Sleep-dependent Memory Consolidation Research Articles

Sleep-Dependent Memory Consolidation in Developmental Disabilities: Cognitive and Neural Factors Driving Heterogeneity Across Diagnoses

Sleep-Dependent Memory Consolidation in Developmental Disabilities: Cognitive and Neural Factors Driving Heterogeneity Across Diagnoses

Effects of evening smartphone use on sleep and declarative memory consolidation in male adolescents and young adults

Abstract Exposure to short-wavelength light before bedtime is known to disrupt nocturnal melatonin secretion and can impair subsequent sleep. However, while it has been demonstrated that older adults are less affected by short-wavelength light, there is limited research exploring differences between adolescents and young adults. Furthermore, it remains unclear whether the effects of evening short-wavelength light on sleep architecture extend to sleep-related processes, such as declarative memory consolidation. Here, we recorded polysomnography from 33 male adolescents (15.42 ± 0.97 years) and 35 male young adults (21.51 ± 2.06 years) in a within-subjects design during three different nights to investigate the impact of reading for 90min either on a smartphone with or without a blue-light filter or from a printed book. We measured subjective sleepiness, melatonin secretion, sleep physiology, and sleep-dependent memory consolidation. While subjective sleepiness remained unaffected, we observed a significant melatonin-attenuation effect in both age groups immediately after reading on the smartphone without a blue-light filter. Interestingly, adolescents fully recovered from the melatonin attenuation in the following 50min before bedtime, whereas adults still, at bedtime, exhibited significantly reduced melatonin levels. Sleep-dependent memory consolidation and the coupling between sleep spindles and slow oscillations were not affected by short-wavelength light in both age groups. Nevertheless, adults showed a reduction in N3 sleep during the first night-quarter. In summary, avoiding smartphone use in the last hour before bedtime is advisable for adolescents and young adults to prevent sleep disturbances. Our research empirically supports general sleep hygiene advice and can inform future recommendations regarding the use of smartphones and other screen-based devices before bedtime.

0071 Does Additional Training on a Motor Sequence Task Improve Sleep-Dependent Memory Consolidation for Older Adults?

0071 Does Additional Training on a Motor Sequence Task Improve Sleep-Dependent Memory Consolidation for Older Adults?

Preoperative recovery sleep ameliorates postoperative cognitive dysfunction aggravated by sleep fragmentation in aged mice by enhancing EEG delta-wave activity and LFP theta oscillation in hippocampal CA1

Sleep fragmentation (SF) is a common sleep problem experienced during the perioperative period by older adults, and is associated with postoperative cognitive dysfunction (POCD). Increasing evidence indicates that delta-wave activity during non-rapid eye movement (NREM) sleep is involved in sleep-dependent memory consolidation and that hippocampal theta oscillations are related to spatial exploratory memory. Recovery sleep (RS), a self-regulated state of sleep homeostasis, enhances delta-wave power and memory performance in sleep-deprived older mice. However, it remains unclear whether RS therapy has a positive effect on cognitive changes following SF in older mouse models. Therefore, this study aimed to explore whether preoperative RS can alleviate cognitive deficits in aged mice with SF. A model of preoperative 24-h SF combined with exploratory laparotomy-induced POCD was established in 18-month-old mice. Aged mice were treated with preoperative 6-h RS following SF and postoperative 6-h RS following surgery, respectively. The changes in hippocampus-dependent cognitive function were investigated using behavioral tests, electroencephalography (EEG), local field potential (LFP), magnetic resonance imaging, and neuromorphology. Mice that underwent 24-h SF combined with surgery exhibited severe spatial memory impairment; impaired cognitive performance could be alleviated by preoperative RS treatment. In addition, preoperative RS increased NREM sleep; enhanced EEG delta-wave activity and LFP theta oscillation in the hippocampal CA1; and improved hippocampal perfusion, microstructural integrity, and neuronal damage. Taken together, these results provide evidence that preoperative RS may ameliorate the severity of POCD aggravated by SF by enhancing delta slow-wave activity and hippocampal theta oscillation, and by ameliorating the reduction in regional cerebral blood flow and white matter microstructure integrity in the hippocampus.

Closed-loop auditory stimulation of slow-wave sleep in chronic insomnia: a pilot study.

Insomnia is a prevalent and disabling condition whose treatment is not always effective. This pilot study explores the feasibility and effects of closed-loop auditory stimulation (CLAS) as a potential non-invasive intervention to improve sleep, its subjective quality, and memory consolidation in patients with insomnia. A total of 27 patients with chronic insomnia underwent a crossover, sham-controlled study with 2 nights of either CLAS or sham stimulation. Polysomnography was used to record sleep parameters, while questionnaires and a word-pair memory task were administered to assess subjective sleep quality and memory consolidation. The initial analyses included 17 patients who completed the study, met the inclusion criteria, and received CLAS. From those, 10 (58%) received only a small number of stimuli. In the remaining seven (41%) patients with sufficient CLAS, we evaluated the acute and whole-night effect on sleep. CLAS led to a significant immediate increase in slow oscillation (0.5-1 Hz) amplitude and activity, and reduced delta (1-4 Hz) and sigma/sleep spindle (12-15 Hz) activity during slow-wave sleep across the whole night. All these fundamental sleep rhythms are implicated in sleep-dependent memory consolidation. Yet, CLAS did not change sleep-dependent memory consolidation or sleep macrostructure characteristics, number of arousals, or subjective perception of sleep quality. Results showed CLAS to be feasible in patients with insomnia. However, a high variance in the efficacy of our automated stimulation approach suggests that further research is needed to optimise stimulation protocols to better unlock potential CLAS benefits for sleep structure and subjective sleep quality in such clinical settings.

Sleep spindle density and temporal clustering are associated with sleep-dependent memory consolidation in Parkinson's disease.

Sleep is required for successful memory consolidation. Sleep spindles, bursts of oscillatory activity occurring during non-REM sleep, are known to be crucial for this process and, recently, it has been proposed that the temporal organization of spindles into clusters might additionally play a role in memory consolidation. In Parkinson's disease, spindle activity is reduced, and this reduction has been found to be predictive of cognitive decline. However, it remains unknown whether alterations in sleep spindles in Parkinson's disease are predictive of sleep-dependent cognitive processes like memory consolidation, leaving open questions about the possible mechanisms linking sleep and more general cognitive state in Parkinson's patients. The current study sought to fill this gap by recording overnight polysomnography and measuring overnight declarative memory consolidation in a sample of thirty-five Parkinson's patients. Memory consolidation was measured using a verbal paired-associates task administered before and after the night of recorded sleep. We found that lower sleep spindle density at frontal leads during non-REM stage 3 was associated with worse overnight declarative memory consolidation. We also found that patients who showed less temporal clustering of spindles exhibited worse declarative memory consolidation. These results suggest alterations to sleep spindles, which are known to be a consequence of Parkinson's disease, might represent a mechanism by which poor sleep leads to worse cognitive function in Parkinson's patients.

Disrupted Nighttime Sleep and Sleep-Dependent Memory Consolidation in Pediatric Narcolepsy Type 1

Disrupted Nighttime Sleep and Sleep-Dependent Memory Consolidation in Pediatric Narcolepsy Type 1

An acute bout of high-intensity exercise affects nocturnal sleep and sleep-dependent memory consolidation.

Acute exercise has been shown to affect long-term memory and sleep. However, it is unclear whether exercise-induced changes in sleep architecture are associated with enhanced memory. Recently, it has been shown that exercise followed by a nap improved declarative memory. Whether these effects transfer to night sleep and other memory domains has not yet been studied. Here, we investigate the influence of exercise on nocturnal sleep architecture and associations with sleep-dependent procedural and declarative memory consolidation. Nineteen subjects (23.68 ± 3.97 years) were tested in a balanced cross-over design. In two evening sessions, participants either exercised (high-intensity interval training) or rested immediately after encoding two memory tasks: (1) a finger tapping task and (2) a paired-associate learning task. Subsequent nocturnal sleep was recorded by polysomnography. Retrieval was conducted the following morning. High-intensity interval training lead to an increased declarative memory retention (p = 0.047, d = 0.40) along with a decrease in REM sleep (p = 0.012, d = 0.75). Neither procedural memory nor NREM sleep were significantly affected. Exercise-induced changes in N2 showed a positive correlation with procedural memory retention which did not withstand multiple comparison correction. Exploratory analyses on sleep spindles and slow wave activity did not reveal significant effects. The present findings suggest an exercise-induced enhancement of declarative memory which aligns with changes in nocturnal sleep architecture. This gives additional support for the idea of a potential link between exercise-induced sleep modifications and memory formation which requires further investigation in larger scaled studies.

Sleep restoration by optogenetic targeting of GABAergic neurons reprograms microglia and ameliorates pathological phenotypes in an Alzheimer’s disease model

BackgroundAlzheimer’s disease (AD) patients exhibit memory disruptions and profound sleep disturbances, including disruption of deep non-rapid eye movement (NREM) sleep. Slow-wave activity (SWA) is a major restorative feature of NREM sleep and is important for memory consolidation.MethodsWe generated a mouse model where GABAergic interneurons could be targeted in the presence of APPswe/PS1dE9 (APP) amyloidosis, APP-GAD-Cre mice. An electroencephalography (EEG) / electromyography (EMG) telemetry system was used to monitor sleep disruptions in these animals. Optogenetic stimulation of GABAergic interneurons in the anterior cortex targeted with channelrhodopsin-2 (ChR2) allowed us to examine the role GABAergic interneurons play in sleep deficits. We also examined the effect of optogenetic stimulation on amyloid plaques, neuronal calcium as well as sleep-dependent memory consolidation. In addition, microglial morphological features and functions were assessed using confocal microscopy and flow cytometry. Finally, we performed sleep deprivation during optogenetic stimulation to investigate whether sleep restoration was necessary to slow AD progression.ResultsAPP-GAD-Cre mice exhibited impairments in sleep architecture including decreased time spent in NREM sleep, decreased delta power, and increased sleep fragmentation compared to nontransgenic (NTG) NTG-GAD-Cre mice. Optogenetic stimulation of cortical GABAergic interneurons increased SWA and rescued sleep impairments in APP-GAD-Cre animals. Furthermore, it slowed AD progression by reducing amyloid deposition, normalizing neuronal calcium homeostasis, and improving memory function. These changes were accompanied by increased numbers and a morphological transformation of microglia, elevated phagocytic marker expression, and enhanced amyloid β (Aβ) phagocytic activity of microglia. Sleep was necessary for amelioration of pathophysiological phenotypes in APP-GAD-Cre mice.ConclusionsIn summary, our study shows that optogenetic targeting of GABAergic interneurons rescues sleep, which then ameliorates neuropathological as well as behavioral deficits by increasing clearance of Aβ by microglia in an AD mouse model.

Overnight exposure to pink noise could jeopardize sleep-dependent insight and pattern detection.

Accumulated evidence from the past decades suggests that sleep plays a crucial role in memory consolidation and the facilitation of higher-level cognitive processes such as abstraction and gist extraction. In addition, recent studies show that applying pink noise during sleep can further enhance sleep-dependent memory consolidation, potentially by modulating sleep physiology through stochastic resonance. However, whether this enhancement extends to higher cognitive processes remains untested. In this study, we investigated how the application of open-loop pink noise during sleep influences the gain of insight into hidden patterns. Seventy-two participants were assigned to three groups: daytime-wake, silent sleep, and sleep with pink noise. Each group completed the number reduction task, an established insight paradigm known to be influenced by sleep, over two sessions with a 12-h interval. Sleep groups were monitored by the DREEM 3 headband in home settings. Contrary to our prediction, pink noise did not induce an increase in insight compared to silent sleep and was statistically more similar to the wake condition despite evidence for its typical influence on sleep physiology. Particularly, we found that pink noise limited the time spent in the initial cycle of N1 just after sleep onset, while time spent in N1 positively predicted insight. These results echo recent suggestions that the time in the initial cycle of N1 plays a critical role in insight formation. Overall, our results suggest that open-loop pink noise during sleep may be detrimental to insight formation and creativity due to the alterations it causes to normal sleep architecture.

P047 Slow Wave Dynamics in Mild Cognitive Impairment compared with Age Matched Controls: A High Density EEG study.

Abstract Introduction Slow wave activity during non-rapid eye movement (NREM) sleep has been linked with memory consolidation in healthy older adults. To date, there has been limited research in mild cognitively impaired populations, particularly looking across the whole brain using high density EEG. We aimed to determine if the dynamics of slow wave activity (delta power) during the first NREM sleep cycle differ between patients with mild cognitive impairment (MCI) and healthy older adults. Methods Participants were assessed for MCI by a panel of neuropsychologists and clinicians. They underwent full polysomnography including high-density EEG (256 electrodes). We computed the delta power (0.5-4.5Hz) for each NREM cycle and slope between sleep onset and the peak of delta in the first NREM sleep cycle (rise-rate) which were compared between groups using t-tests. Results 17 older adults with MCI and 21 older healthy controls were assessed. The mean delta power in the first NREM cycle did not differ between MCI and controls across the whole brain, but the global rise-rate (1/min) of MCI and controls was 0.0015 and 0.0032 respectively (t-value -2.35, p=0.025). Discussion Global slow wave dynamics in the first NREM period appear to be altered in patients with MCI compared with age-matched controls. The gentler slope of rise-rate to the first delta peak in MCI patients than in healthy controls may indicate the dysfunction of sleep homeostasis in MCI patients. Regional slow wave dynamics, ultra-low frequency delta (0.25-1Hz), and associations with sleep dependent memory consolidation will further be explored.

Sleep Stage Transitions and Sleep-Dependent Memory Consolidation in Children with Narcolepsy-Cataplexy.

Electroencephalographic sleep stage transitions and altered first REM sleep period transitions have been identified as biomarkers of type 1 narcolepsy in adults, but not in children. Studies on memory complaints in narcolepsy have not yet investigated sleep-dependent memory consolidation. We aimed to explore stage transitions; more specifically altered REM sleep transition and its relationship with sleep-dependent memory consolidation in children with narcolepsy. Twenty-one children with narcolepsy-cataplexy and twenty-three healthy control children completed overnight polysomnography and sleep-dependent memory consolidation tests. Overnight transition rates (number of transitions per hour), global relative transition frequencies (number of transitions between a stage and all other stages/total number of transitions × 100), overnight transitions to REM sleep (transition from a given stage to REM/total REM transitions × 100), and altered first REM sleep period transitions (transitions from wake or N1 to the first REM period) were computed. Narcoleptic children had a significantly higher overnight transition rate with a higher global relative transition frequencies to wake. A lower sleep-dependent memory consolidation score found in children with narcolepsy was associated with a higher overnight transition frequency. As observed in narcoleptic adults, 90.48% of narcoleptic children exhibited an altered first REM sleep transition. As in adults, the altered sleep stage transition is also present in children with narcolepsy-cataplexy, and a higher transition rate could have an impact on sleep-dependent memory consolidation. These potential biomarkers could help diagnose type 1 narcolepsy in children more quickly; however, further studies with larger cohorts, including of those with type 2 narcolepsy and hypersomnia, are needed.

Human REM sleep recalibrates neural activity in support of memory formation.

The proposed mechanisms of sleep-dependent memory consolidation involve the overnight regulation of neural activity at both synaptic and whole-network levels. Now, there is a lack of in vivo data in humans elucidating if, and how, sleep and its varied stages balance neural activity, and if such recalibration benefits memory. We combined electrophysiology with in vivo two-photon calcium imaging in rodents as well as intracranial and scalp electroencephalography (EEG) in humans to reveal a key role for non-oscillatory brain activity during rapid eye movement (REM) sleep to mediate sleep-dependent recalibration of neural population dynamics. The extent of this REM sleep recalibration predicted the success of overnight memory consolidation, expressly the modulation of hippocampal-neocortical activity, favoring remembering rather than forgetting. The findings describe a non-oscillatory mechanism how human REM sleep modulates neural population activity to enhance long-term memory.

The effects of closed-loop auditory stimulation on sleep oscillatory dynamics in relation to motor procedural memory consolidation.

Healthy aging and many disorders show reduced sleep-dependent memory consolidation and corresponding alterations in non-rapid eye movement sleep oscillations. Yet sleep physiology remains a relatively neglected target for improving memory. We evaluated the effects of closed-loop auditory stimulation during sleep (CLASS) on slow oscillations (SOs), sleep spindles, and their coupling, all in relation to motor procedural memory consolidation. Twenty healthy young adults had two afternoon naps: one with auditory stimulation during SO upstates and another with no stimulation. Twelve returned for a third nap with stimulation at variable times in relation to SO upstates. In all sessions, participants trained on the motor sequence task prior to napping and were tested afterward. Relative to epochs with no stimulation, upstate stimuli disrupted sleep and evoked SOs, spindles, and SO-coupled spindles. Stimuli that successfully evoked oscillations were delivered closer to the peak of the SO upstate and when spindle power was lower than stimuli that failed to evoke oscillations. Across conditions, participants showed similar significant post-nap performance improvement that correlated with the density of SO-coupled spindles. Despite its strong effects on sleep physiology, CLASS failed to enhance motor procedural memory. Our findings suggest methods to overcome this failure, including better sound calibration to preserve sleep continuity and the use of real-time predictive algorithms to more precisely target SO upstates and to avoid disrupting endogenous SO-coupled spindles and their mnemonic function. They motivate continued development of CLASS as an intervention to manipulate sleep oscillatory dynamics and improve memory.

Sleep sculpts circuits in every species studied

In this issue of Cell, we see first evidence of sleep-dependent circuit remodeling alongside behavioral memory consolidation in C.elegans. Examining memory of a never-rewarded odor during post-training sleep from synapse to behavior all in one organism opens the opportunity to use this well-mapped nervous system to study mechanisms of sleep-dependent memory consolidation.

0588 DNS and Sleep-Dependent Memory Consolidation in Pediatric Narcolepsy Type 1

Abstract Introduction Disrupted nighttime sleep (DNS) is common in narcolepsy type 1 (NT1), yet its impact on cognitive function is unknown. Given known associations between sleep-dependent memory consolidation and N2 sleep spindles, we hypothesized that NT1 impairs memory consolidation, due to fragmented N2 sleep and altered N2 sleep spindles in the NT1 group. Methods In this case-control study, we trained n=23 NT1 participants [mean age 15.8 years (3.2)] and n=28 healthy control (HC) patients [13.6 years (3.7)] to criterion on a spatial declarative memory task before a nocturnal in-lab polysomnogram and then gave them a cued recall test upon awakening in the morning. NT1 participants could take SSRI/SNRI medication for cataplexy but were weaned off wake-promoting medications and excluded if on an oxybate. We extracted wake and sleep stage bout numbers from sleep and N2 spindle characteristics from the polysomnogram and conducted linear regression with memory consolidation results across groups. Results Adjusting for age, NT1 participants had longer sleep duration than HC, more N1%, lower N3%, higher Wake/N1 Index, as well as more bouts per hour of Wake, N1, N2, REM than controls (p’s < 0.04). Compared to HC, NT1 subjects had similar N2 spindle density, amplitude, and sigma power, but shorter duration of N2 spindles (p=0.009). More NT1 participants could not meet performance criterion on the initial learning task and required an easier memory task vs. HC (p=0.02) despite being older than HC. NT1 participants showed a trend for impaired memory consolidation vs. HC across a night of sleep after adjusting for age, gender, and total sleep time (p=0.07). Across groups, shorter N2 spindle duration (p=0.02) but not increased N2 bout number was associated with worse sleep-dependent memory consolidation. Conclusion Compared to controls, NT1 participants showed encoding difficulties but only a trend difference in memory consolidation despite greater sleep fragmentation. NT1 participants had briefer N2 sleep spindles and overall, these shorter N2 spindles were associated with greater memory consolidation deficits. Future sleep therapeutic studies are needed to determine if sleep-dependent memory consolidation can be improved to address daytime cognitive problems in NT1 patients. Support (if any) Jazz Pharmaceuticals and National Institutes of Health grant 5K23NS104267-2

0059 Acoustic enhancement of sleep slow oscillations nested to spindles relative to delta waves improves memory consolidation

Abstract Introduction The nesting of electroencephalographic (EEG) sleep slow oscillations (SOs) to spindles has been shown to be important for sleep-dependent memory consolidation. However, recent evidence indicates that a higher proportion of SOs nested to spindles, relative to δ waves, might be even more critical for sleep-dependent memory consolidation. Acoustic stimulation during slow wave sleep has been shown to be effective in improving memory consolidation. Here, we examined the contribution of SOs nested to spindles relative to δ waves on sleep-dependent declarative memory consolidation associated with acoustic stimulation. Methods Twenty subjects (18-35 years, 75% females) participated in a randomized cross-over study. At each visit participants received either stimulation (stim) or sham following an adaption night. Stim occurred in blocks of 5 pulses (ON intervals) followed by a period of equal length with no stimulation (OFF intervals). Participants learned 40 Arabic-English word pairs and were tested before sleep and after sleep in the morning and again in the afternoon. Detection of SOs (< 2 Hz), δ waves (2-4 Hz), spindles (11-16Hz), and the ratio (%) of spindles nested to SO over δ waves (SO/δ Nesting Index) were calculated during ON intervals for stim and sham conditions. Results Overnight mean (SD) percentage change in word recall between conditions was similar in the morning (stim 6(3)%, sham 4(6)%, p=0.68), but was higher in the afternoon in stim compared to the sham condition (stim 10(4)%, sham 4(6)%, p=0.02). The SO/δ Nesting Index was higher in stim compared to the sham condition (stim 21(13)%, sham 13(10%), p=0.004). Within-subject improvement from sham to stim condition in afternoon memory was associated with a greater change in SO/δ Nesting Index (R=0.63, p=0.03), this association was not observed for spindles nested to SOs (R=0.33, p=0.202) or spindles nested to δ waves (R=-0.18, p=0.811). Conclusion Enhancement of memory consolidation with acoustic stimulation may be dependent on its ability to increase SOs nested to spindles relative to δ waves. Dynamic changes in the relationships between SOs, δ waves and spindles can help inform novel EEG-derived markers and targets to enhance sleep-dependent memory consolidation. Support (if any) DARPA award W911NF-16- 2-0021

Sleep-dependent memory consolidation in schizophrenia: A systematic review and meta-analysis

Sleep disturbances and cognitive impairment are both persistent and common features of schizophrenia. Accumulating evidence indicates that sleep-dependent memory consolidation might be impaired in patients with schizophrenia compared to healthy controls. The current systematic review was performed in accordance with PRISMA guidelines. A random-effects model was used to calculate effect sizes (Hedge's g). In the quantitative review, three separate meta-analyses were conducted for procedural memory in healthy controls, schizophrenia, and comparison between healthy controls and schizophrenia. Additionally, separate meta-analyses were conducted for the studies using finger tapping motor sequence task, as it is the most commonly used task. The current systematic review included 14 studies including 304 patients with schizophrenia and 209 healthy controls. The random-effects model analyses for sleep-dependent procedural memory consolidation resulted in a small effect size in schizophrenia (g=0.26), a large effect size in healthy controls (g=0.98), a moderate effect size in healthy controls vs schizophrenia (g=0.64). For the studies using finger tapping motor sequence task, meta-analyses resulted in a small effect size in schizophrenia (g=0.19), a large effect size in healthy controls (g=1.07), a moderate effect size in healthy controls vs schizophrenia (g=0.70). In the qualitative review, there was also impaired sleep-dependent declarative memory consolidation in schizophrenia compared to healthy controls. Current findings support that sleep improves memory consolidation in healthy adults, but there is a deficit in sleep-dependent memory consolidation in people with schizophrenia. Future studies investigating sleep-dependent consolidation of different memory subtypes with polysomnography in different stages of psychotic disorders are needed.

Selectivity in sleep-dependent memory consolidation

Memory is not uniformly stored in the brain. There are various types of memories and only some are retained over time. Much is forgotten, and of those memories retained, their representations are transferred into long-term stores, a process called consolidation, which occurs predominantly during sleep. Sorting out how sleep contributes to memory has not been straightforward, but nonetheless, emerging data suggest that sleep plays a causal role in how our memories are formed and ultimately stored. One of the intriguing aspects of sleep-dependent memory consolidation is its selectivity. Memories of future relevance are tagged during encoding and prioritized for consolidation during subsequent sleep, leading to the discriminatory selection for memories that are emotional, show difficultly during learning, have high retrieval expectancy, or are associated with rewards. Several brain regions, electrophysiological oscillations and neurotransmitters are at the heart of this process, guiding each organism through its unique life.

Neural dynamic transitions caused by changes of synaptic strength in heterogeneous networks

Sleep-dependent memory consolidation (SDMC) is an unaddressed and challenging functional issue regarding neural dynamics. Based on experimental findings, the synaptic homeostasis hypothesis for understanding SDMC implies a link between changes of synaptic strength and transitions of neural dynamics (including tonic and bursting activities). However, the causality of the link has been unclear. Recently, it has been found that, the synaptic changes can cause the dynamical transitions and so can produce the slow-wave activity (SWA) similar to that observed during sleep in a homogeneous network (Zhou et al., 2021). Since many real neural networks are heterogeneous in topology, we herein further investigated the transitions and the SWA driven by the synaptic changes in heterogeneous networks. It was found that synaptic changes can also cause the dynamical transitions and the SWA. Differently, the transitions in heterogeneous networks are hierarchical for neurons with different degrees, whether in electrically or chemically coupled networks. The critical synaptic strengths related to the transitions for neurons depend strongly on their degrees. The larger the degree, the smaller the critical synaptic strength. We showed that, they obey power-law relations, both in electrically coupled networks and in chemically coupled networks in the presence of inhibitory synapses. Particularly, it was found that the networked critical synaptic strength depends only on the networked maximum degree in electrically coupled networks. We showed, both numerically and analytically, that they also satisfy a power-law function. In general, our study revealed a possible causal relationship between changes of synaptic strength and transitions of neural dynamics in heterogeneous networks. Further interesting and challenging investigations are briefly discussed as well.