Boosting Focally-Induced Brain Plasticity by Dopamine

Kuo, Min‐Fang; Paulus, Walter; Nitsche, Michael A.

doi:10.1093/cercor/bhm098

Cited by 248 publications

(222 citation statements)

References 34 publications

Supporting

Mentioning

195

Contrasting

Unclassified

Order By: Relevance

“…Moreover, because of the randomized order of conditions, we would not expect a systematic impact of any minor carryover effect on the results. Finally, previous studies of our group in which a similar procedure was performed showed PAS plasticity effects in the placebo medication conditions, which are comparable to the experiments of other groups, in which not such a frequent repetition of sessions was performed (Kuo et al, 2008;Monte-Silva et al, 2009;Monte-Silva et al, 2010;Stefan et al, 2000;Stefan et al, 2004;Thirugnanasambandam et al, 2012). Therefore, late-phase plasticity is unlikely to have compromised the results of the present experiments.…”

Section: General Remarkssupporting

confidence: 89%

“…Accordingly, activation of 5-HT2 receptors has a facilitatory effect on NMDA receptor-dependent LTP induction in the visual cortex of adult rats (Park et al, 2012). Finally, serotonin affects cholinergic (Consolo et al, 1994;Matsumoto et al, 2001;Yamaguchi et al, 1997), GABAergic (Roerig and Katz, 1997;Waider et al, 2012), nicotinergic (Zaniewska et al, 2009), and dopaminergic (Gobert and Millan, 1999;Wood and Wren, 2008) systems, which have a major impact on stimulation-induced plasticity in humans Kuo et al, 2008;Monte-Silva et al, 2009;Monte-Silva et al, 2010;Nitsche et al, 2004;Thirugnanasambandam et al, 2012). While it cannot be ruled out completely that serotonin enhancement affected plasticity partially by its impact on one of these neuromodulatory systems, a profound contribution seems unlikely, because the impact of citalopram on tDCS-, and PAS-induced plasticity differs relevantly from those of other neuromodulators.…”

Section: Proposed Mechanisms Of Actionmentioning

confidence: 99%

“…Specifically, dopamine, acetylcholine, and nicotine have a focusing, or signal-enhancing effect on facilitatory plasticity Kuo et al, 2008;Monte-Silva et al, 2010;Thirugnanasambandam et al, 2012). These substances abolish tDCS-induced non-focal, but enhance PAS-generated focal facilitatory plasticity.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

Batsikadze

Paulus

Kuo

et al. 2013

Neuropsychopharmacol

View full text Add to dashboard Cite

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.

show abstract

Section: General Remarkssupporting

confidence: 89%

Section: Proposed Mechanisms Of Actionmentioning

confidence: 99%

See 1 more Smart Citation

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

Batsikadze

Paulus

Kuo

et al. 2013

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Indeed there is ample evidence that the somatosensory cortex influences brain DA activity including striatal DA release (Huttunen et al, 2003;Rossini et al, 1995;Chen et al, 2007). There is also evidence that DA modulates the somatosensory cortex in the human brain (Kuo et al, 2007). Inasmuch as DA stimulation signals saliency and facilitates conditioning (Zink et al, 2003, Kelley, 2004), DA's modulation of the somatosensory cortex's response to food is likely to play a role in the formation of conditioned association between food and food-related environmental cues and in the enhanced reinforcing value of food that occurs in obesity (Epstein et al, 2007).…”

Section: Correlation Between D2r and Somatosensory Cortexmentioning

confidence: 99%

Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: Possible contributing factors

et al. 2008

View full text Add to dashboard Cite

Dopamine's role in inhibitory control is well recognized and its disruption may contribute to behavioral disorders of discontrol such as obesity. However, the mechanism by which impaired dopamine neurotransmission interferes with inhibitory control is poorly understood. We had previously documented a reduction in dopamine D2 receptors in morbidly obese subjects. To assess if the reductions in dopamine D2 receptors were associated with activity in prefrontal brain regions implicated in inhibitory control we assessed the relationship between dopamine D2 receptor availability in striatum with brain glucose metabolism (marker of brain function) in ten morbidly obese subjects (BMI>40 kg/m 2 ) and compared it to that in twelve non-obese controls. PET was used with [ 11 C]raclopride to assess D2 receptors and with [ 18 F] FDG to assess regional brain glucose metabolism. In obese subjects striatal D2 receptor availability was lower than controls and was positively correlated with metabolism in dorsolateral prefrontal, medial orbitofrontal, anterior cingulate gyrus and somatosensory cortices. In controls correlations with prefrontal metabolism were not significant but comparisons with those in obese subjects were not significant, which does not permit to ascribe the associations as unique to obesity. The associations between striatal D2 receptors and prefrontal metabolism in obese subjects suggest that decreases in striatal D2 receptors could contribute to overeating via their modulation of striatal prefrontal pathways, which participate in inhibitory control and salience attribution. The association between striatal D2 receptors and metabolism in somatosensory cortices (regions that process palatability) could underlie one of the mechanisms through which dopamine regulates the reinforcing properties of food. KeywordsOrbitofrontal cortex; Cingulate gyrus; Dorsolateral prefrontal; Dopamine transporters; Raclopride, PET The increase in obesity and associated metabolic diseases seen over the past decade has raised concern that if not controlled this may become the number one preventable public health threat for the 21st century (Sturm, 2002 (Berthoud, 2007). The extent to which individuals differ in their ability to inhibit these responses and control how much they eat is likely to modulate their risk for overeating in our current food rich environments (Berthoud, 2007).We had shown that in healthy individuals D2 receptor availability in the striatum modulated eating behavioral patterns (Volkow et al., 2003). Specifically the tendency to eat when exposed to negative emotions was negatively correlated with D2 receptor availability (the lower the D2 receptors the higher the likelihood that an individual would eat if emotionally stressed). In addition, in a different study, we showed that morbidly obese subjects (BMI>40) had lower than normal D2 receptor availability and these reductions were proportional to their BMI (Wang et al., 2001). These findings led us to postulate that low D2 receptor availability could put an...

show abstract

“…In the dopaminergic system, levodopa enhances its magnitude and duration (Kuo et al, 2008) but no longer when D2 receptors are blocked by sulpiride ). On the other hand, the D2 receptor agonist ropinirole decreases PASinduced LTP-like plasticity dose dependently in an inverted U-shaped manner ).…”

Section: Introductionmentioning

confidence: 99%

Neuromodulatory Neurotransmitters Influence LTP-Like Plasticity in Human Cortex: A Pharmaco-TMS Study

Korchounov

Ziemann

2011

Neuropsychopharmacol

View full text Add to dashboard Cite

Long-term potentiation (LTP) of synaptic efficacy is considered a fundamental mechanism of learning and memory. At the cellular level a large body of evidence demonstrated that the major neuromodulatory neurotransmitters dopamine (DA), norepinephrine (NE), and acetylcholine (ACh) influence LTP magnitude. Noninvasive brain stimulation protocols provide the opportunity to study LTP-like plasticity at the systems level of human cortex. Here we applied paired associative stimulation (PAS) to induce LTP-like plasticity in the primary motor cortex of eight healthy subjects. In a double-blind, randomized, placebo-controlled, crossover design, the acute effects of a single oral dose of the neuromodulatory drugs cabergoline (DA agonist), haloperidol (DA antagonist), methylphenidate (indirect NE agonist), prazosine (NE antagonist), tacrine (ACh agonist), and biperiden (ACh antagonist) on PAS-induced LTP-like plasticity were examined. The antagonists haloperidol, prazosine, and biperiden depressed significantly the PAS-induced LTP-like plasticity observed under placebo, whereas the agonists cabergoline, methylphenidate, and tacrine had no effect. Findings demonstrate that antagonists in major neuromodulatory neurotransmitter systems suppress LTP-like plasticity at the systems level of human cortex, in accord with evidence of their modulating action of LTP at the cellular level. This provides further supportive evidence for the known detrimental effects of these drugs on LTP-dependent mechanisms such as learning and memory.

show abstract

Boosting Focally-Induced Brain Plasticity by Dopamine

Cited by 248 publications

References 34 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

Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: Possible contributing factors

Neuromodulatory Neurotransmitters Influence LTP-Like Plasticity in Human Cortex: A Pharmaco-TMS Study

Contact Info

Product

Resources

About