Melatonin inhibits voltage-sensitive Ca2+ channel-mediated neurotransmitter release

Choi, Tae-Yong; Kwon, Ji Eun; Durrance, Eunice Sung; Jo, Su‐Hyun; Choi, Se‐Young; Kim, Kyong‐Tai

doi:10.1016/j.brainres.2014.02.023

Cited by 27 publications

(27 citation statements)

References 38 publications

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“…Because a decrease of both parameters indicates an increase in glutamate release, we concluded that MLT enhances glutamatergic synaptic transmission to MLHb neurons by a presynaptic increase in glutamate release. Interestingly, previous studies have shown that MLT decreases glutamate release at Schaffer collateral CA1 hippocampal synapses (Choi et al, 2014). The discrepancy between this study and our finding could be attributed to the differing concentration of MLT, subtype/distribution of receptors, as well as, regional and cell specific effects.…”

Section: Discussioncontrasting

confidence: 99%

Melatonin receptor activation increases glutamatergic synaptic transmission in the rat medial lateral habenula

Evely

Hudson

Dubocovich

et al. 2016

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Melatonin (MLT) is secreted from the pineal gland and mediates its physiological effects through activation of two G protein-coupled receptors, MT1 and MT2 . These receptors are expressed in several brain areas, including the habenular complex, a pair of nuclei that relay information from forebrain to midbrain and modulate a plethora of behaviors, including sleep, mood, and pain. However, so far, the precise mechanisms by which MLT control the function of habenula neurons remain unknown. Using whole cell recordings from male rat brain slices, we examined the effects of MLT on the excitability of medial lateral habenula (MLHb) neurons. We found that MLT had no significant effects on the intrinsic excitability of MLHb neurons, but profoundly increased the amplitude of glutamate-mediated evoked excitatory post-synaptic currents (EPSC). The increase in strength of glutamate synapses onto MLHb neurons was mediated by an increase in glutamate release. The MLT-induced increase in glutamatergic synaptic transmission was blocked by the competitive MT1 /MT2 receptor antagonist luzindole (LUZ). These results unravel a potential cellular mechanism by which MLT receptor activation enhances the excitability of MLHb neurons. The MLT-mediated control of glutamatergic inputs to the MLHb may play a key role in the modulation of various behaviors controlled by the habenular complex.

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Section: Discussioncontrasting

confidence: 99%

Melatonin receptor activation increases glutamatergic synaptic transmission in the rat medial lateral habenula

Evely

Hudson

Dubocovich

et al. 2016

Synapse

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“…In addition to epileptic seizures, an overload of intracellular Ca 2+ concentration in epilepsy induces ROS production, apoptosis, and caspase activations ( Figure). Melatonin reduces ROS production and intracellular Ca 2+ concentration through regulation of cation channels, preventing apoptosis (Molina-Carballo et al, 2007;Choi et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

Nazıroğlu¹

2015

Turk J Biol

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Calcium ion (Ca 2+ ) accumulation and excessive oxidative stress in the hippocampus and brain cortex have long been known as major contributors to the etiology of epilepsy. I have reviewed the role of Ca 2+ signaling through cation channels and mitochondriamediated oxidative stress on epilepsy in human and animals. A review of the relevant papers and results from recent studies were obtained from PubMed and the Science Citation Index. Current literature findings indicate that melatonin and agomelatine reduce activation of hippocampal transient receptor potential (TRP), glutamate receptors, and voltage-gated calcium channels that are critical for the development of abnormal Ca 2+ homeostasis and oxidative stress and associated mitochondrial dysfunction. In addition, low doses of melatonin induce anticonvulsant action through increase of GABA levels in the hippocampus and brain cortex. The accumulating evidence implicates a modulator role of melatonin on excessive oxidative stress products, plus mitochondrial and Ca 2+ dysregulations in epilepsy. The evidence indicates that modulation of oxidative stress and neuronal Ca 2+ handling occurs through effects on TRP channels, suggesting an increasingly viable approach for therapeutic interventions against epilepsy.

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“…The hormone and its metabolites act as free radical scavengers and antioxidants. The results from a recent study have shown that melatonin inhibits neurotransmitter release through the blocking of voltage-sensitive Ca 2þ channels suggesting a possible mechanism for the antiepileptic effect of melatonin [101].…”

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confidence: 98%

An insight into the scientific background and future perspectives for the potential uses of melatonin

Anwar

Muhammad²,

Bader³

et al. 2015

Egyptian Journal of Basic and Applied Sciences

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Antiepileptic Antiosteoporotic Antioxidant Cardiovascular disease Circardian rhythm Hypnotic Immunodulatory Melatonin a b s t r a c t Melatonin is one of the most versatile and ubiquitous molecule widely distributed in nature has been reported to play a role in a wide variety of physiological responses including reproduction, circadian homeostasis, sleep, retinal neuromodulation, and vasomotor responses. In most vertebrates, including humans, melatonin is synthesized primarily in the pineal gland and is regulated by the environmental light ⁄ dark cycle via the suprachiasmatic nucleus. Melatonin is synthesized in all areas of the body such as gastrointestinal tract, skin, bone marrow, retina and in lymphocytes, from which it may influence other physiological functions through paracrine signalling. In addition to regulation of circadian rhythm of melatonin a variety of other physiological effects such as hypnotic, antidepressant, antiepileptic, oncostatic, immunomodulatory, antiosteoporotic, in cardiovascular disease, neuromodulatory and cerebral ischaemic condition have been reported.Moreover there is scarcity of literature that reviewed the scientific evidence for its use in these conditions. Therefore in this article we review recent advances in this research field, which is preceded by a concise account of general information about melatonin, melatonin receptors and intracellular signalling pathways for melatonin actions.

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Melatonin inhibits voltage-sensitive Ca2+ channel-mediated neurotransmitter release

Cited by 27 publications

References 38 publications

Melatonin receptor activation increases glutamatergic synaptic transmission in the rat medial lateral habenula

Melatonin receptor activation increases glutamatergic synaptic transmission in the rat medial lateral habenula

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

An insight into the scientific background and future perspectives for the potential uses of melatonin

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