Fluvoxamine suppresses the long-term potentiation in the hippocampal CA1 field of anesthetized rats: an effect mediated via 5-HT1A receptors

Kojima, Taku; Matsumoto, Machiko; Togashi, Hiroko; Tachibana, Kaori; Kemmotsu, Osamu; Yoshioka, Mitsuhiro

doi:10.1016/s0006-8993(02)03756-3

Cited by 55 publications

(31 citation statements)

References 21 publications

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“…However, serotonin enhancement or activation of serotonergic receptors via specific agonists resulted in divergent effects in other studies. In some studies, serotonin or 5-HT receptor activation reduced or abolished LTP (Huang and Kandel, 2007;Kojima et al, 2003). This might be explained by the activation of different 5-HT receptor subtypes, the concentration of 5-HT agonists and antagonists, and different brain sites of action (Mori et al, 2001;Staubli and Otaky, 1994).…”

Section: Discussionmentioning

confidence: 99%

Chronic Enhancement of Serotonin Facilitates Excitatory Transcranial Direct Current Stimulation-Induced Neuroplasticity

Kuo

Paulus

Batsikadze

et al. 2015

Neuropsychopharmacol

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Serotonin affects memory formation via modulating long-term potentiation (LTP) and depression (LTD). Accordingly, acute selective serotonin reuptake inhibitor (SSRI) administration enhanced LTP-like plasticity induced by transcranial direct current stimulation (tDCS) in humans. However, it usually takes some time for SSRI to reduce clinical symptoms such as anxiety, negative mood, and related symptoms of depression and anxiety disorders. This might be related to an at least partially different effect of chronic serotonergic enhancement on plasticity, as compared with single-dose medication. Here we explored the impact of chronic application of the SSRI citalopram (CIT) on plasticity induced by tDCS in healthy humans in a partially double-blinded, placebo (PLC)-controlled, randomized crossover study. Furthermore, we explored the dependency of plasticity induction from the glutamatergic system via N-methyl-D-aspartate receptor antagonism. Twelve healthy subjects received PLC medication, combined with anodal or cathodal tDCS of the primary motor cortex. Afterwards, the same subjects took CIT (20 mg/day) consecutively for 35 days. During this period, four additional interventions were performed (CIT and PLC medication with anodal/cathodal tDCS, CIT and dextromethorphan (150 mg) with anodal/cathodal tDCS). Plasticity was monitored by motor-evoked potential amplitudes elicited by transcranial magnetic stimulation. Chronic application of CIT increased and prolonged the LTP-like plasticity induced by anodal tDCS for over 24 h, and converted cathodal tDCS-induced LTD-like plasticity into facilitation. These effects were abolished by dextromethorphan. Chronic serotonergic enhancement results in a strengthening of LTP-like glutamatergic plasticity, which might partially explain the therapeutic impact of SSRIs in depression and other neuropsychiatric diseases.

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Section: Discussionmentioning

confidence: 99%

Chronic Enhancement of Serotonin Facilitates Excitatory Transcranial Direct Current Stimulation-Induced Neuroplasticity

Kuo

Paulus

Batsikadze

et al. 2015

Neuropsychopharmacol

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“…However, activation of serotoninergic receptors also had opposing results on plasticity in other studies. Some studies have shown negative or no effect of serotonin on LTP induction (Edagawa et al, 1998;Huang and Kandel, 2007;Kojima et al, 2003;Normann et al, 2007;Sanberg et al, 2006), which can be explained by activation of different serotoninergic receptor subtypes, stage of brain development or dosage and frequency of application of 5-HT agonists or antagonists Park et al, 2012;Staubli and Otaky, 1994). To explore the reasons of such opposing results, future studies should address specific serotoninergic receptor subtypes, using different 5-HTreceptor agonist or antagonist drugs.…”

Section: Discussionmentioning

confidence: 99%

Effect of Serotonin on Paired Associative Stimulation-Induced Plasticity in the Human Motor Cortex

Batsikadze

Paulus

Kuo

et al. 2013

Neuropsychopharmacol

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Serotonin modulates diverse brain functions. Beyond its clinical antidepressant effects, it improves motor performance, learning and memory formation. These effects might at least be partially caused by the impact of serotonin on neuroplasticity, which is thought to be an important foundation of the respective functions. In principal accordance, selective serotonin reuptake inhibitors enhance long-term potentiation-like plasticity induced by transcranial direct current stimulation (tDCS) in humans. As other neuromodulators have discernable effects on different kinds of plasticity in humans, here we were interested to explore the impact of serotonin on paired associative stimulation (PAS)-induced plasticity, which induces a more focal kind of plasticity, as compared with tDCS, shares some features with spike timing-dependent plasticity, and is thought to be relative closely related to learning processes. In this single-blinded, placebo-controlled, randomized crossover study, we administered a single dose of 20 mg citalopram or placebo medication and applied facilitatory-and excitability-diminishing PAS to the left motor cortex of 14 healthy subjects. Cortico-spinal excitability was explored via single-pulse transcranial magnetic stimulation-elicited MEP amplitudes up to the next evening after plasticity induction. After citalopram administration, inhibitory PAS-induced after-effects were abolished and excitatory PAS-induced after-effects were enhanced trendwise, as compared with the respective placebo conditions. These results show that serotonin modulates PAS-induced neuroplasticity by shifting it into the direction of facilitation, which might help to explain mechanism of positive therapeutic effects of serotonin in learning and medical conditions characterized by enhanced inhibitory or reduced facilitatory plasticity, including depression and stroke.

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“…Studies investigating the effect of stress on longterm potentiation (LTP) have also indicated that a serotonergic system has a variety of modulatory effects on LTP depending on the learning events (e.g. stressed or non-stressed learning) (Corradetti et al, 1992;Shakesby et al, 2002;Kojima et al, 2003;Dupin et al, 2006;Vouimba et al, 2006;Ryan et al, 2008). Serotonergic systems have also been implicated in the mediation of arousal responses in molluscan models.…”

Section: Introductionmentioning

confidence: 99%

The role of serotonin in the enhancement of long-term memory resulting from predator detection in Lymnaea

Il-Han

Janes

Lukowiak

2010

Journal of Experimental Biology

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SUMMARYSerotonergic systems play important roles in modulating stress-induced arousal and vigilance behaviours. The pond snail, Lymnaea, shows multiple defensive vigilance behaviours in response to the stress associated with predator detection. Predator detection elicited by crayfish effluent (CE), increases the time to re-emerge from the shell and enhances the shadow withdrawal response. More importantly, in Lymnaea, CE enhances the ability to form long-term memory (LTM). We investigated the role of the serotonergic system in these anti-predator responses in Lymnaea. Using a serotonin-receptor antagonist, mianserin, we found that two defensive vigilance behaviours (e.g. increasing the time to re-emerge from their shell and shadow response) elicited by CE were not observed when the serotonergic system was disrupted. Also, methysergide, another serotonin antagonist, blocked the enhanced LTM formation after training in CE. Importantly, mianserin did not alter LTM formation in pond water (PW). These data suggest that a serotonergic system is activated only when Lymnaea detect a predator. When snails were trained in CE using a training procedure that in PW produces a 24-h LTM, a more persistent form of LTM (5days) occurred. This more persistent form of LTM was abolished after mianserin treatment. Increasing 5-HT levels in the snail by the injection of 5-HT was also associated with enhanced LTM formation. Lastly, we tested whether the osphradium is implicated in CE detection and subsequent enhanced formation of LTM. Cutting the osphradial nerve to the CNS resulted in the loss of the ability to form enhanced LTM in CE. Together, these findings support the hypothesis that the serotonergic system plays a key role in modulating the predator-induced stress responses in Lymnaea.

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Fluvoxamine suppresses the long-term potentiation in the hippocampal CA1 field of anesthetized rats: an effect mediated via 5-HT1A receptors

Cited by 55 publications

References 21 publications

Chronic Enhancement of Serotonin Facilitates Excitatory Transcranial Direct Current Stimulation-Induced Neuroplasticity

Chronic Enhancement of Serotonin Facilitates Excitatory Transcranial Direct Current Stimulation-Induced Neuroplasticity

Effect of Serotonin on Paired Associative Stimulation-Induced Plasticity in the Human Motor Cortex

The role of serotonin in the enhancement of long-term memory resulting from predator detection in Lymnaea

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