Long-Term Plasticity of Visually Evoked Potentials in Humans is Altered in Major Depression

Normann, Claus; Schmitz, Daniela; Fürmaier, Andrea; Döing, Carsten; Bach, Michael

doi:10.1016/j.biopsych.2006.10.006

Cited by 209 publications

(235 citation statements)

References 48 publications

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“…It abolishes focal LTD-like and trendwise enhances focal LTP-like plasticity induced by PAS10 and PAS25, respectively. These results go in line with previous studies Normann et al, 2007). Chronic application of SSRI enhanced facilitatory plasticity and resulted in a shift of inhibitory plasticity of early visual-evoked potentials (VEPs) toward excitation or restored LTP induction and suppressed LTD facilitation in distressed animals ( Von Frijtag et al, 2001).…”

Section: Discussionsupporting

confidence: 91%

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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Section: Discussionsupporting

confidence: 91%

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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“…Researchers reported significant increases in VEPs in subjects after a train of patterned visual stimuli. However, increases in VEP amplitude were significantly smaller in depressed subjects compared with healthy controls (Normann et al, 2007). Impairment of synaptic plasticity in depression has also been proposed to occur in other telencephalic regions such as the hippocampus.…”

Section: Discussionmentioning

confidence: 92%

“…First, the majority of depressed subjects were on antidepressant medications. This is important because there is some experimental evidence that antidepressant medications may affect neuroplasticity, although these studies found that they tended to enhance rather than reduce plasticity (Normann et al, 2007;Rocher et al, 2004). Further analysis of medicated and non-medicated depressed subjects found no difference in MEP changes after PAS between these groups, although both differed significantly from healthy controls.…”

Section: Discussionmentioning

confidence: 98%

“…Dysfunctional neuroplasticity has been implicated in depression-related cognitive and behavioral changes such as impaired learning and memory and inability to respond appropriately to stress or aversive stimuli (Pittenger and Duman, 2008). However, only one prior study has examined neuroplasticity in depression using an objective neurological test (Normann et al, 2007). This study used changes in visual evoked potentials (VEPs) in response to repeated visual stimuli as a means of examining changes in synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

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Neuroplasticity in Depressed Individuals Compared with Healthy Controls

Player

Taylor

Weickert

et al. 2013

Neuropsychopharmacol

105

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Several lines of evidence suggest that neuroplasticity is impaired in depression. This study aimed to compare neuroplasticity in 23 subjects with DSM-IV major depressive episode and 23 age-and gender-matched healthy controls, using an objective test that is independent of subject effort and motivation. Neuroplasticity was assessed in the motor cortex using a brain stimulation paradigm known as paired associative stimulation (PAS), which induces transient changes in motor cortical function. Motor cortical excitability was assessed before and after PAS using single-pulse transcranial magnetic stimulation (TMS) to induce motor evoked potentials (MEPs) in a hand muscle. After PAS, MEP amplitudes significantly increased in healthy controls compared with depressed subjects (P ¼ 0.002). The functional significance of motor cortical changes was assessed using a motor learning task-a computerized version of the rotor pursuit task. Healthy controls also performed better on motor learning (P ¼ 0.02). BDNF blood levels and genotype were assayed to determine any relationship with motor cortical plasticity. However, PAS results did not correlate with motor learning, nor appear to be related to BDNF measures. The significance of these findings is that it provides one of the first direct demonstrations of reduced neuroplasticity in depressed subjects, using an objective test.

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“…LTP is an important physiological derivate of learning and memory formation (Rioult-Pedotti et al, 2000). Deficient LTP and left prefrontal hypo-activity are present in depression and are restituted after antidepressant treatment; thus, respective restitution of brain physiology and reduction of symptoms seem to be associated (Henriques and Davidson., 1991;Rocher et al, 2004;Norman et al, 2007). Taken together, these findings suggest that the enhancement of cortical excitability and LTP-like plasticity may contribute to adaptive changes induced by antidepressant treatment and therefore improve learning and cognition.…”

Section: Functional Relevancementioning

confidence: 80%

Acute and chronic noradrenergic effects on cortical excitability in healthy humans

Kuo

Paulus

et al. 2017

Brain Stimulation

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Long-Term Plasticity of Visually Evoked Potentials in Humans is Altered in Major Depression

Cited by 209 publications

References 48 publications

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

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

Neuroplasticity in Depressed Individuals Compared with Healthy Controls

Acute and chronic noradrenergic effects on cortical excitability in healthy humans

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