Different effects of anxiolytic agents, diazepam and 5-HT1A agonist tandospirone, on hippocampal long-term potentiation in vivo

Mori, Kiyoshi; Togashi, Hiroko; Kojima, Taku; Matsumoto, Machiko; Ohashi, Satoshi; Ueno, Kenichi; Yoshioka, Mitsuhiro

doi:10.1016/s0091-3057(01)00546-9

Cited by 48 publications

(28 citation statements)

References 31 publications

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“…Repeated application of SSRI can enhance LTP (Kojic et al, 1997;Mori et al, 2001). In addition, chronic application of the SSRI fluvoxamine prevented stress-induced facilitation of LTD and increased LTP both in stressed and non-stressed animals (Holderbach et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…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). To explore the reasons for these inconsistent results and to learn more about the impact of serotonin on neuroplasticity in humans, future studies should consider specific serotonergic receptor subtypes, apply different 5-HT-receptor agonists and antagonists, and explore the impact of different dosages, which might be a relevant factor for the strength and direction of effects, as seen for other neuromodulators, which have nonlinear effects on plasticity (Frensnoza et al, 2014;Monte-Silva et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Animal experiments have shown that serotonin can affect long-term potentiation (LTP) and long-term depression (LTD) in slice preparations. The direction of the effects depends on receptor subtypes, dosage of respective drugs, duration of 5-HT receptor activation, and site of action (Kemp and Manahan-Vaughan, 2005;Kojic et al, 1997;Mori et al, 2001). Both LTP-enhancing and -abolishing effects were described in different studies (Kojic et al, 1997;Park et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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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%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Kuo

Paulus

Batsikadze

et al. 2015

Neuropsychopharmacol

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“…Student's t-tests revealed no significant differences between conditions (p40.05). Impact of serotonin on neuroplasticity G Batsikadze et al animal studies have shown that serotonin can enhance LTP (Huang and Kandel, 2007;Kojic et al, 1997;Machacek et al, 2001;Mori et al, 2001;Ohashi et al, 2002;Park et al, 2012), block the stress-caused inhibition of LTP (Ryan et al, 2008) or block LTD . Activation of 5-HT receptors was furthermore shown to reverse LTD induction or convert it into LTP (Costa et al, 2012;Kemp and Manahan-Vaughan, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…One important foundation for these effects might be its impact on neuroplasticity. Activation of serotoninergic subreceptors is shown to affect long-term potentiation (LTP) or longterm depression (LTD) in animal slice preparations, depending on subreceptor type, location and frequency of application (Huang and Kandel, 2007;Kojic et al, 1997;Mori et al, 2001).…”

Section: Introductionmentioning

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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Early postnatal stress alters the 5-HTergic modulation to emotional stress at postadolescent periods of rats

et al. 2005

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Several lines of evidence have shown that traumatic events during the early postnatal stage might precipitate long-lasting alteration in the functional properties underlying emotional expression. The aim of the present study was to examine whether the early postnatal stress alters the 5-HTergic mechanism underlying regulation of emotional stress, focusing on the 5-HT(1A) receptor-mediated synaptic responses in adult rats. Pups were exposed to aversive stimulus, footshock (FS) at the postnatal period of the second (2W) and the third week (3W). At postadolescent period (10-12-week-old), electrophysiological and behavioral studies were performed. The 5-HT(1A) receptor agonist tandospirone (10 mg/kg body wt, i.p.) blocked the long-term potentiation (LTP) in the hippocampal CA1 field of 3W-FS, as well as non-FS control, whereas this inhibition was not observed in 2W-FS group. Fear-related freezing behavior observed during exposure to contextual fear conditioning markedly attenuated in 2W-FS, but not in 3W-FS. These data suggest that aversive stress exposed at 2W is attributable to changes in the 5-HT(1A) receptor-mediated synaptic plasticity, which may be responsible for the attenuation of freezing behavior. Thus, 5-HT(1A) receptors appear to play a key role in the 5-HTergic mechanism underlying regulation of emotional stress on the postnatal development of the brain. In other words, the second postnatal week may be the "critical period" for establishing proper behavioral responses to emotional stress in adult rats. (c) 2005 Wiley-Liss, Inc.

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Different effects of anxiolytic agents, diazepam and 5-HT1A agonist tandospirone, on hippocampal long-term potentiation in vivo

Cited by 48 publications

References 31 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

Early postnatal stress alters the 5-HTergic modulation to emotional stress at postadolescent periods of rats

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