Characteristics of Antinociception Induced by Noncatecholic Phenylethylamine Derivatives: The Relation of Endogenous Norepinephrine to Phenylethylamine Analog-Induced Antinociception

Matsuoka, Yutaka; Sakuma, Mayumi; Sugioka, Toshihiko; Terawaki, Yasufumi; Uruno, Tsutomu; Kubota, Keiichi

doi:10.1254/jjp.48.263

Cited by 4 publications

(4 citation statements)

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“…PEA decreased norepinephrine in the brain and tended to increase the norepinephrine metabolite normetanephrine 15 minutes after administration, indicating a release of norepinephrine in the central nervous system, inducing antinociception. 19 To evaluate the hypothesis that norepinephrine is involved in mediating peripheral cannabinoid antinociception in our model, we studied this effect in rats treated with guanethidine, a depletor of peripheral sympathomimetic amines, 28 and the norepinephrine reuptake inhibitor, reboxetine. 67 Without the presence of norepinephrine, guanethidine induced an approximately 70% reversal of the peripheral effect of anandamide and PEA.…”

Section: Anesthesia and Analgesiamentioning

confidence: 99%

“…18 Three lines of evidence suggesting an antinociceptive interaction between the adrenergic and the cannabinoid systems have also been proposed. [19][20][21] First, both α 2 adrenoceptor and cannabinoid receptors induce antinociception through inhibition of postsynaptic membrane excitation, Ca 2+ -inducing neurotransmitter release, [22][23][24] and the opening of adenosine triphosphate-sensitive K + channels. 7,25 Second, some cannabinoid receptor agonists, such as N-palmitoylethanolamine (PEA), release norepinephrine in the central nervous system, inducing antinociception.…”

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confidence: 99%

“…7,25 Second, some cannabinoid receptor agonists, such as N-palmitoylethanolamine (PEA), release norepinephrine in the central nervous system, inducing antinociception. 19 Third, there is synergy in the antinociceptive effect between the cannabinoid agonist WIN 55,212-2 and the α 2 adrenoceptor agonist clonidine at the spinal level. 21 The aim of this study was to determine whether the CB 1 and CB 2 cannabinoid agonists anandamide and PEA, respectively, induce peripheral antinociception through an interaction with the endogenous noradrenergic system.…”

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confidence: 99%

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CB1 and CB2 Cannabinoid Receptor Agonists Induce Peripheral Antinociception by Activation of the Endogenous Noradrenergic System

Romero

Resende²,

Guzzo³

et al. 2013

Anesthesia &Amp; Analgesia

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Section: Anesthesia and Analgesiamentioning

confidence: 99%

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CB1 and CB2 Cannabinoid Receptor Agonists Induce Peripheral Antinociception by Activation of the Endogenous Noradrenergic System

Romero

Resende²,

Guzzo³

et al. 2013

Anesthesia &Amp; Analgesia

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“…Amphetamine, one of the noncatecholic phenylethylamine derivatives, produces a slight but significant antinociceptive action (5). We (6,7) have also reported that PEA derivatives such as PEA, OHPEA and amphetamine have antinociceptive action which may involve endogenous serotonin, norepineph rine and opioid peptides.…”

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confidence: 94%

Characteristics of Antinociception Induced by Noncatecholic Phenylethylamine Derivatives: The Involvement of Alpha-2-Adrenoceptors

Matsuoka

Sugioka

Terawaki

et al. 1993

Japanese Journal of Pharmacology

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ABSTRACT-Characteristicsof the antinociceptive action of phenylethylamine derivatives, amphetamine, (3-phenylethylamine (PEA) and (3-hydroxyphenylethylamine (OHPEA), were examined. The antinocicep tion induced by PEA derivatives was enhanced by intracisternal injection of norepinephrine or clonidine and attenuated by intracisternal injection of phentolamine or yohimbine, but was not affected by intracister nal injection of prazosin in the mouse hot plate method. PEA derivatives induced a contraction of the rat vas deferens, and this contraction by PEA derivatives was attenuated by the application of phentolamine. The contractions induced by PEA or OHPEA in the reserpinized vas deferens were much smaller than those in the normal one. PEA derivatives inhibited the electrical stimulation-evoked contractions of the vas deferens, and the inhibition by PEA derivatives was reversed by the application of yohimbine. These findings indicate that PEA derivatives may induce the antinociception as a result of stimulating the a2 adrenoceptors. The stimulation of a2-adrenoceptors by PEA derivatives may result from the release of endo genous norepinephrine and/or from direct action on the a2-adrenoceptors.

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Analgesic Effects of β-Phenylethylamine and Various Methylated Derivatives in Mice

Mosnaim

Hudzik

Wolf³

2014

Neurochem Res

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Administration of β-phenylethylamine (PEA), the simplest endogenous neuroamine, and various methylated PEA derivatives including α-methyl PEA (amphetamine, AMP) elicits analgesia in mice. Five or 20 min after intraperitoneal PEA injection of as little as 6 mg/kg resulted in an increased latency response time (from 2.4 ± 0.4 to 8.5 ± 2.3 or 7.0 ± 3.0 s, respectively) to the thermal stimulus (hot-plate test), which reached statistical significance at the 15 mg/kg (20 min; 13.1 ± 0.4 s) or 25 mg/kg dose (5 min; 15.3 ± 4.1 s). This PEA effect, was dose-dependent (albeit non-linear: 6, 12, 15, 25, 50 and 100 mg/kg), reached the cut-off time of 45 s at the upper PEA dose (5 min), and it was consistently enhanced by pretreatment with the monoamine oxidase inhibitor pargyline (P). Methylated PEA derivatives (15 and 100 mg/kg dose) produced various degrees of analgesia (in decreasing order p-Me PEA > PEA > N,N-diMe PEA > N-Me PEA) which, likewise to PEA itself, were consistently increased by P and declined over time (mice tested 5, 20 and 60 min after amine injection); small but statistically significant o- and β-Me PEA antinociceptive effects (5 min) were observed only at the higher dose (in the presence of P for β-Me PEA). A small analgesic effect was observed after the administration of AMP (5 or 10 mg/kg) which failed, even after P, to reach statistically significance. Independent of the amine and concentration tested, individual compound's antinociceptive properties were reliably increased by P (exception of AMP), decreased by reserpine (R) or haloperidol (H), and remained essentially unchanged after naloxone (N) administration suggesting the involvement of catecholamines, but not opioid peptides, in their observed analgesic effects. Injection of P + N produced results similar to those seen after P alone. Under the experimental conditions described neither P, R, H or N had any effects by themselves. These findings suggest additional understanding of the mechanism of action responsible for the analgesic effects of these amines would be of interest, leading further to controlled studies on their alleged usefulness as weight reducing agents and sport performance enhancers.

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Characteristics of Antinociception Induced by Noncatecholic Phenylethylamine Derivatives: The Relation of Endogenous Norepinephrine to Phenylethylamine Analog-Induced Antinociception

Cited by 4 publications

References 14 publications

CB1 and CB2 Cannabinoid Receptor Agonists Induce Peripheral Antinociception by Activation of the Endogenous Noradrenergic System

CB1 and CB2 Cannabinoid Receptor Agonists Induce Peripheral Antinociception by Activation of the Endogenous Noradrenergic System

Characteristics of Antinociception Induced by Noncatecholic Phenylethylamine Derivatives: The Involvement of Alpha-2-Adrenoceptors

Analgesic Effects of β-Phenylethylamine and Various Methylated Derivatives in Mice

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