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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.

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.