scholarly journals How rhythms of the sleeping brain tune memory and synaptic plasticity

SLEEP ◽  
2019 ◽  
Vol 42 (7) ◽  
Author(s):  
Carlos Puentes-Mestril ◽  
James Roach ◽  
Niels Niethard ◽  
Michal Zochowski ◽  
Sara J Aton
Keyword(s):  
Synaptic Plasticity ◽  
Eye Movement ◽  
Neural Circuits ◽  
Declarative Memory ◽  
Rapid Eye Movement ◽  
Brain Areas ◽  
Brain Circuits ◽  
New Information ◽  
Procedural Task ◽  
Synaptic Changes

Abstract Decades of neurobehavioral research has linked sleep-associated rhythms in various brain areas to improvements in cognitive performance. However, it remains unclear what synaptic changes might underlie sleep-dependent declarative memory consolidation and procedural task improvement, and why these same changes appear not to occur across a similar interval of wake. Here we describe recent research on how one specific feature of sleep—network rhythms characteristic of rapid eye movement and non-rapid eye movement—could drive synaptic strengthening or weakening in specific brain circuits. We provide an overview of how these rhythms could affect synaptic plasticity individually and in concert. We also present an overarching hypothesis for how all network rhythms occurring across the sleeping brain could aid in encoding new information in neural circuits.

scholarly journals EEG Bands of Wakeful Rest, Slow-Wave and Rapid-Eye-Movement Sleep at Different Brain Areas in Rats

2016 ◽  
Vol 10 ◽  
Author(s):  
Wei Jing ◽  
Yanran Wang ◽  
Guangzhan Fang ◽  
Mingming Chen ◽  
Miaomiao Xue ◽  
...  
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Brain Areas

scholarly journals Specific changes in sleep oscillations after blocking human metabotropic glutamate receptor 5 in the absence of altered memory function

2021 ◽  
pp. 026988112110056
Author(s):  
Gordon B Feld ◽  
Til O Bergmann ◽  
Marjan Alizadeh-Asfestani ◽  
Viola Stuke ◽  
Jan-Philipp Wriede ◽  
...  
Keyword(s):  
Eye Movement ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Declarative Memory ◽  
Rapid Eye Movement ◽  
Metabotropic Glutamate Receptor 5 ◽  
Memory Processing ◽  
Metabotropic Glutamate ◽  
Healthy Humans ◽  
Nonrem Sleep

Background: Sleep consolidates declarative memory by repeated replay linked to the cardinal oscillations of non-rapid eye movement (NonREM) sleep. However, there is so far little evidence of classical glutamatergic plasticity induced by this replay. Rather, we have previously reported that blocking N-methyl-D-aspartate (NMDA) or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors does not affect sleep-dependent consolidation of declarative memory. Aims: The aim of this study was to investigate the role of metabotropic glutamate receptor 5 (mGluR5) in memory processing during sleep. Methods: In two placebo-controlled within-subject crossover experiments with 20 healthy humans each, we used fenobam to block mGluR5 during sleep. In Experiment I, participants learned word-pairs (declarative task) and a finger sequence (procedural task) in the evening, then received the drug and recall was tested the next morning. To cover possible effects on synaptic renormalization processes during sleep, in Experiment II participants learned new word-pairs in the morning after sleep. Results/outcomes: Surprisingly, fenobam neither reduced retention of memory across sleep nor new learning after sleep, although it severely altered sleep architecture and memory-relevant EEG oscillations. In NonREM sleep, fenobam suppressed 12–15 Hz spindles but augmented 2–4 Hz delta waves, whereas in rapid eye movement (REM) sleep it suppressed 4–8 Hz theta and 16–22 Hz beta waves. Notably, under fenobam NonREM spindles became more consistently phase-coupled to the slow oscillation. Conclusions/interpretations: Our findings indicate that mGluR5-related plasticity is not essential for memory processing during sleep, even though mGlurR5 are strongly implicated in the regulation of the cardinal sleep oscillations.

scholarly journals Medulla glutamatergic neurons control wake-sleep transitions

2021 ◽  
Author(s):  
Sasa Teng ◽  
Fenghua Zhen ◽  
Jose Canovas Schalchli ◽  
Xinyue Chen ◽  
Hao Jin ◽  
...  
Keyword(s):  
Eye Movement ◽  
Animal Species ◽  
Preoptic Area ◽  
Nrem Sleep ◽  
Brain Structures ◽  
Rapid Eye Movement ◽  
Glutamatergic Neurons ◽  
Sleep Maintenance ◽  
Brain Circuits

SUMMARYSleep is a ubiquitous behavior in animal species. Yet, brain circuits controlling sleep remain poorly understood. Previous studies have identified several brain structures that promote sleep, but whether these structures are involved in sleep initiation or sleep maintenance remains largely unknown. Here we identified a population of glutamatergic neurons in the medulla that project to the preoptic area (POA), a prominent sleep-promoting region. Chemogenetic silencing of POA-projecting medulla neurons disrupts the transitions from wakefulness to Non-Rapid Eye Movement (NREM) sleep, whereas chemogenetic activation of these neurons promotes NREM sleep. Moreover, we show that optogenetic activation of medulla glutamatergic neurons or their projections in the POA reliably initiates long-lasting NREM sleep in awake mice. Together, our findings uncover a novel excitatory brainstem-hypothalamic circuit that controls the wake-sleep transitions.

scholarly journals SYNPLA: A synapse-specific method for identifying learning-induced synaptic plasticity loci

2018 ◽  
Author(s):  
Kim Dore ◽  
Yvonne Pao ◽  
Jose Soria Lopez ◽  
Sage Aronson ◽  
Huiqing Zhan ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
High Throughput ◽  
Neural Circuits ◽  
Synaptic Strength ◽  
Proximity Ligation Assay ◽  
Specific Method ◽  
Neural Pathways ◽  
Proximity Ligation ◽  
Synaptic Changes ◽  
Specific Learning

AbstractWhich neural circuits undergo synaptic changes when an animal learns? Although it is widely accepted that changes in synaptic strength underlie many forms of learning and memory, it remains challenging to connect changes in synaptic strength at specific neural pathways to specific behaviors and memories. Here we introduce SYNPLA (SYNaptic Proximity Ligation Assay), a synapse-specific, high-throughput and potentially brain-wide method capable of detecting circuit-specific learning-induced synaptic plasticity.

scholarly journals GABA neurons in the ventral tegmental area regulate non-rapid eye movement sleep in mice

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Srikanta Chowdhury ◽  
Takanori Matsubara ◽  
Toh Miyazaki ◽  
Daisuke Ono ◽  
Noriaki Fukatsu ◽  
...  
Keyword(s):  
Ventral Tegmental Area ◽  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Neural Circuitry ◽  
Acid Decarboxylase ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Brain Areas ◽  
Ventral Tegmental

Sleep/wakefulness cycle is regulated by coordinated interactions between sleep- and wakefulness-regulating neural circuitry. However, the detailed mechanism is far from understood. Here, we found that glutamic acid decarboxylase 67-positive GABAergic neurons in the ventral tegmental area (VTAGad67+) are a key regulator of non-rapid eye movement (NREM) sleep in mice. VTAGad67+ project to multiple brain areas implicated in sleep/wakefulness regulation such as the lateral hypothalamus (LH). Chemogenetic activation of VTAGad67+ promoted NREM sleep with higher delta power whereas optogenetic inhibition of these induced prompt arousal from NREM sleep, even under highly somnolescent conditions, but not from REM sleep. VTAGad67+ showed the highest activity in NREM sleep and the lowest activity in REM sleep. Moreover, VTAGad67+ directly innervated and inhibited wake-promoting orexin/hypocretin neurons by releasing GABA. As such, optogenetic activation of VTAGad67+ terminals in the LH promoted NREM sleep. Taken together, we revealed that VTAGad67+ play an important role in the regulation of NREM sleep.

scholarly journals SYNPLA, a method to identify synapses displaying plasticity after learning

2020 ◽  
Vol 117 (6) ◽  
pp. 3214-3219 ◽  
Author(s):  
Kim Dore ◽  
Yvonne Pao ◽  
Jose Soria Lopez ◽  
Sage Aronson ◽  
Huiqing Zhan ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
High Throughput ◽  
Neural Circuits ◽  
Synaptic Strength ◽  
Proximity Ligation Assay ◽  
Neural Pathways ◽  
Proximity Ligation ◽  
Synaptic Changes ◽  
Specific Learning

Which neural circuits undergo synaptic changes when an animal learns? Although it is widely accepted that changes in synaptic strength underlie many forms of learning and memory, it remains challenging to connect changes in synaptic strength at specific neural pathways to specific behaviors and memories. Here we introduce SYNPLA (synaptic proximity ligation assay), a synapse-specific, high-throughput, and potentially brain-wide method capable of detecting circuit-specific learning-induced synaptic plasticity.

scholarly journals Central control of cardiovascular function during sleep

2013 ◽  
Vol 305 (12) ◽  
pp. H1683-H1692 ◽  
Author(s):  
Alessandro Silvani ◽  
Roger A. L. Dampney
Keyword(s):  
Eye Movement ◽  
Neural Circuits ◽  
Preoptic Area ◽  
Current Knowledge ◽  
Cardiovascular Function ◽  
Neural Pathways ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Physiological Mechanisms ◽  
Medullary Nuclei

There is increasing evidence that cardiovascular control during sleep is relevant for cardiovascular risk. This evidence warrants increased experimental efforts to understand the physiological mechanisms of such control. This review summarizes current knowledge on autonomic features of sleep states [non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS)] and proposes some testable hypotheses concerning the underlying neural circuits. The physiological reduction of blood pressure (BP) during the night (BP dipping phenomenon) is mainly caused by generalized cardiovascular deactivation and baroreflex resetting during NREMS, which, in turn, are primarily a consequence of central autonomic commands. Central commands during NREMS may involve the hypothalamic ventrolateral preoptic area, central thermoregulatory and central baroreflex pathways, and command neurons in the pons and midbrain. During REMS, opposing changes in vascular resistance in different regional beds have the net effect of increasing BP compared with that of NREMS. In addition, there are transient increases in BP and baroreflex suppression associated with bursts of brain and skeletal muscle activity during REMS. These effects are also primarily a consequence of central autonomic commands, which may involve the midbrain periaqueductal gray, the sublaterodorsal and peduncular pontine nuclei, and the vestibular and raphe obscurus medullary nuclei. A key role in permitting physiological changes in BP during sleep may be played by orexin peptides released by hypothalamic neurons, which target the postulated neural pathways of central autonomic commands during NREMS and REMS. Experimental verification of these hypotheses may help reveal which central neural pathways and mechanisms are most essential for sleep-related changes in cardiovascular function.

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