Noncompetitive inhibition of the glycine receptor-mediated current by melatonin in cultured neurons

Wu, Fong‐Sen; Yang, Ying-Chen; Tsai, Jing-Jane

doi:10.1016/s0006-8993(00)02804-3

Cited by 12 publications

(6 citation statements)

References 12 publications

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“…Our findings are consistent with those of a previous study showing that, at higher doses (60 mg/kg and 120 mg/kg), melatonin produced effective antinociception in the tail-flick test, starting 15 minutes after melatonin administration and peaking after 30 minutes, with the effect lasting over 100 minutes 16. In addition, a previous study of intrathecal melatonin administration showed antiallodynic activity in rats with neuropathic pain, with the effect observed from 30 minutes through 240 minutes after administration 17. In diabetic rats, the best antinociceptive effect was observed with 60 minutes’ pretreatment (300 mg/kg orally) in the formalin test 3…”

Section: Discussionsupporting

confidence: 91%

“…The possible mechanisms of action for the antinociceptive effect of melatonin include activation of supraspinal sites16 and inhibition of “spinal windup.”23 Thus, the reduction in secondary inflammatory hyperalgesia in our study could indicate that melatonin reduces the excitability of pain transmission in dorsal horn neurons by acting on membrane-bound MT1 and MT2 receptors 9. There is also experimental evidence to suggest that the analgesic effect of melatonin is mediated by opioids1 and by gamma-aminobutyric acid (GABAergic) systems 17…”

Section: Discussionmentioning

confidence: 65%

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Melatonin administration reduces inflammatory pain in rats

Laste¹,

Macedo²,

Rozisky³

et al. 2012

JPR

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In view of the broad range of effects attributed to melatonin, this study evaluated its analgesic effect on inflammatory pain induced by complete Freund’s adjuvant (CFA) in Wistar rats. Inflammation was induced by intradermal CFA injection in the hind paw of all animals, which were then divided into two groups that received either 60 mg/kg of melatonin or vehicle (1% alcohol in saline), intraperitoneally, for three days. The analgesic effect of melatonin was assessed by the hot-plate test, immediately and thereafter at 30, 60, 90, and 120 minutes after the first administration and 24 hours after once-daily administration for 2 more days. After CFA injection, melatonin administration increased withdrawal latency at 60 minutes after the first dose. After the end of treatment, melatonin showed a significant analgesic effect on inflammatory pain. This study paves the way for exploration of how brief courses of treatment could improve this analgesic effect in the late phases of inflammatory pain.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 65%

Melatonin administration reduces inflammatory pain in rats

Laste¹,

Macedo²,

Rozisky³

et al. 2012

JPR

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“…No evidence is now available, demonstrating melatonin receptor-mediated effects on glycine currents in any central neurons. In cultured chick spinal cord neurons melatonin of micromolar concentrations noncompetitively inhibited the glycine currents in a dose-dependent manner, with an EC 50 of 934 mM [21]. It is highly possible that such effect might be due to the allosteric action caused by melatonin of higher concentrations.…”

Section: Discussionmentioning

confidence: 99%

Melatonin modulates glycine currents of retinal ganglion cells in rat

Zhang

Cao²,

Yang³

2007

NeuroReport

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Melatonin is a hormone participating in the modulation of various physiological functions via binding to specific melatonin receptors. In the retina, melatonin is synthesized and released by photoreceptors and may play a neuromodulatory role. By using patch clamp techniques, we demonstrate for the first time that glycine-induced currents from a population of isolated ganglion cells in the rat retina are potentiated by melatonin of nanomolar concentrations by increasing the efficacy and the channel conductance of the strychnine-sensitive glycine receptor. The melatonin effect is blocked by 4-P-PDOT, indicating the mediation of the MT2 receptor. These results suggest that melatonin, along with the MT2 receptor, may be involved in retinal information processing by modulating glycine receptor-mediated inhibition.

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“…In several neuronal populations, melatonin has been found to control neuronal excitabilities, synaptic events, and neurotransmitter release in concentrations ranging from nanomolar to millimolar [ 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 ]. For example, the γ-aminobutyric acid (GABA) response was inhibited by melatonin in nanomolar to micromolar ranges in brain slices of rat trigeminal ganglion neurons [ 45 ] and GnRH neurons [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Melatonin Suppresses the Kainate Receptor-Mediated Excitation on Gonadotropin-Releasing Hormone Neurons in Female and Male Prepubertal Mice

Rijal

Cho

Park³

et al. 2020

IJMS

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Melatonin, a pineal gland secretion, is an amphiphilic neurohormone involved in the biological and physiologic regulation of bodily functions. Numerous studies have shown the effects of melatonin on the release of gonadotropins and their actions at one or several levels of the hypothalamic–pituitary–gonadal axis. However, direct melatonin action on gonadotropin-releasing hormone (GnRH) neurons and its mechanism of action remain unclear. Here, plasma melatonin levels were measured and the effect of melatonin on GnRH neurons was assessed using brain slice patch clamp techniques. The plasma melatonin levels in prepubertal mice were higher than those in the adults. Melatonin itself did not change the firing activity of GnRH neurons. Interestingly, the kainate receptor-mediated responses but not the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)- and N-methyl-D-aspartic acid (NMDA)-induced responses were suppressed by melatonin in both the voltage clamp and current clamp modes. The inhibitory effects of the kainate-induced response by melatonin tended to increase with higher melatonin concentrations and persisted in the presence of tetrodotoxin, a voltage-sensitive Na+ channel blocker, or luzindole, a non-selective melatonin receptor antagonist. However, the response was completely abolished by pretreatment with pertussis toxin. These results suggest that melatonin can regulate GnRH neuronal activities in prepubertal mice by partially suppressing the excitatory signaling mediated by kainate receptors through pertussis toxin-sensitive G-protein-coupled receptors.

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Noncompetitive inhibition of the glycine receptor-mediated current by melatonin in cultured neurons

Cited by 12 publications

References 12 publications

Melatonin administration reduces inflammatory pain in rats

Melatonin administration reduces inflammatory pain in rats

Melatonin modulates glycine currents of retinal ganglion cells in rat

Melatonin Suppresses the Kainate Receptor-Mediated Excitation on Gonadotropin-Releasing Hormone Neurons in Female and Male Prepubertal Mice

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