4 results on '"Sarah Maywald"'
Search Results
2. Indices of cortical plasticity after therapeutic sleep deprivation in patients with major depressive disorder
- Author
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Christoph Nissen, Marion Kuhn, Florian Mainberger, Aliza Bredl, Elias Wolf, Claus Normann, Sarah Maywald, Maike Michel, Jonathan G. Maier, Nicola Sendelbach, Dieter Riemann, Bernd Feige, Stefan Klöppel, and Anne Eckert
- Subjects
medicine.medical_treatment ,Long-Term Potentiation ,Electroencephalography ,03 medical and health sciences ,0302 clinical medicine ,Neuroplasticity ,Humans ,Medicine ,Depressive Disorder, Major ,Neuronal Plasticity ,medicine.diagnostic_test ,business.industry ,Long-term potentiation ,Evoked Potentials, Motor ,medicine.disease ,Transcranial Magnetic Stimulation ,030227 psychiatry ,Transcranial magnetic stimulation ,Psychiatry and Mental health ,Clinical Psychology ,Sleep deprivation ,Synaptic plasticity ,Sleep Deprivation ,Antidepressant ,Major depressive disorder ,medicine.symptom ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Background Therapeutic sleep deprivation (SD) presents a unique paradigm to study the neurobiology of major depressive disorder (MDD). However, the rapid antidepressant mechanism, which differs from today's slow first-line treatments, is not sufficiently understood. We recently integrated two prominent hypotheses of MDD and sleep, the synaptic plasticity hypothesis of MDD and the synaptic homeostasis hypothesis of sleep-wake regulation, into a synaptic plasticity model of therapeutic SD in MDD. Here, we further tested this model positing that homeostatically elevating net synaptic strength through therapeutic SD shifts the initially deficient inducibility of associative synaptic long-term potentiation (LTP)-like plasticity in patients with MDD into a more favorable window of associative plasticity. Methods We used paired associative stimulation (PAS), a transcranial magnetic stimulation protocol (TMS), to quantify cortical LTP-like plasticity after one night of therapeutic sleep deprivation in 28 patients with MDD. Results We demonstrate a significantly different inducibility of associative plasticity in clinical responders to therapeutic SD (> 50% improvement on the 6-item Hamilton-Rating-Scale for Depression, n=13) compared to non-responders (n=15), which was driven by a long-term depression (LTD)-like response in SD-non-responders. Indices of global net synaptic strength (wake EEG theta activity, intracortical inhibition and BDNF serum levels) were increased after SD in both groups, with responders showing a generally lower intracortical inhibition than non-responders. Limitations Repetitive assessments prior to and after treatment would be needed to further determine potential mechanisms. Conclusion After a night of therapeutic SD, clinical responders show a significantly higher inducibility of associative LTP-like plasticity than non-responders.
- Published
- 2020
3. Synaptic plasticity model of therapeutic sleep deprivation in major depression
- Author
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Sarah Maywald, Elias Wolf, Florian Mainberger, Dieter Riemann, Jonathan G. Maier, Christoph Nissen, Stefan Klöppel, Annette Sterr, Claus Normann, Knut Biber, Aliza Bredl, Dietrich van Calker, and Marion Kuhn
- Subjects
0301 basic medicine ,Pulmonary and Respiratory Medicine ,03 medical and health sciences ,0302 clinical medicine ,Physiology (medical) ,mental disorders ,Neuroplasticity ,Metaplasticity ,medicine ,Animals ,Humans ,Wakefulness ,Depressive Disorder, Major ,Neuronal Plasticity ,Long-term potentiation ,medicine.disease ,Sleep deprivation ,030104 developmental biology ,Synaptic fatigue ,Neurology ,Synaptic plasticity ,Sleep Deprivation ,Major depressive disorder ,Antidepressant ,Neurology (clinical) ,medicine.symptom ,Sleep ,Psychology ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Therapeutic sleep deprivation (SD) is a rapid acting treatment for major depressive disorder (MDD). Within hours, SD leads to a dramatic decrease in depressive symptoms in 50-60% of patients with MDD. Scientifically, therapeutic SD presents a unique paradigm to study the neurobiology of MDD. Yet, up to now, the neurobiological basis of the antidepressant effect, which is most likely different from today's first-line treatments, is not sufficiently understood. This article puts the idea forward that sleep/wake-dependent shifts in synaptic plasticity, i.e., the neural basis of adaptive network function and behavior, represent a critical mechanism of therapeutic SD in MDD. Particularly, this article centers on two major hypotheses of MDD and sleep, the synaptic plasticity hypothesis of MDD and the synaptic homeostasis hypothesis of sleep-wake regulation, and on how they can be integrated into a novel synaptic plasticity model of therapeutic SD in MDD. As a major component, the model proposes that therapeutic SD, by homeostatically enhancing cortical synaptic strength, shifts the initially deficient inducibility of associative synaptic long-term potentiation (LTP) in patients with MDD in a more favorable window of associative plasticity. Research on the molecular effects of SD in animals and humans, including observations in the neurotrophic, adenosinergic, monoaminergic, and glutamatergic system, provides some support for the hypothesis of associative synaptic plasticity facilitation after therapeutic SD in MDD. The model proposes a novel framework for a mechanism of action of therapeutic SD that can be further tested in humans based on non-invasive indices and in animals based on direct studies of synaptic plasticity. Further determining the mechanisms of action of SD might contribute to the development of novel fast acting treatments for MDD, one of the major health problems worldwide.
- Published
- 2016
4. Sleep recalibrates homeostatic and associative synaptic plasticity in the human cortex
- Author
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Volker Mall, Elias Wolf, Sarah Maywald, Florian Mainberger, Anne Eckert, Dieter Riemann, Christoph Nissen, Janine Reis, Claus Normann, Marion Kuhn, Nikolai H. Jung, Hanna Schmid, Stefan Klöppel, Bernd Feige, Annette Sterr, Kai Spiegelhalder, Jonathan G. Maier, and Jan Bürklin
- Subjects
0301 basic medicine ,Adult ,Male ,Science ,Long-Term Potentiation ,General Physics and Astronomy ,Nonsynaptic plasticity ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Article ,03 medical and health sciences ,Young Adult ,0302 clinical medicine ,Homeostatic plasticity ,Synaptic augmentation ,Metaplasticity ,Homeostasis ,Humans ,Wakefulness ,Neuroscience of sleep ,Multidisciplinary ,Synaptic scaling ,Neuronal Plasticity ,Motor Cortex ,Electroencephalography ,General Chemistry ,Evoked Potentials, Motor ,Electrophysiological Phenomena ,030104 developmental biology ,Synaptic fatigue ,Synaptic plasticity ,Sleep Deprivation ,Female ,Sleep ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Sleep is ubiquitous in animals and humans, but its function remains to be further determined. The synaptic homeostasis hypothesis of sleep–wake regulation proposes a homeostatic increase in net synaptic strength and cortical excitability along with decreased inducibility of associative synaptic long-term potentiation (LTP) due to saturation after sleep deprivation. Here we use electrophysiological, behavioural and molecular indices to non-invasively study net synaptic strength and LTP-like plasticity in humans after sleep and sleep deprivation. We demonstrate indices of increased net synaptic strength (TMS intensity to elicit a predefined amplitude of motor-evoked potential and EEG theta activity) and decreased LTP-like plasticity (paired associative stimulation induced change in motor-evoked potential and memory formation) after sleep deprivation. Changes in plasma BDNF are identified as a potential mechanism. Our study indicates that sleep recalibrates homeostatic and associative synaptic plasticity, believed to be the neural basis for adaptive behaviour, in humans., Sleep deprivation is believed to lead to homeostatic increases in synaptic strength and reduced inducibility of associative LTP, based mainly on findings from animal studies. Here, Kuhn et al. demonstrate similar sleep-dependent synaptic plasticity changes in humans along with altered plasma BDNF levels.
- Published
- 2016
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