Publications by authors named "Jidong Fang"

Background: Identifying biomarkers that predict substance use disorder propensity may better strategize antiaddiction treatment. Melanin-concentrating hormone (MCH) neurons in the lateral hypothalamus critically mediate interactions between sleep and substance use; however, their activities are largely obscured in surface electroencephalogram (EEG) measures, hindering the development of biomarkers.

Methods: Surface EEG signals and real-time calcium (Ca) activities of lateral hypothalamus MCH neurons (Ca) were simultaneously recorded in male and female adult rats.

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Background: Identifying biomarkers that predict substance use disorder (SUD) propensity may better strategize anti-addiction treatment. The melanin-concentrating hormone (MCH) neurons in the lateral hypothalamus (LH) critically mediates interactions between sleep and substance use; however, their activities are largely obscured in surface electroencephalogram (EEG) measures, hindering the development of biomarkers.

Methods: Surface EEG signals and real-time Ca activities of LH MCH neurons (Ca) were simultaneously recorded in male and female adult rats.

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Introduction: Sleep disturbances are prominent in drug use disorders, including those involving opioids in both humans and animals. Recent studies have shown that administration of liraglutide, a glucagon-like peptide-1 agonist, significantly reduces heroin taking and seeking in rats. In an effort to further understand the action of this substance on physiological functions and to evaluate safety issues for its potential clinical use, the aim of the present study was to determine whether the dose of liraglutide found effective in reducing responding for an opioid also could improve sleep in drug-naïve rats.

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Background: Persistent sleep disruptions following withdrawal from abused drugs may hold keys to battle drug relapse. It is posited that there may be sleep signatures that predict relapse propensity, identifying which may open new avenues for treating substance use disorders.

Methods: We trained male rats (approximately postnatal day 56) to self-administer cocaine.

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Background: Sleep slow wave activity (SWA) peaks during childhood and declines in the transition to adolescence during typical development (TD). It remains unknown whether this trajectory differs in youth with neuropsychiatric disorders.

Methods: We analyzed sleep EEGs of 664 subjects 6 to 21 y (449 TD, 123 unmedicated, 92 medicated) and 114 subjects 7-12 y (median 10.

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Study Objectives: Psychiatric/learning disorders are associated with sleep disturbances, including those arising from abnormal cortical activity. The odds ratio product (ORP) is a standardized electroencephalogram metric of sleep depth/intensity validated in adults, while ORP data in youth are lacking. We tested ORP as a measure of sleep depth/intensity in adolescents with and without psychiatric/learning disorders.

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Sleep spindles, bursts of electroencephalogram (EEG) activity in the σ-frequency (11-16 Hz) range, may be biomarkers of cortical development. Studies capturing the transition to adolescence are needed to delineate age-related, sex-related, and pubertal-related changes in sleep spindles at the population-level. We analyzed the sleep EEG of 572 subjects 6-21 years (48% female) and 332 subjects 5-12 years (46% female) followed-up at 12-22 years.

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Article Synopsis
  • The study examines changes in sleep patterns during adolescence by analyzing brain activity, focusing on slow wave activity (SWA) and sleep depth (measured by odds ratio product - ORP) in a diverse group of participants aged 6-21 years.
  • Results show that SWA is stable from ages 6-10, decreases from 11-17, and plateaus at ages 18-21, with notable differences between males and females regarding the rate of decline.
  • ORP increases with age without significant differences between sexes or puberty stages, indicating that while SWA reflects specific brain maturation processes, ORP provides insights into overall sleep depth regulation during adolescent development.
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Trazodone and cognitive-behavioural treatment for insomnia (CBT-I) are widely used to treat patients with chronic insomnia. Although both treatments improve sleep continuity, no study has compared their comparative effectiveness in modifying spectral electroencephalographic (EEG) activity during sleep in humans. In this study, participants included 19 men and women with chronic insomnia who were randomized to either trazodone (n = 8) or CBT-I (n = 11) treatment for 3 months.

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Sleep abnormalities are often a prominent contributor to withdrawal symptoms following chronic drug use. Notably, rapid eye movement (REM) sleep regulates emotional memory, and persistent REM sleep impairment after cocaine withdrawal negatively impacts relapse-like behaviors in rats. However, it is not understood how cocaine experience may alter REM sleep regulatory machinery, and what may serve to improve REM sleep after withdrawal.

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Chronic intermittent hypoxia (CIH) is the main symptom of obstructive sleep apnea syndrome (OSAS) and causes neural damage and cognitive deficits via neuroinflammation. Toll-like receptors (TLRs), especially TLR2, play an important role in neuroinflammation. However, the mechanisms by which TLR2 participates in CIH-induced cognitive deficits remain unclear.

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Rapid-eye-movement (REM) sleep without atonia (RSWA), a marker of REM sleep behavior disorder (RBD), is frequently comorbid with Parkinson's disease (PD). Although rodent models are commonly used for studying PD, the neurobiological and behavioral correlates of RBD remain poorly understood. Therefore, we developed a behavior-based criteria to identify RSWA in the hemiparkinsonian rat model of PD.

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Study Objectives: A major challenge in treating insomnia is to find effective medicines with fewer side effects. Activation of G-protein-gated inward rectifying K+ channels (GIRKs) by GABAB agonists baclofen or γ-hydroxybutyric acid (GHB) promotes nonrapid eye movement (NREM) sleep and consolidates sleep. However, baclofen has poor brain penetration, GHB possesses abuse liability, and in rodents both drugs cause spike-wave discharges (SWDs), an absence seizure activity.

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Background: Insomnia has been associated in cross-sectional studies with increased beta (15-35 Hz) electroencephalogram (EEG) power during nonrapid eye movement (NREM) sleep, an index of cortical hyperarousal. However, it is unknown whether this cortical hyperarousal is present before individuals with insomnia develop the disorder. To fill this gap, we examined the association of childhood sleep high-frequency EEG activity with incident insomnia symptoms (i.

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Study Objectives: To examine whether insomnia is associated with spectral electroencephalographic (EEG) dynamics in the beta (15-35Hz) range during sleep in an adolescent general population sample.

Methods: A case-control sample of 44 adolescents from the Penn State Child Cohort underwent a 9-h polysomnography, clinical history and physical examination. We examined low-beta (15-25 Hz) and high-beta (25-35 Hz) relative power at central EEG derivations during sleep onset latency (SOL), sleep onset (SO), non-rapid eye movement (NREM) sleep, and wake after sleep onset (WASO).

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The goal of this study was to examine how heroin self-administration, abstinence, and extinction/reinstatement affect circadian sleep-wake cycles and the associated sleep architecture. We used electroencephalography (EEG) and electromyography (EMG) to measure sleep patterns in male Sprague-Dawley rats over 16 trials of heroin self-administration (acquisition), 14 days of abstinence, and a single day of extinction and drug-induced reinstatement. Rats self-administering heroin showed evidence of reversed (diurnal) patterns of wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep throughout acquisition.

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Sleep pattern disruption, specifically REM sleep behavior disorder (RBD), is a major nonmotor cause of disability in PD. Understanding the pathophysiology of these sleep pattern disturbances is critical to find effective treatments. 24-hour polysomnography (PSG), the gold standard for sleep studies, has never been used to test sleep dysfunction in the standard 6-OHDA lesioned hemiparkinsonian (HP) rat PD model.

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Background: We have recently shown that mice with experimental autoimmune encephalomyelitis (EAE) have increased sleep fragmentation (SF) and reduced sleep efficiency, and that the extent of SF correlates with the severity of disease. It is not yet clear whether and how sleep promotes recovery from autoimmune attacks. We hypothesized that SF promotes leukocyte infiltration across the blood-spinal cord barrier, impairs immune regulation, and thus worsens EAE.

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Substance abuse and sleep deprivation are major problems in our society. Clinical studies suggest that measures of poor sleep quality effectively predict relapse to substance abuse. Previously, our laboratory has shown that acute sleep deprivation increases the rate and efficiency (i.

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1. To facilitate investigation of diverse rodent behaviours in rodents' home cages, we have developed an integrated modular platform, the SmartCage(™) system (AfaSci, Inc. Burlingame, CA, USA), which enables automated neurobehavioural phenotypic analysis and in vivo drug screening in a relatively higher-throughput and more objective manner.

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Risk-taking behaviors involve increased motor activity and reduced anxiety in humans. Total sleep deprivation (SD) in animals produces a similar change in motor and fear behaviors. Investigators studied region-specific brain levels of glutamate in rats after TSD, an animal model of risk-taking behavior.

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A simple method is described for using principal component analysis (PCA) to score rat sleep recordings as awake, rapid-eye-movement (REM) sleep, or non-REM (NREM) sleep. PCA was used to reduce the dimensionality of the features extracted from each epoch to three, and the projections were then graphed in a scatterplot where the clusters were visually apparent. The clusters were then directly manually selected, classifying the entire recording at once.

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Relapse to drug seeking and drug taking is elicited by exposure to stress, drug-associated cues, or drugs of abuse themselves. According to the clinical literature, relapse also can be elicited in humans by sleep deprivation. Even so, the effect of sleep deprivation on drug-seeking and drug-taking behaviors has received relatively little attention in the laboratory (i.

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Entrainment of anticipatory activity and wakefulness to nutrient availability is a poorly understood component of energy homeostasis. Restricted feeding (RF) paradigms with a periodicity of 24 h rapidly induce entrainment of rhythms anticipating food presentation that are independent of master clocks in the suprachiasmatic nucleus (SCN) but do require other hypothalamic structures. Here, we report that the melanocortin system, which resides in hypothalamic structures required for food entrainment, is required for expression of food entrainable rhythms.

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Objective: To determine whether weight loss could reverse excessive sleep in high-fat diet-induced obesity.

Design: Three groups of mice participated in the study. A weight gain/loss group was fed with high-fat food for 6 weeks (weight gain), and regular food again for 4 weeks (weight loss).

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