Melatonin administration impairs visuo-spatial performance and inhibits neocortical long-term potentiation in rats

Soto-Moyano, Rubén; Burgos, Héctor; Flores, Francisco; Valladares, Luis; Sierralta, Walter; Fernández, Vı́ctor; Pérez, Hernán; Hernández, Paula; Hernández, Alejandro

doi:10.1016/j.pbb.2006.09.009

Cited by 20 publications

(18 citation statements)

References 53 publications

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“…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). Because melatonin secretion is subjected to circadian rhythms, the present study was undertaken to examine contribution of dark rearingrelated enhancement of melatonin secretion on the baseline activity and induction of LTP in the CA1 area of hippocampus.…”

Section: Introductionmentioning

confidence: 99%

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: Introductionmentioning

confidence: 99%

Light deprivation improves melatonin related suppression of hippocampal plasticity

2009

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“…In addition to its impact on hippocampal synaptic plasticity, melatonin was shown to prevent the induction of neocortical LTP and impair spatial performance in the radial maze (393). Neonatal rats given low doses of melatonin exhibited impaired hippocampal LTP and displayed learning and memory deficits.…”

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confidence: 99%

“…This may seem surprising as it might be expected that an antioxidant should improve cognition rather than making it worse. However, these studies (77,92,139,318,393,408,430) were performed in the absence of excessive oxidative stress. Going back to the first part of this review, we described numerous studies indicating that ROS are important signaling molecules necessary for proper LTP induction, and therefore scavenging radicals with melatonin likely explains the detrimental effects of melatonin on synaptic plasticity.…”

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confidence: 99%

Reactive Oxygen Species in the Regulation of Synaptic Plasticity and Memory

Massaad

Klann

2011

Antioxidants & Redox Signaling

468

350

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The brain is a metabolically active organ exhibiting high oxygen consumption and robust production of reactive oxygen species (ROS). The large amounts of ROS are kept in check by an elaborate network of antioxidants, which sometimes fail and lead to neuronal oxidative stress. Thus, ROS are typically categorized as neurotoxic molecules and typically exert their detrimental effects via oxidation of essential macromolecules such as enzymes and cytoskeletal proteins. Most importantly, excessive ROS are associated with decreased performance in cognitive function. However, at physiological concentrations, ROS are involved in functional changes necessary for synaptic plasticity and hence, for normal cognitive function. The fine line of role reversal of ROS from good molecules to bad molecules is far from being fully understood. This review focuses on identifying the multiple sources of ROS in the mammalian nervous system and on presenting evidence for the critical and essential role of ROS in synaptic plasticity and memory. The review also shows that the inability to restrain either age-or pathology-related increases in ROS levels leads to opposite, detrimental effects that are involved in impairments in synaptic plasticity and memory function.

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“…Ozdemir et al (2005) pointed out that melatonin significantly attenuates trauma induced neuronal death in hippocampal CA1, CA3 regions and dentate gyrus, and improves spatial memory deficits. Some others have indicated that this hormone has adverse effects on spatial memory and learning (Rogers et al 2003;Uysal et al 2005;Soto-Moyano et al 2006). Soto-Moyano et al (2006) showed that melatonin can impair visuo-spatial performance of rats in radial arm maze.…”

Section: Introductionmentioning

confidence: 99%

Interaction of visual experience and melatonin in the spatial task learning

Salami

Talaei

Davari

et al. 2012

Biological Rhythm Research

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During a postnatal critical period, sensory experience modifications cause changes in electrophysiological and behavioral considerations. Pineal melatonin secretion follows a circadian rhythm, rising during darkness and waning by light. This study evaluated interaction of visual signals and melatonin on spatial performance of animals reared on 12 light/dark cycle (control; CO), constant light (light reared; LR) and total darkness (dark reared; DR). Each group was administered vehicle and/or melatonin (5 mg/kg) intraperitonealy. The animals were introduced to a water maze task 4 trials/day for 5 days. The time spent and distance traveled to find the platform were measured. We found a superiority of the CO rats on both LR and DR groups. Melatonin impaired the task learning in the CO animals. Conversely, the LR and DR animals were insensitive to melatonin. Conclusively, visual experience modifications, whether light or dark deprivation, impaired the spatial learning. Also, exogenous melatonin influenced behavior of only normally reared animals.

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Melatonin administration impairs visuo-spatial performance and inhibits neocortical long-term potentiation in rats

Cited by 20 publications

References 53 publications

Light deprivation improves melatonin related suppression of hippocampal plasticity

Light deprivation improves melatonin related suppression of hippocampal plasticity

Reactive Oxygen Species in the Regulation of Synaptic Plasticity and Memory

Interaction of visual experience and melatonin in the spatial task learning

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