The modulation of neuronal activity by melatonin: In vitro studies on mouse hippocampal slices

Hogan, Michael V.; El-Sherif, Yasir; Wieraszko, Andrzej

doi:10.1034/j.1600-079x.2001.300204.x

Cited by 61 publications

(53 citation statements)

References 55 publications

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“…HFS (right upward arrow) induced a significant LTP in the EPSPs from both the LR (open square; P < 0.0001) and DR (closed square; P < 0.0001), which was markedly higher in magnitude and longer in maintenance in the former (P < 0.0001). Semm, 1985;Musshoff et al, 2002) and alter synaptic transmission between neurons in this region (Wan et al, 1999;Hogan et al, 2001;El-Sherif et al, 2002). This may lead to the postsynaptic facilitations reported here and increased firing rate of neurons in the CA1 regions (Musshoff et al, 2002).…”

Section: Similar Effect Of Light Deprivation and Melatonin On The Evomentioning

confidence: 70%

“…Binding sites for melatonin have been found in the hippocampus of several mammals (Musshoff et al, 2002;Savaskan et al, 2005;Stewart and Leung, 2005;Wan et al, 1999). Both in vivo and in vitro studies have revealed that melatonin displays inhibitory effects on CA3 area (Zeise and Semm, 1985), CA1 area (Hogan et al, 2001), SCN (Stehle et al, 1989) and striatum (León et al, 1998a), and, facilitatory effects on striatum (León et al, 1998b), cultured ocular tissues (Rich et al, 1999) and SCN (Wan et al, 1999). There are also reports demonstrating that melatonin inhibits induction of LTP in slices taken from CA1 (Wang et al, 2005;Ozcan et al, 2006) and visual cortex (Soto-Moyano et al, 2006).…”

Section: Introductionmentioning

confidence: 91%

“…On the other hand, other studies have indicated that melatonin reduced the amplitude of synaptically evoked responses (Hogan et al, 2001;El-Sherif et al, 2003) or had no effect on synaptic transmission (Collins and Davies, 1997;Wang et al, 2005).…”

Section: Similar Effect Of Light Deprivation and Melatonin On The Evomentioning

confidence: 96%

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Light deprivation improves melatonin related suppression of hippocampal plasticity

2009

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In early postnatal life, sensory inputs deeply influence development as well as function of the brain. Plasticity of synaptic transmission including its experimentally induced form, long-term potentiation (LTP), is affected by sensory deprivation in neocortex. This study is devoted to assess if dark rearing and a dark phase synthesized hormone melatonin influence LTP in the hippocampus, an area of brain involved in learning and memory. In vivo experiments were carried out on two groups of 45-days-old male Wistar rats kept in standard 12-h light/dark condition [light reared (LR) tested during the light phase] or in complete darkness [dark reared (DR)] since birth to testing. Each group, in turn, was divided to two, vehicle- and melatonin-treated, groups. Stimulating the Schaffer collaterals of CA3 area of hippocampus extracellular postsynaptic potentials (EPSPs) were recorded in the CA1 area. Having the stable baseline responses to the test pulses, the hippocampus was perfused by either vehicle or 2 microg melatonin and EPSPs were recorded for 30 min. Then, for induction of LTP, the tetanus was applied to the Schaffer collaterals and the field potentials were pooled for 120-min post-tetanus. The light deprivation resulted in a significant augmentation in the amplitude of baseline responses. Also, we observed a melatonin-induced increase in amplitude of the baseline recordings in either LR or DR animals. Tetanic stimulation elicited LTP of EPSPs in both LR and DR groups, robustly in the former where it lasted for about 90 min. Generally, melatonin inhibited the production of LTP in the two groups especially in the LR animals leading to a noticeable depression. We concluded that higher level of neuronal activity in the DR rats gives rise to a lower level of LTP. Weaker effect of melatonin on blocking the potentiation of post-tetanus EPSPs in the DR rats may be the result of a desensitization of melatonin receptors due to chronically increased levels of this hormone in the visually deprived rats.

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Section: Similar Effect Of Light Deprivation and Melatonin On The Evomentioning

confidence: 70%

Section: Introductionmentioning

confidence: 91%

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Light deprivation improves melatonin related suppression of hippocampal plasticity

2009

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“…Data derived from mice carrying the targeted disruption of MT1 and the treatment with an MT2-selective antagonist indicate that to some extent MT2 mediates the effects of melatonin on neural firing in the suprachiasmatic nucleus and hippocampus [34,35,36]. In contrast, studies using MT2 knockout mice and hamsters naturally lacking functional MT2 genes suggest that MT1 predominantly mediates the modulatory action of melatonin in reproductive functions [9,10].…”

Section: Discussionmentioning

confidence: 99%

Cetrorelix, a Gonadotropin-Releasing Hormone Antagonist, Induces the Expression of Melatonin Receptor 1a in the Gonadotropin-Releasing Hormone Neuronal Cell Line GT1–7

Ishii

Sato²,

Yin³

et al. 2009

Neuroendocrinology

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Melatonin has been implicated in the control of the reproductive system, and the modulatory actions of melatonin on gonadotropin-releasing hormone (GnRH) neurons have been assumed to be indirectly mediated through afferent neurons. However, our previous studies demonstrate sexually dimorphic modulation of A-type γ-aminobutyric acid (GABA) receptor (GABA_AR) currents by melatonin in adult rat GnRH neurons and a preferential expression of melatonin 1a receptor (MT1) in male GnRH neurons. Using immortalized GnRH neurons (GT1–7 cells), the present study investigated the mechanism by which the expression of melatonin receptors is regulated in GnRH neurons. Like endogenous GnRH neurons, GT1–7 cells express both GnRH and GnRH receptor mRNAs, indicating that the cells have a self-stimulatory system. A 2-iodomelatonin binding assay and RT-PCR analysis demonstrated that the cells expressed neither MT1 nor MT2. However, treatment of GT1–7 cells with the GnRH antagonist cetrorelix significantly increased 2-iodomelatonin binding and induced a time- and concentration-dependent MT1 mRNA expression. The GABA_AR currents were then measured using a perforated patch-clamp technique to examine whether the treatment with cetrorelix changed the responses to melatonin. Melatonin augmented the GABA_AR currents in GT1–7 cells treated with 1 μM cetrorelix for 24 h, while melatonin decreased the currents in the cells not treated with cetrorelix, probably via receptor-independent processes. The present results suggest that GnRH downregulates the expression of MT1 via an autocrine-paracrine mechanism in GT1–7 cells, and modifies the melatonin-induced modulation of GABA_AR currents. These findings may provide one possible mechanism for the sexually dimorphic responses to melatonin in adult rat GnRH neurons.

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“…There is likely some mechanistic benefit beyond the reductions in peri-hematomal free-radical injury. Hippocampal neurons have receptors for melatonin (Morgan et al, 1994;Musshoff et al, 2002), and the administration of this hormone is known to alter excitability and synaptic transmission within the hippocampus (Hogan et al, 2001;Musshoff et al, 2002;Wan et al, 1999), and melatonin has been shown to alter hippocampal synaptic plasticity through the MT2-mediated regulation of the adenylate cyclase-protein kinase A (AC-PKA) pathway (Wang et al, 2005). The synaptic plasticity in the hippocampus and other brain regions has recently gained attention as an important means by which melatonin may augment its neuroprotective effects beyond reductions in oxidative stress alone (Baydas et al, 2005;Bob and Fedor-Freybergh, 2008;Fukunaga et al, 2002;Gorfine and Zisapel, 2007;Larson et al, 2006;Talaei et al, 2009;Wang et al, 2005).…”

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confidence: 99%

Protective Effect of Melatonin upon Neuropathology, Striatal Function, and Memory Ability after Intracerebral Hemorrhage in Rats

Lekic

Hartman

Rojas

et al. 2010

Journal of Neurotrauma

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Since free radicals play a role in the mechanisms of brain injury after hemorrhagic stroke, the effect of melatonin (a potent antioxidant and free-radical scavenger) on outcomes was investigated after intracerebral hemorrhage (ICH) in rats. ICH was induced by clostridial collagenase infusion into the right caudate putamen, and several time points and doses of melatonin were studied. Brain edema and neurological function at 24 h were unchanged in comparison with vehicle-treated groups, in spite of oxidative stress reductions. Repeated treatment with the lower dose of melatonin (5 mg=kg) given at 1 h and every 24 h thereafter for 3 days after ICH, led to normalization of striatal function and memory ability over the course of 8 weeks, and less brain atrophy 2 weeks later. These results suggest that melatonin is safe for use after ICH, reduces oxidative stress, provides brain protection, and could be used for future investigations of free radical mechanisms after cerebral hemorrhage.

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The modulation of neuronal activity by melatonin: In vitro studies on mouse hippocampal slices

Cited by 61 publications

References 55 publications

Light deprivation improves melatonin related suppression of hippocampal plasticity

Light deprivation improves melatonin related suppression of hippocampal plasticity

Cetrorelix, a Gonadotropin-Releasing Hormone Antagonist, Induces the Expression of Melatonin Receptor 1a in the Gonadotropin-Releasing Hormone Neuronal Cell Line GT1–7

Protective Effect of Melatonin upon Neuropathology, Striatal Function, and Memory Ability after Intracerebral Hemorrhage in Rats

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