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Background/Aim: The same neural processes may govern older people’s motor and cognitive abilities since an inability to switch between actions develops with aging. In this study, a dexterity test was used to measure motor and cognitive perseverance, which required participants to move their fingers fast and correctly on hole boards. Materials and Methods: An electroencephalography (EEG) recording was used to evaluate how healthy young and older adults process brain signals when performing the test. Results: A significant difference was found between the young and older groups in the average time taken to complete the test, with the older group taking 87.4 s and the young group taking 55.21 s. During motor movement, young participants showed alpha desynchronization over the cortex (Fz, Cz, Oz, Pz, T5, T6, P3, P4) in comparison to the resting state. However, compared to the younger group, no alpha desynchronization was found in the aging group during motor performance. It was noteworthy that alpha power (Pz, P3, and P4) in the parietal cortex was significantly lower in older compared to young adults. Conclusion: Age-related slowdown in motor performance may be caused by deteriorating alpha activity in the parietal cortex, which functions as a sensorimotor interface. This study provides new insights into how perception and action are distributed between brain regions.

Background/Aim: The dorsal striatum is a brain area integrating information for movement output. The local field potentials (LFPs) reflect the neuronal activity that can be used for monitoring brain activities and controlling movement. Materials and Methods: Rhythmic low gamma power activity (30.1-45 Hz) in the dorsal striatum was monitored according to voluntary motor movement in rotarod and bar tests in 0.5 mg/kg haloperidol-induced mice. Results: Haloperidol can effectively induce movement impairment indicated by decreased low gamma LFP with the lessened rotarod test’s latency fall, and the enhanced bar test’s descending latency. L-DOPA was used for the induction of a dopamine-dependent signal. The results showed that 25 mg/kg of L-DOPA could reverse the effect of haloperidol by enhancing low gamma oscillation concomitantly with the improvement in behavioral movement as fast as 60 min after administration, suggesting that dopamine signaling increases low gamma frequency of LFP in correlation with the improved mice movement. This work supports quantitative LFP assessment as a monitoring tool to track drug action on the nervous system. Conclusion: In animal models of motor impairment, oral dopaminergic treatment can be effective in restoring motor dysfunction by stimulating low gamma power activity in the dorsal striatum.

Background Citrus essential oil (EO) has been used for mood elevation and sedative hypnotic purposes. However, scientific proofs of its central nervous system (CNS) action remained largely unexplored. This study investigated chemotypes, electrical brain waves and sleep-wake effects of the essential oil from Citrus reticulata in rat model. Methods Chemical contents of citrus EO were analyzed using gas chromatography-mass spectrometry (GC–MS). Male Wistar rats implanted with electrodes on the frontal and parietal skulls were used for electroencephalographic (EEG) recording while inhaling the citrus EO (200 μl on cotton wool). Diazepam (10 mg/kg, p.o.) was used as a standard anxiolytic drug. EEG frequency analyses were performed by using Fast Fourier transform. All data were statistical analyzed using One-way ANOVA followed by Tukey's test. Results GC–MS analysis reveal d -limonene (95.7%) as a major constituent of citrus EO. The EEG results showed that overall EEG patterns of citrus EO effects were relatively similar to that of diazepam. However, significant differences between treatments were seen from sleep-wake analyses. Diazepam significantly increased episode numbers of awake and non-rapid eye movement (REM) sleep and reduced averaged episode duration. On the other hand, the citrus EO significantly decreased REM sleep latency and increased total time and episode numbers of REM sleep. Conclusion These findings demonstrated unique CNS effects of C. reticulata EO with EEG fingerprints and sleep-wake profiles. The data might be useful for citrus essential oil sub-classification and clinical application.

The efficacy of pseudoephedrine (PSE) as a nasal decongestant has been well‑demonstrated; however, PSE is strictly prescribed as a control substance due to its controversial psychostimulant effects. Although standard stimulatory drugs increase exploratory behavior and stimulate the dopamine system, the exact effects of PSE on locomotion and electrical activity in the striatum have not been determined. This study aimed to examine and compare the locomotor activities, local field potential (LFP) and sleep‑wake patterns produced by PSE and morphine, which is a standard drug used to promote psychomotor activity. Male Swiss albino mice were anesthetized and implanted with an intracranial electrode into the striatum. Animals were divided into four groups, which received either saline, PSE or morphine. Locomotor activity and LFP signals were continuously monitored following pseudoephedrine or morphine treatment. One‑way ANOVA revealed that locomotor count was significantly increased by morphine, but not PSE. Frequency analyses of LFP signals using fast Fourier transform also revealed significant increases in spectral powers of low‑ and high‑gamma waves following treatment with morphine, but not PSE. Sleep‑wake analysis also confirmed significant increases in waking and decreases in both non‑rapid eye movement and rapid eye movement sleep following morphine treatment. Sleep‑wakefulness did not appear to be disturbed by PSE treatment. These findings indicate that acute PSE administration, even at high doses, does not have psychostimulatory effects and may be relatively safe for the treatment of non‑chronic nasal congestion.

Ethnopharmacological relevance Lavandula angustifolia Mill. Essential oil (Lavender EO) has a long history of medicinal use and is particularly claimed to possess anxiolytic and sedative properties. Lavender EO aromatherapy has been used to reduce distress and improve insomnia naturally. Increasing evidence appeared to show similarities between the effects of lavender EO and the anxiolytic drugs, benzodiazepines. However, its effects on sleep-wake and electrical brain patterns in comparison to that of the standard anxiolytic, diazepam, remained to be explored. Aim of the study The aim of this work was to investigate electroencephalography (EEG) profiles and sleep-pattern elicited by lavender EO inhalation compared to that of diazepam, a standard anxiolytic drug in in vivo rat model. Materials and methods Adult male Wistar rats were anesthetized for electrode implantation on the frontal and parietal skulls. EEG signals were recorded for 180 min following intraperitoneal injection of diazepam (10 mg/kg) or during continuous inhalation of lavender EO (200 μL) or distilled water (control). Fast Fourier transform was used for the analyses of EEG power spectra and sleep-wake parameters. Results During a 30–60 min period, diazepam and lavender EO significantly increased frontal powers of 0.78–45.31 and 7.03–18.36 Hz, respectively. Both treatments also increased parietal powers with lower magnitudes of significant change. Significant increases in some frequency ranges remained until a 60–90 min period. Sleep-wake analyses also revealed that diazepam significantly reduced time spent in wake, increased time spent in non-rapid eye movement (NREM), increased episode duration of NREM, decreased numbers of wake episode and decreased rapid eye movement (REM) sleep latency. On the other hand, lavender EO only significantly decreased wake episodes and latency to REM sleep. Lavender EO inhalation reduced numbers of wake episode but maintain normal time spent in wake, NREM and REM sleeps. Conclusions These findings might suggest beneficial and distinct anxiolytic-like effects of lavender EO for sleep enhancing purposes.

Eating motivation is induced not only by negative energy balance but also food related cues. However, neural processing for acquisition of learned food preference remains to be established. This study aimed to identify hippocampal neural signaling in response to olfactory cue (chocolate scent) after completion of repetitive chocolate sessions. Male Swiss albino mice implanted with intracranial electrode into the hippocampus were used for local field potential (LFP) recording. Animals were given chocolate sessions (a piece of 2g chocolate per each mouse to eat on day 1, 3, 5 and 7). Hippocampal CA1 LFP signals and exploratory behavior of animals receiving chocolate scent were analyzed before and after chocolate sessions. The experiment was performed in a place preference-like apparatus with the zones of normal food pellet and chocolate (both kept in a small perforated cup for smell dispersion) at the opposite ends. Following chocolate sessions, time spent in a chocolate zone and CA1 LFP patterns were analyzed in comparison to control levels. Two-way ANOVA revealed significant increase in time spent seeking for chocolate. Frequency analysis of LFP power spectra revealed significant increases in delta and theta powers. Phase-amplitude analysis showed significant increase in maximal modulation index and decrease in frequency for phase of theta-high gamma coupling. Taken together, neural signaling in the hippocampus was sensitive to chocolate olfactory cue that might underlie learning process in response to repeated chocolate consumptions that primed intense food approaching behavior. Ultimately, these LFP patterns might reflect motivation to eat and predict feeding probability.

Previously, satiated animals or human subjects can still be motivated to eat by palatable food-associated cues. However, neural circuitries of hedonic hunger have not been well investigated. This study identified neural network connectivities between major brain areas in response to chocolate-associated cues following repeated exposures to chocolate. Adult male Swiss albino ICR mice were anesthetized and implanted with intracranial electrodes in the lateral hypothalamus (LHa), nucleus accumbens (NAc), olfactory bulb (OB) and hippocampus (HP) for local field potential (LFP) recording. LFP oscillations were recorded before and after repeated exposures to chocolate for chocolate experienced group whereas control group was not exposed to chocolate. On testing days, satiated animals were individually put into a place preference-like apparatus with two opposite chambers of chocolate and normal chow scent cues, separately. The results showed that chocolate experienced group significantly increased time spent in chocolate chamber whereas control group did not. One-way ANOVA revealed significant influence of chocolate sessions on LFP spectral powers of multiple frequencies in the LHa (delta, low gamma and high gamma) and NAc (high gamma). Moreover, coherence function analyses also highlighted significant increases in LHa-NAc and LHa-OB, and decrease in LHa-HP coherent activities in response to olfactory cues of chocolate. This study demonstrated modifications of neural network connectivity and associative learning following multiple exposures to palatable food. These findings might explain why energy homeostatic hunger is overridden by hedonic hunger.

Neural adaptation associated with formation of morphine conditioned place preference remained largely unexplored. This study monitored longitudinal changes in neural signaling during pre-conditioning, conditioning and post-conditioning periods of morphine conditioned place preference (CPP) paradigm for investigation of adaptive mechanisms of opiate addiction. Male Swiss albino mice implanted with intracranial electrodes into the nucleus accumbens (NAc), striatum (STr) and hippocampus (HC) were used for recording of local field potentials (LFPs). Animals received a 10-day schedule for associative learning to pair the specific compartment of the chamber with morphine effects. Exploratory behavior and LFP signals were recorded during pre-conditioning (baseline level), conditioning (day 1, 5 and 10) and post-conditioning (day 1, 4 and 7) periods. Repeated measures one-way ANOVA followed by Tukey test revealed significant increases in number of visit and time spent in morphine compartment during post-conditioning days. Frequency analysis of LFP highlighted the increases in alpha activity (12 – 18 Hz) in the NAc from post-conditioning day 1 until day 7. Moreover, significantly increased coherent activities between the pair of NAc-HC were developed within gamma frequency range (35 – 42 Hz) on morphine conditioning day 10 and disappeared during post-conditioning days. Taken together, these findings emphasized NAc LFP signaling and neural connectivities between the NAc and HC associated with morphine CPP. These adaptive changes might underlie the formation of morphine conditioned place preference and behavioral consequences such as craving and relapse.

Food deprivation is known to trigger hunger sensation and motivation to eat for energy replenishing. However, brain mechanisms associated with hunger and neural circuitries that mediate hunger driven responses remained to be investigated. To understand neural signaling of hunger, local field potentials (LFPs) in the lateral hypothalamus (LHa), nucleus accumbens (NAc), dorsal hippocampus (HP) and olfactory bulb (OB) and their interconnectivities were studied in freely moving adult male Albino mice during 18–20 h food deprivation and fed periods. Raw LFP signals were recorded and analyzed for mean values of spectral frequency power and coherence values. One-way repeated measures ANOVA revealed significant increases in spectral powers of beta and gamma frequency ranges induced by food deprivation in the LHa, HP, NAc but not OB. No change of spectral power in these brain regions was induced by food feeding. The analyses of coherent activity between brain regions also deliniated some distributed neural network activities correlated with hunger. In particular, coherent function indicated the increased beta and gamma phase synchrony between the pairs of LHa-HP and NAc-OB regions, and decreased gamma synchrony between the pairs of LHa-NAc and NAc-HP induced by food deprivation. It was found that plasma glucose level, locomotor count, travelled distance and time spent on moving were not altered by food deprivation. These results suggest that changes in LFP hallmarks in these brain regions were associated with hunger driven by negative energy balance.

The lateral hypothalamus plays an important role in homeostasis. It is sensitive to negative energy balance and believed to interact with other brain regions to mediate food seeking behavior. However, no neural signaling of hunger in the lateral hypothalamus has been studied. Male Swiss albino mice implanted with intracranial electrodes into the lateral hypothalamus and the hippocampus were randomly treated with drinking water for control condition, 18-20 h deprivation of food for hunger condition, and fluid food for satiety condition. Therefore, local field potential (LFP) and locomotor activity of animals were simultaneously recorded. One way ANOVA with Tukey's post hoc test was used for statistical analysis. Frequency analysis of LFP revealed that food deprivation significantly increased the power of gamma oscillation (65-95 Hz) in the lateral hypothalamus and the hippocampus. However, satiety did not change the oscillation in these regions. Moreover, no significant difference among groups was observed for locomotor count and speed. The analysis of coherence values between neural signaling of these two brain areas also confirmed significant increase within a frequency range of 61-92 Hz for hunger. No change in coherence value was induced by satiety. In summary, this study demonstrated neural signaling of the lateral hypothalamus in response to hunger with differential power spectrum of LFP and the interplay with the hippocampus. The data may suggest critical roles of the lateral hypothalamus in detection of negative energy balance and coordination of other higher functions for food related learning or behaviors through the connectivity with the hippocampus.

Glucocorticoids arising from chronic stress and long-term inflammatory treatment with corticosteroids are both associated with neuropathology and cognitive impairments. Many previous studies have focused on changes in brain morphology and deficits in learning behavior. However, effects of long-term exposure to stress hormones on electrical brain signaling and sleep-wake patterns have remained largely unexplored. This study aimed to monitor electroencephalographic (EEG) patterns induced by prolonged dexamethasone exposure. Adult male Wistar rats implanted with electrodes on the skull over the frontal and parietal cortices were intraperitoneally injected with either saline or dexamethasone (0.5 mg/kg) once daily for 21 consecutive days. Longitudinal EEG recording was performed on day 6, 11, 16 and 21. Fast Fourier transform was used for frequency power analysis. One-way ANOVA revealed significant increases in parietal EEG power of slow frequencies (delta, theta and alpha) particularly, with the dominant theta activity seen as early as day 11 of dexamethasone treatment. Sleep-wake analysis on day 21 confirmed a significant reduction of rapid-eye movement (REM) sleep and increased slow frequency oscillations mainly in the parietal cortex during the awake period. The number of high-voltage spindles (HVSs) (6-10 Hz EEG oscillation) was significantly increased during awake and slow wave sleep (SWS) periods following dexamethasone treatment. These findings demonstrated that distinct frequency oscillations, sleep-wakefulness and sleep spindles may be parameters of neuropathology produced by long-term dexamethasone exposure. Early detection of these parameters might be predictive of neuropathology in long-term corticosteroid users.