Lavender essential oil (LEO), extracted from the flowers and upper parts of the lavender plant, has attracted considerable interest in the field of aromatherapy due to its anxiolytic, antidepressant, and hypnotic properties. However, the mechanisms underlying these effects of LEO remain inadequately elucidated, presenting challenges for its clinical application and promotion. This review aims to systematically analyze existing studies from a biological perspective to clarify the role and potential mechanisms of LEO in the contexts of anxiety, depression, and insomnia. The findings indicate that LEO exhibits anxiolytic effects by enhancing GABA receptor binding, increasing serotonin levels in the synaptic cleft, inhibiting glutamate release and its receptor interactions, and suppressing acetylcholine release at the neuromuscular junction. The antidepressant properties of LEO are attributed to its promotion of neurogenesis in the hippocampus, inhibition of inflammatory responses, and exertion of antioxidant effects. Furthermore, LEO has been demonstrated to possess hypnotic effects by elevating levels of melatonin and serotonin, reducing c-Fos expression in the prefrontal cortex, ventral hippocampus, and amygdala, and modulating GABAergic neurons in the central amygdala. These findings contribute to a deeper understanding of the biological effects of LEO and provide a substantial theoretical foundation for its clinical application.

Plateau zokors (Eospalax baileyi), endemic to the Qinghai-Tibet Plateau (QTP), are solitary subterranean rodents that spend their lifespan within underground burrows. Although the activity rhythms of the plateau zokors have been slightly documented, their sleep-wake patterns and seasonal variations remain unclear. Here, we investigated the sleep-wake patterns of wild-caught plateau zokors during spring and autumn using polysomnographic (PSG) recordings in the lab, and compared the findings with those of Sprague-Dawley (SD) rats. We found that plateau zokors exhibit three clearly distinguishable brain states: wakefulness (W), non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep. Under complete darkness in spring, they showed rhythmic-like activity. Compared with daytime periods, they spent significantly more time in wakefulness (398.88 ± 15.02 min vs. 320.55 ± 23.69 min, P < 0.05), and less time both in NREM sleep (257.32 ± 11.28 min vs. 312.23 ± 18.18 min, P < 0.05) and REM sleep (63.80 ± 6.63 min vs. 87.22 ± 7.27 min, P < 0.05) during the nocturnal period (local time). Although the plateau zokors in autumn did not exhibit significant rhythmic-like activity, they showed higher levels of wakefulness in the awake state and shallower sleep during sleep. Notably, plateau zokors had longer and more stable REM sleep compared to SD rats. These findings provide new empirical evidence for adaptive strategies in sleep ecophysiology and help reveal the functions and evolutionary strategies of sleep.

STUDY OBJECTIVES:Ponto-geniculo-occipital (PGO) waves are a hallmark feature of paradoxical sleep (PS), emerging just before PS onset during the transition from slow-wave sleep (SWS) to PS (TSWS-PS) and persisting throughout the PS phase in adult cats. These waves are considered a biomarker for the maturation of PS. However, their developmental trajectory in mammals remains poorly understood. This study investigated the emergence and maturation of PGO waves during PS in developing kittens. METHODS:Electrodes were stereotaxically implanted into the lateral geniculate nucleus, accurately localized using magnetic resonance imaging. Recording included cortical electroencephalogram, nuchal muscle activity, PGO waves, and rapid eye movements (REMs). RESULTS:Despite the presence of abundant PS and frequent muscle twitches accompanied by REMs in neonatal kittens, PGO spikes were first detected at postnatal day (PND) 16, with an average onset at PND 19. Initially, these waves appeared with lower density and amplitude during the TSWS-PS and PS phases. Over the following weeks, PGO wave density and amplitude increased, along with prolonged durations during both TSWS-PS and PS. Type I waves (singlet and bigeminy) predominated during TSWS-PS, while type II waves (clusters) were more frequent during PS. The proportion of type II waves and their co-occurrence with REMs increased with age. The adult-like pattern of PGO waves was fully established by PND 50. CONCLUSIONS:The emergence and maturation of PGO waves during PS are closely linked to the development of the sleep-wake cycle and may play a role in learning and memory processes.

ETHNOPHARMACOLOGICAL RELEVANCE:The use of lavender as sleep aid or hypnotic agent can be traced back as early as ancient Romans and Greeks. Yet, objective experimental data on whether and how lavender enhances sleep duration or/and sleep quality remain lacking. AIM OF THE STUDY:We aimed to characterize the sleep-wake regulating effects of lavender in the mouse and to demonstrate the brain targets and neural circuits involved. MATERIALS AND METHODS:A self-made precise odor delivery system combined with chronic polysomnographic recordings was employed to assess the sleep-wake effects of inhalation with lavender essential oil (LEO, extracted from lavender) and its different constituents during the light and dark phases in free-moving C57BL/6J mice. Neuroviral labeling, in situ hybridization and pharmacogenetics were combined to identify the neural circuits and targets involved. Finally, an insomniac model of DL-4-Chlorophenylalanine (PCPA)-treated mice was established to examine the sleep-inducing potential of LEO. RESULTS:We found that inhalation of LEO with a concentration at 25.0% during the light (inactive) phase significantly shortened the latency to non-rapid eye movement (NREM) sleep, increased the total amount of NREM sleep at the expense of wakefulness (W), and enhanced cortical EEG slow wave activities, notably delta power spectra density. We further identified linalool, d-limonene, 1,8-cineole, linalyl acetate and terpinene-4-ol as the major effective sleep-promoting monomer components. Importantly, we found that LEO no longer produced any of the above sleep-promoting effect following either nasal injection of zinc sulfate which interrupts the olfactory pathway, or pharmacogenetics silencing of central amygdala GABAergic neurons. Finally, LEO reestablished NREM sleep with short latency in PCPA-treated insomniac mice, effects comparable with those induced by a potent sedative diazepam. CONCLUSIONS:We have characterized the quantitative and qualitative sleep-promoting effects of LEO and its effective components via the olfactory pathway and central amygdala GABA neuronal targets. The hypnotic property of LEO is reinforced by its ability to restore sleep in insomnia. Our study thus establishes a neurobiological basis for aromatherapy of sleep disorders using lavender.

Sleep regulation depends on the complex interplay between homeostatic and circadian processes synchronized by the light/dark cycle. Sleep is also directly regulated by light via the retinal inputs to the preoptic area (POA). Although the light-responsive POA neurons project to several wake-promoting structures, including histaminergic neurons in the tuberomammillary nucleus (TMn), there is no functional evidence for their involvement in light-induced sleep. To bridge this gap, we used histidine decarboxylase (HDC, the histamine-synthetizing enzyme) knockout mice (HDC−/−, n=7) and hM4Di-HDC-cre mice (HDC+/+, n=8) subjected to an ultradian light/dark protocol (LD 1h:1h over 24h), and another group of hM4Di-HDC-cre mice (n=8) exposed to a 1-h light pulse. We found that light pulses during the biological night enhanced slow wave sleep and increased cortical EEG power in the delta range (0.5-3Hz), and that these effects were significantly attenuated both in HDC−/− (83 vs 23 min/6h, p=0.005) under LD 1h:1h condition and in hM4Di-HDC-cre mice after acute chemogenetic silencing of histamine neurons by the DREADD ligand deschloroclozapine (15 vs 6 min/h, p=0.0016) under a 1-h light pulse. In addition, the sleep-inducing effect of light was circadian dependent, with the strongest effect at the beginning and end of the night but no effect at all during the biological day in HDC+/+mice. Our study provides functional evidence that the acute sleep-inducing effects of light on sleep require histamine neurotransmission in mice. ### Competing Interest Statement The authors have declared no competing interest. Inserm, https://ror.org/02vjkv261 Agence Nationale de la Recherche Chinese Scholarship Council (CSC)

The Hodgkin-Huxley model assumes independent ion channel activation, although mutual interactions are common in biological systems. This raises the problem why neurons would favor independent over cooperative channel activation. In this study, we evaluate how cooperative activation of sodium channels affects the neuron's information processing and energy consumption. Simulations of the stochastic Hodgkin-Huxley model with cooperative activation of sodium channels show that, while cooperative activation enhances neuronal information processing capacity, it greatly increases the neuron's energy consumption. As a result, cooperative activation of sodium channel degrades the energy efficiency for neuronal information processing. This discovery improves our understanding of the design principles for neural systems, and may provide insights into future designs of the neuromorphic computing devices as well as systematic understanding of pathological mechanisms for neural diseases.

Rapid eye movement (REM) sleep is the main sleep correlate of dreaming. Ponto-geniculo-occipital (PGO) waves are a signature of REM sleep. They represent the physiological mechanism of REM sleep that specifically limits the processing of external information. PGO waves look just like a message sent from the pons to the lateral geniculate nucleus of the visual thalamus, the occipital cortex, and other areas of the brain. The dedicated visual pathway of PGO waves can be interpreted by the brain as visual information, leading to the visual hallucinosis of dreams. PGO waves are considered to be both a reflection of REM sleep brain activity and causal to dreams due to their stimulation of the cortex. In this review, we summarize the role of PGO waves in potential neural circuits of two major theories, i.e., (1) dreams are generated by the activation of neural activity in the brainstem; (2) PGO waves signaling to the cortex. In addition, the potential physiological functions during REM sleep dreams, such as memory consolidation, unlearning, and brain development and plasticity and mood regulation, are discussed. It is hoped that our review will support and encourage research into the phenomenon of human PGO waves and their possible functions in dreaming.

Hemopressin and related peptides have shown to function as the endogenous ligands or the regulator of cannabinoid receptors. The previous studies demonstrated that the endocannabinoid system played important roles in modulating several physiological functions such as sleep, olfaction, emotion, learning and memory, and reward behaviors. Mouse VD-hemopressin (α) [(m)VD-HPα], an 11-residue peptide derived from the α1 chain of hemoglobin, was recently presumed as a selective agonist of the CB 1 receptor. The present study was undertaken to investigate the effects of (m)VD-HPα on the sleep–wake cycle and power spectrum of cortical EEG in freely moving rats and the potential neurons in the brain activated by (m)VD-HPα. The results showed that 20.1 nmol of (m)VD-HPα i.c.v. administration increased non-rapid eye movement (NREM) sleep in the first 2 h section accompanied by an increase in EEG delta (0.5–4 Hz) activity. The (m)VD-HPα-induced NREM sleep enhancement was due to extended episode duration instead of the episode number. In addition, the effect of (m)VD-HPα (20.1 nmol) on sleep–wake states was significantly attenuated by an antagonist of the CB 1 receptor, AM251 (20 nmol, i.c.v.) but not by the CB 2 receptor antagonist, AM630 (20 nmol, i.c.v.). In comparison with vehicle, (m)VD-HPα increased Fos-immunoreactive (-ir) neurons in the ventrolateral preoptic nucleus (VLPO), but reduced Fos-ir neurons in the lateral hypothalamus (LH), tuberomammillary nucleus (TMN), and locus coeruleus (LC). These findings suggest that (m)VD-HPα promotes NREM sleep via the CB 1 cannabinoid receptor to probably activate VLPO GABAergic neurons, but inactivates the LH orexinergic, LC noradrenergic, and TMN histaminergic neurons.

Precise and reliable presentation of odorants to animals is crucial for olfactory studies. Although odor stimulation systems in anesthetized or awake, head-fixed animals are well established, temporally precise odor presentation in awake, freely moving animals remains a challenge. Here, we describe a new odor stimulation system which presents odors directly to the nostrils of freely moving mice. The system comprises 3 modules: an odor-delivery module, an odor-generation module, and a control module. The new system is precise and temporally reliable, and odor stimulation can be triggered by specific sniffing phases or other events. Moreover, the system can be combined with neural recordings, such as electrophysiology, and olfactory behavioral tests to investigate how neurons in the brain represent odor information during individual olfactory behaviors. This innovative odor stimulation system may replace traditional stimulation systems: It will enable precise odor presentation in a wide range of olfactory studies in freely moving animals.

Recently, researchers have paid progressively more attention to the study of neural development in infant rats. However, due to the lack of complete intracerebral localization information, such as clear nuclear cluster boundaries, identified main brain structures, and reliable stereotaxic coordinates, it is difficult and restricted to apply technical neuroscience to infant rat’s brain. The present study was undertaken to refine the atlas of infant rats. As such, we established a stereotaxic atlas of the infant rat’s brain at postnatal days 7–13. Furthermore, dye calibration surgery was performed in P7–P13 infant rats by injecting Methylene blue, and sections were incubated in Nissl solutions. From the panoramic images of the brain sections, atlases were made. Our article has provided the appearance and measurements of P7–P13 Sprague–Dawley rat pups. Whereas the atlas contains a series of about 530 coronal brain section images from olfactory bulbs to the brainstem, a list of abbreviations of the main brain structures, and reliable stereotaxic coordinates, which were demonstrated by vertical and oblique injections with fluorescent dye DiI. The present findings demonstrated that our study of P7–P13 atlases has reasonable nucleus boundaries and accurate and good repeatability of stereotaxic coordinates, which can make up for the shortage of postnatal rat brain atlas currently in the field.

The ontogenetic sleep hypothesis suggested that rapid eye movement (REM) sleep is ontogenetically primitive. Namely, REM sleep plays an imperative role in the maturation of the central nervous system. In coincidence with a rapidly developing brain during the early period of life, a remarkably large amount of REM sleep has been identified in numerous behavioral and polysomnographic studies across species. The abundant REM sleep appears to serve to optimize a cerebral state suitable for homeostasis and inherent neuronal activities favorable to brain maturation, ranging from neuronal differentiation, migration, and myelination to synaptic formation and elimination. Progressively more studies in Mammalia have provided the underlying mechanisms involved in some REM sleep-related disorders (e.g., narcolepsy, autism, attention deficit hyperactivity disorder (ADHD)). We summarize the remarkable alterations of polysomnographic, behavioral, and physiological characteristics in humans and Mammalia. Through a comprehensive review, we offer a hybrid of animal and human findings, demonstrating that early-life REM sleep disturbances constitute a common feature of many neurodevelopmental disorders. Our review may assist and promote investigations of the underlying mechanisms, functions, and neurodevelopmental diseases involved in REM sleep during early life.

Neuropeptide S (NPS) acts by activating its cognate receptor (NPSR). High level expression of NPSR in the posterior medial amygdala suggests that NPS-NPSR system should be involved in regulation of social behaviors induced by social pheromones. The present study was undertaken to investigate the effects of central administration of NPS or with NPSR antagonist on the alarm pheromone (AP)-evoked defensive and risk assessment behaviors in mice. Furthermore, H129-H8, a novel high-brightness anterograde multiple trans-synaptic virus, c-Fos and NPSR immunostaining were employed to reveal the involved neurocircuits and targets of NPS action. The mice exposed to AP displayed an enhancement in defensive and risk assessment behaviors. NPS (0.1–1 nmol) intracerebroventricular (i.c.v.) injection significantly attenuated the AP-evoked defensive and risk assessment behaviors. NPSR antagonist [D-Val5]NPS at the dose of 40 nmol completely blocked the effect of 0.5 nmol of NPS which showed the best effective among dose range. The H129-H8-labeled neurons were observed in the bilateral posterodorsal medial amygdala (MePD) and posteroventral medial amygdala (MePV) 72 h after the virus injection into the unilateral olfactory bulb (OB), suggesting that the MePD and MePV receive olfactory information inputs from the OB. The percentage of H129-H8-labeled neurons that also express NPSR were 90.27 ± 3.56% and 91.67 ± 2.46% in the MePD and MePV, respectively. NPS (0.5 nmol, i.c.v.) remarkably increased the number of Fos immunoreactive (-ir) neurons in the MePD and MePV, and the majority of NPS-induced Fos-ir neurons also expressed NPSR. The behavior characteristic of NPS or with [D-Val5]NPS can be better replicated in MePD/MePV local injection within lower dose. The present findings demonstrated that NPS, via selective activation of the neurons bearing NPSR in the posterior medial amygdala, attenuates the AP-evoked defensive and risk assessment behaviors in mice.

甘丙肽(GAL)及其受体(GalRs)广泛分布于中枢神经系统,参与多种生理功能调节.下丘脑前部腹外侧视前核(VLPO) 80％神经元含GAL并与γ-氨基丁酸共存,发出下行投射至多个觉醒核团,抑制结节乳头体核、中缝背核和蓝斑核神经元活动而促进睡眠.本研究回顾GAL-GalRs系统在中枢神经系统的发现,聚焦多项利用神经示踪、神经药理学、分子生物学、化学遗传和光遗传学等方法研究进展,证明VLPO GAL能神经元调控生理条件下慢波睡眠的产生和维持以及参与阿尔茨海默症、焦虑、抑郁、癫痫和成瘾等疾病及伴随睡眠障碍的机制,总结性地提出尚未清晰的问题和研究方向.

睡眠觉醒发育与脑发育密切相关,多数动物睡眠觉醒节律发育规律与人类相似,由脑内生物钟、睡眠觉醒中枢和内平衡稳态等因素调节.成人的觉醒与睡眠呈昼夜节律性出现,整夜睡眠20％为快动眼(REM)睡眠,80％为非快动眼(NREM)睡眠.NREM-REM睡眠转换周期为90～110 min,表现为次昼夜节律.足月新生儿觉醒与睡眠昼夜均匀分布,睡眠常以REM睡眠起始,REM与NREM睡眠各占50％,转换周期为50～60 min;3月龄开始显现昼夜节律分布,睡眠周期以NREM睡眠起始,10岁后NREM-REM睡眠周期呈现近似成年次昼夜节律水平.睡眠与觉醒的昼夜节律及次昼夜节律的发育参与个体的生理和心理发育过程,了解睡眠觉醒节律调控及发育,为理解脑发育和新生儿睡眠节律异常导致的疾病奠定理论基础.

Neuropeptide S (NPS) is an endogenous peptide recently recognized to be presented in the brainstem and believed to play an important role in maintaining memory. The deletion of NPS or NPS receptor (NPSR) in mice shows a deficit in memory formation. Our recent studies have demonstrated that central administration of NPS facilitates olfactory function and ameliorates olfactory spatial memory impairment induced by muscarinic cholinergic receptor antagonist and N-methyl-D-aspartate receptor antagonist. However, it remains to be determined if endogenous NPS is an indispensable neuromodulator in the control of the olfactory spatial memory. In this study, we examined the effects of NPSR peptidergic antagonist [D-Val5]NPS (10 and 20 nmol, intracerebroventricular) and nonpeptidergic antagonist SHA 68 (10 and 50 mg/kg, intraperitoneal) on the olfactory spatial memory using computer-assisted 4-hole-board olfactory spatial memory test in mice. Furthermore, immunofluorescence was employed to identify the distributions of c-Fos and NPSR immunoreactive (-ir) neurons in olfactory system and hippocampal formation known to closely relate to the olfactory spatial memory. [D-Val5]NPS dosing at 20 nmol and SHA 68 dosing at 50 mg/kg significantly decreased the number of visits to the 2 odorants interchanged spatially, switched odorants, in recall trial, and simultaneously reduced the percentage of Fos-ir in NPSR-ir neurons, which were densely distributed in the anterior olfactory nucleus, piriform cortex, subiculum, presubiculum, and parasubiculum. These findings suggest that endogenous NPS is a key neuromodulator in olfactory spatial memory.

系统解剖学作为一门形态学课程,是医学生认识人体结构的必修课.为给学生提供更多的学习资源并提高教学效果,我们利用动画、图片等辅助教学形式和基础与临床密切结合的方法制作了椎间盘的微课,用以帮助学生在实验室外对相关解剖结构进行再学习.本文详细整理了作者微课作品的教学方案,并希望通过不断提高微课的质量,努力打造辅助系统解剖学课堂教学的"金课".

The thalamus is the gate of the cerebral cortex, the ultimate target for the neural networks controlling behavioral states and cognitive functions. According to the reticular theory initially proposed by Moruzzi and Magoun, excitatory inputs from large reticular zones of the brainstem via widespread intra-and extra-thalamocortical systems finally activate the cerebral cortex to cause generalized cortical

Sleep-wake development in postnatal rodent life could reflect the brain maturational stages. As the altricial rodents, rats are born in a very undeveloped state. Continuous sleep recording is necessary to study the sleep-wake cycle profiles. However, it is difficult to realize in infant rats since they rely on periodic feeding before weaning and constant warming and appropriate EEG electrodes. We developed a new approach including two types of EEG electrodes and milk-feeding system and temperature-controlled incubator to make continuously polysomnographic (PSG) recording possible. The results showed that there was no evident difference in weight gaining and behaviors between pups fed through the milk-feeding system and warmed with temperature-controlled incubator and those kept with their dam. Evolutional profiles of EEG and electromyogram (EMG) activities across sleep-wake states were achieved perfectly during dark and light period from postnatal day (P) 11 to P75 rats. The ontogenetic features of sleep-wake states displayed that the proportion of rapid eye movement (REM) was 57.0 ± 2.4% and 59.7 ± 1.7% and non-REM (NREM) sleep was 5.2 ± 0.8% and 4.9 ± 0.5% respectively, in dark and light phase at P11, and then REM sleep progressively decreased and NREM sleep increased with age. At P75, REM sleep in dark and light phase respectively, reduced to 6.3 ± 0.6% and 6.9 ± 0.5%, while NREM correspondingly increased to 37.5 ± 2.1% and 58.4 ± 1.7%. Wakefulness from P11 to P75 in dark phase increased from 37.8 ± 2.2% to 56.2 ± 2.6%, but the change in light phase was not obvious. P20 pups began to sleep more in light phase than in dark phase. The episode number of vigilance states progressively decreased with age, while the mean duration of that significantly increased. EEG power spectra in 0.5-4 Hz increased with age accompanied with prolonged duration of cortical slow wave activity. Results also indicated that the dramatic changes of sleep-wake cycle mainly occurred in the first month after birth. The novel approaches used in our study are reliable and valid for continuous PSG recording for infant rats and unravel the ontogenetic features of sleep-wake cycle.

Olfactory dysfunction is a major non-motor symptom that appears during the early stages of Parkinson's Disease (PD), a neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra (SN). Depletion of SN dopaminergic neurons by 6-hydroxydopamine (6-OHDA) is widely used as a model for PD and ultimately results in motor deficits. However, it is largely unknown whether olfactory behavior and, more importantly, neural activity in the olfactory bulb (OB) are impaired prior to the appearance of motor deficits. We partially depleted the SN dopaminergic population in mice by injection of 6-OHDA. Seven days after injection of 6-OHDA, motor ability was unchanged but olfactory-driven behaviors were significantly impaired. Injection of 6-OHDA into the SN significantly increased the power of the ongoing local field potential in the OB for all frequency bands, and decreased odor-evoked excitatory beta responses and inhibitory high-gamma responses. Moreover, 6-OHDA treatment led to increased odor-evoked calcium responses in the mitral cells in the OB of awake mice. These data suggest that the olfactory deficits caused by depletion of the SN dopaminergic population are likely due to abnormal hyperactivity of the mitral cells in the OB.

Disturbed sleep is a common subjective complaint among individuals with anxiety disorders. Sleep deprivation increases general and specific anxiety symptoms among healthy individuals. The amygdala is critical for regulating anxiety and also involved in mediating the effects of emotions on sleep. Neuropeptide S (NPS) and NPS receptors (NPSR) are reported as a novel endogenous arousal and anxiolytic system, but it is unclear yet whether this system is involved in anxiety-like behavior and sleep caused by sleep deprivation, and how it plays anxiolytic effect underlying the comorbid condition. In the present study, we demonstrate that paradoxical sleep deprivation (PSD) induced by modified multiple platform method (MMPM) for 24 h caused anxiety-like behavior, a prolonged sleep latency and subsequent paradoxical sleep (PS) rebound accompanied by an increase in electroencephalogram (EEG) theta (4.5-8.5 Hz) activities across light and dark phase in rats. The increase of PS after PSD was due to an increase of episode number during light phase and both episode number and duration during dark phase. Central action of NPS (1 nmol) attenuated PSD-induced anxiety-like behavior, and altered PSD-induced sleep-wake disturbances through increasing wakefulness, and suppressing PS and EEG theta activities. The reduction in PS time following NPS administration during light phase was because of a decreased episode number. Furthermore, sleep amount in 24 h in PSD rats given NPS was lesser than that given saline. PSD significantly enhanced NPSR mRNA expression level in the amygdala. NPS remarkably increased the number of Fos-ir neurons in the basolateral amygdala (BLA), the central amygdala (CeA) and medial amygdala (MeA). The majority of Fos-ir neurons induced by NPS also expressed NPSR. These results suggest that NPSR upregulation in the amygdala is presumably related to the PSD-induced anxiety-like behavior and sleep disturbances, and that NPS counteracts PSD-induced anxiety-like behavior and sleep disturbances possibly through activating the neurons bearing NPSR in the amygdala. In addition, the little sleep increase in PSD rats treated with NPS suggests that NPS can function as an anxiolytic without causing a subsequent sleep rebound.