methylbenzylpiperazine (MBZP)
  • Methylenedioxyamphetamine (MDA)
  • Methylenedioxybenzylpiperazine (MDBZP)
  • Methylenedioxyethylamphetamine (MDEA)
  • Methylenedioxyethylcathinone (MDEC, bk-MDEA; Ethylone)
  • Methylenedioxymethamphetamine (MDMA; "Ecstasy", "Adam")
  • Methylenedioxymethcathinone (MDMC, bk-MDMA; Methylone)[3]
  • Methylenedioxymethoxyamphetamine (MMDA)
  • para-Fluorophenylpiperazine (pFPP; Fluoperazine)
  • para-Methoxyamphetamine (PMA)
  • para-Methoxyethylamphetamine (PMEA)
  • para-Methoxymethamphetamine (PMMA)
  • para-Methoxymethcathinone (bk-PMMA; Methedrone)
  • Trifluoromethylphenylpiperazine (TFMPP)[9]
Research chemicals
  • 2-Aminodilin (2-AD)
  • 2-Aminoindane (2-AI)
  • 2-Aminotetralin (2-AT)
  • 4-Benzylpiperidine (4-BP)
  • 4-Methylamphetamine (4-MA)
  • 4-Methylmethamphetamine (4-MMA)
  • 5-Aminopropyldihydrobenzofuran (5-APDB)
  • 5-Carboxamidotryptamine (5-CT)[12]
  • 5-Methoxytryptamine (5-MT)[12]
  • 8-Hydroxydipropylaminotetralin (8-OH-DPAT)[12]
  • Clominorex
  • Cyclazodone
  • Cypenamine
  • D-Deprenyl
  • Dimethylamphetamine
  • Ethyltrifluoromethylaminoindane (ETAI)
  • Fluminorex
  • Indanylaminopropane (IAP)
  • Methoxymethamphetamine (MMA)
  • Methoxymethylaminoindane (MMAI)
  • Methylenedioxyaminoindane (MDAI)
  • Methylenedioxymethylaminoindane (MDMAI)
  • Naphthylaminopropane (NAP; PAL-287)
  • para-Bromoamphetamine (PBA)
  • para-Chloroamphetamine (PCA)
  • para-Iodoamphetamine (PIA)
  • Propylamphetamine
  • Thozalinone
  • Trifluoromethylaminoindane (TAI)
Trace amines

Comparison of binding profiles

The selectivities of a number of releasing agents have been compared below:[14][15][16][17][18]

Compound NA (Release) DA (Release) 5-HT (Release)
4-Fluoroamphetamine 28 51.5 939
4-Methylamphetamine 22.2 44.1 53.4
Aminorex 26.4 49.4 193
(d)-Amphetamine 7.07 24.8 1,765
Benzylpiperazine 62 175 6,050
Cathine 15.0 68.3 -
(l)-Cathinone 12.4 18.5 2,366
Chlorphentermine - 2,650 30.9
Ephedrine 130.5 1,170 -
Fenfluramine 739 - 79.3
(d)-Methamphetamine 12.3 24.5 736
(l)-Methamphetamine 28.5 416 4,640
(l)-Methcathinone 13.1 14.8 1,772
MDA 108 190 160
MDMA 110 278 72
Naphthylaminopropane 11.1 12.6 3.4
Norfenfluramine 168 1,925 104
Phenmetrazine 50.4 131 7,765
Phentermine 39.4 262 3,511
Phenylpropanolamine 89.5 836.6 -
Pseudoephedrine 2,158 5,556.6 -
Tyramine 40.6 119 2,775

The values above are expressed as equilibrium dissociation constants (EC50 (nM)). Lower values correspond to higher binding at the site, or in other words, less is more. NE, DA, and 5-HT correspond to the abilities of the compounds to induce the release of norepinephrine, dopamine, and serotonin, respectively. All compounds listed are racemic unless noted otherwise.

See also

References

  1. ↑ Question: Is release restricted to MAs only?
  2. ↑ Krebs KM, Geyer MA (1993). Behavioral characterization of alpha-ethyltryptamine, a tryptamine derivative with MDMA-like properties in rats. Psychopharmacology 113 (2): 284–7.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Nagai F, Nonaka R, Satoh Hisashi Kamimura K (March 2007). The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain. European Journal of Pharmacology 559 (2-3): 132–7.
  4. ↑ Marsden CA (November 1979). Evidence for the release of hippocampal 5-hydroxytryptamine by alpha-methyltryptamine [proceedings]. British Journal of Pharmacology 67 (3): 438P–439P.
  5. ↑ Yamaguchi T, Ohyama M, Suzuki M, et al. (September 1998). Neurochemical and behavioral characterization of potential antidepressant properties of indeloxazine hydrochloride. Neuropharmacology 37 (9): 1169–76.
  6. ↑ Driessen B, Reimann W (January 1992). Interaction of the central analgesic, tramadol, with the uptake and release of 5-hydroxytryptamine in the rat brain in vitro. British Journal of Pharmacology 105 (1): 147–51.
  7. ↑ Bamigbade TA, Davidson C, Langford RM, Stamford JA (September 1997). Actions of tramadol, its enantiomers and principal metabolite, O-desmethyltramadol, on serotonin (5-HT) efflux and uptake in the rat dorsal raphe nucleus. British Journal of Anaesthesia 79 (3): 352–6.
  8. ↑ Reimann W, Schneider F (May 1998). Induction of 5-hydroxytryptamine release by tramadol, fenfluramine and reserpine. European Journal of Pharmacology 349 (2-3): 199–203.
  9. ↑ 9.0 9.1 Baumann MH, Clark RD, Budzynski AG, Partilla JS, Blough BE, Rothman RB (October 2004). Effects of "Legal X" piperazine analogs on dopamine and serotonin release in rat brain. Annals of the New York Academy of Sciences 1025: 189–97.
  10. ↑ Eriksson E, Engberg G, Bing O, Nissbrandt H (March 1999). Effects of mCPP on the extracellular concentrations of serotonin and dopamine in rat brain. Neuropsychopharmacology 20 (3): 287–96.
  11. ↑ Baumann MH, Ayestas MA, Dersch CM, Rothman RB (May 2001). 1-(m-chlorophenyl)piperazine (mCPP) dissociates in vivo serotonin release from long-term serotonin depletion in rat brain. Neuropsychopharmacology 24 (5): 492–501.
  12. ↑ 12.0 12.1 12.2 12.3 Wölfel R, Graefe KH (February 1992). Evidence for various tryptamines and related compounds acting as substrates of the platelet 5-hydroxytryptamine transporter. Naunyn-Schmiedeberg's Archives of Pharmacology 345 (2): 129–36.
  13. ↑ 13.0 13.1 Schönfeld CL, Trendelenburg U (April 1989). The release of 3H-noradrenaline by p- and m-tyramines and -octopamines, and the effect of deuterium substitution in alpha-position. Naunyn-Schmiedeberg's Archives of Pharmacology 339 (4): 433–40.
  14. ↑ Rothman RB, Baumann MH, Dersch CM, Romero DV, Rice KC, Carroll FI et al. (2001). Amphetamine-type central nervous system stimulants release norepinephrine more potently than they release dopamine and serotonin.. Synapse 39 (1): 32–41.
  15. ↑ Rothman RB, Baumann MH (2006). Therapeutic potential of monoamine transporter substrates.. Curr Top Med Chem 6 (17): 1845–59.
  16. ↑ Rothman RB, Vu N, Partilla JS, Roth BL, Hufeisen SJ, Compton-Toth BA et al. (2003). In vitro characterization of ephedrine-related stereoisomers at biogenic amine transporters and the receptorome reveals selective actions as norepinephrine transporter substrates.. J Pharmacol Exp Ther 307 (1): 138–45.
  17. ↑ Rothman RB, Blough BE, Woolverton WL, Anderson KG, Negus SS, Mello NK et al. (2005). Development of a rationally designed, low abuse potential, biogenic amine releaser that suppresses cocaine self-administration.. J Pharmacol Exp Ther 313 (3): 1361–9.
  18. ↑ Wee S, Anderson KG, Baumann MH, Rothman RB, Blough BE, Woolverton WL (2005). Relationship between the serotonergic activity and reinforcing effects of a series of amphetamine analogs.. J Pharmacol Exp Ther 313 (2): 848–54.

Template:Releasers

v·d·e
Neuromodulation
Types
Classes

see Enzyme inhibition

Calcium channel blocker (CCB) • Potassium channel blocker (PCB) • Sodium channel blocker (SCB) • Potassium channel opener (PCO)



Adrenergic receptor agonist (α, β (1, 2)) • Adrenergic receptor antagonist (α (1, 2), β) • Adrenergic reuptake inhibitor (ARI)

Dopamine receptor agonist • Dopamine receptor antagonist • Dopamine reuptake inhibitor (DRI)

Histamine receptor agonist • Histamine receptor antagonist (H1, H2, H3)

Serotonin receptor agonist • Serotonin Receptor Antagonist (5-HT3) • Serotonin reuptake inhibitor (SRI) • Serotonin reuptake enhancer (SRE)



GABA receptor agonist • GABA receptor antagonist • GABA reuptake inhibitor (GRI)

Glutamate receptor agonist (AMPA) • Glutamate receptor antagonist (NMDA)


Acetylcholine receptor agonist (Muscarinic, Nicotinic) • Acetylcholine receptor antagonist (Muscarinic, Nicotinic (Ganglionic, Muscular))

Cannabinoid receptor agonist • Cannabinoid receptor antagonist

Opioid receptor agonist • Opioid receptor antagonist

Other

Adenosine reuptake inhibitor (AdoRI) • Angiotensin II receptor antagonist • Endothelin receptor antagonist • NK1 receptor antagonist • Vasopressin receptor antagonist


Miscellaneous

Cofactor (see Enzyme cofactors) • Precursor (see Amino acids)

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