Tokushima University i.school Its Conception, Realization, and Outlook

徳島大学i.school の構想と実現，そしてその展望

Journal of University Education Research


Exposure to an Extremely-Low-Frequency Magnetic Field Stimulates Adrenal Steroidogenesis via Inhibition of Phosphodiesterase Activity in a Mouse Adrenal Cell Line

Extremely low-frequency magnetic fields (ELF-MFs) are generated by power lines and household electrical devices. In the last several decades, some evidence has shown an association between ELF-MF exposure and depression and/or anxiety in epidemiological and animal studies. The mechanism underlying ELF-MF-induced depression is considered to involve adrenal steroidogenesis, which is triggered by ELF-MF exposure. However, how ELF-MFs stimulate adrenal steroidogenesis is controversial. In the current study, we investigated the effect of ELF-MF exposure on the mouse adrenal cortex-derived Y-1 cell line and the human adrenal cortex-derived H295R cell line to clarify whether the ELF-MF stimulates adrenal steroidogenesis directly. ELF-MF exposure was found to significantly stimulate adrenal steroidogenesis (p < 0.01-0.05) and the expression of adrenal steroid synthetic enzymes (p < 0.05) in Y-1 cells, but the effect was weak in H295R cells. Y-1 cells exposed to an ELF-MF showed significant decreases in phosphodiesterase activity (p < 0.05) and intracellular Ca2+ concentration (p < 0.01) and significant increases in intracellular cyclic adenosine monophosphate (cAMP) concentration (p < 0.001-0.05) and cAMP response element-binding protein phosphorylation (p < 0.05). The increase in cAMP was not inhibited by treatment with NF449, an inhibitor of the Gs alpha subunit of G protein. Our results suggest that ELF-MF exposure stimulates adrenal steroidogenesis via an increase in intracellular cAMP caused by the inhibition of phosphodiesterase activity in Y-1 cells. The same mechanism may trigger the increase in adrenal steroid secretion in mice observed in our previous study.


Anxiety affects amplitudes of red and green color-elicited flash visual evoked potentials in humans

It has been reported that negative emotional changes and conditions affect the visual faculties of humans at the neural level. On the other hand, the effects of emotion on color perception in particular, which are based on evoked potentials, are unknown. In the present study, we investigated whether different anxiety levels affect the color information processing for each of 3 wavelengths by using flash visual evoked potentials (FVEPs) and State-Trait Anxiety Inventory. In results, significant positive correlations were observed between FVEP amplitudes and state or trait anxiety scores in the long (sensed as red) and middle (sensed as green) wavelengths. On the other hand, short-wavelength-evoked FVEPs were not correlated with anxiety level. Our results suggest that negative emotional conditions may affect color sense processing in humans.

The Journal of Medical Investigation : JMI


Evaluation of blood flow velocity waveform in common carotid artery using multi-branched arterial segment model of human arteries

Arteriosclerosis is considered to be a major cause of cardiovascular diseases, which account for approximately 30% of the causes of death in the world. We have recently demonstrated a strong correlation between arteriosclerosis (arterial elasticity) and two characteristics: maximum systolic velocity (S1) and systolic second peak velocity (S2) of the common carotid artery flow velocity waveform (CCFVW). The CCFVW can be measured by using a small portable measuring device. However, there is currently no theoretical evidence supporting the causes of the relation between CCFVW and arterial elasticity, or the origin of the CCFVW characteristics. In this study, the arterial blood flow was simulated using a one-dimensional systemic arterial segments model of human artery in order to conduct a qualitative evaluation of the relationship between arterial elasticity and the characteristics of CCFVW. The simulation was carried out based on the discretized segments with the physical properties of a viscoelastic tube (the cross-sectional area at the proximal and terminal ends, the length, and the compliance per unit area of the tube (CS)). The findings obtained through this study revealed that the simulated CCFVW had shape similar characteristics to that of the measured CCFVW. Moreover, when the compliance CS of the model was decreased, the first peak of the simulated-CCFVW decreased and the second peak increased. Further, by separating the anterograde pulse wave and the reflected pulse wave, which form the CCFVW, we found that the decrease in the first peak of the simulated CCFVW was due to the arrival of a reflected pulse wave from the head after the common carotid artery toward the arrival of a anterograde pulse wave ejected directly from the heart and that the increase in the second peak resulted from the arrival of the peak of the reflected pulse wave from the thoracic aorta. These results establish that the CCFVW characteristics contribute to the assessment of arterial elasticity.

総頸動脈血流速度波形と動脈弾性の関係について，1次元流体解析モデルを用いて検討している．動脈モデルはヒトの全身の主要な動脈を多枝セグメントモデルとして構築したものを用い，動脈弾性を変化させた時の総頸動脈の血流速度波形を求めた結果，動脈弾性の変化により血流速度波形が変化することを示した．これにより総頸動脈の血流速度波形を調べることにより動脈硬化を評価することができる可能性を示した．

Biomedical Signal Processing and Control


The retinoic acid receptor agonist Am80 increases hippocampal ADAM10 in aged SAMP8 mice

The retinoic acid (RA, a vitamin A metabolite) receptor (RAR) is a transcription factor. Vitamin A/RA administration improves the Alzheimer's disease (AD)- and age-related attenuation of memory/learning in mouse models. Recently, a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) was identified as a key molecule in RA-mediated anti-AD mechanisms. We investigated the effect of chronic administration of the RAR agonist Am80 (tamibarotene) on ADAM10 expression in senescence-accelerated mice (SAMP8). Moreover, we estimated changes in the expression of the amyloid precursor protein (APP), amyloid beta (Aβ), and hairy/enhancer of split (Hes), which are mediated by ADAM10. Spatial working memory and the levels of a hippocampal proliferation marker (Ki67) were also assessed in these mice. ADAM10 mRNA and protein expression was significantly reduced in the hippocampus of 13-month-old SAMP8 mice; their expression improved significantly after Am80 administration. Further, after Am80 administration, the expression levels of Hes5 and Ki67 were restored and the deterioration of working memory was suppressed, whereas APP and Aβ levels remained unchanged. Our results suggest that Am80 administration effectively improves dementia by activating the hippocampal ADAM10-Notch-Hes5 proliferative pathway.


Maternal Dietary Restriction Alters Offspring's Sleep Homeostasis.

Nutritional state in the gestation period influences fetal growth and development. We hypothesized that undernutrition during gestation would affect offspring sleep architecture and/or homeostasis. Pregnant female mice were assigned to either control (fed ad libitum; AD) or 50% dietary restriction (DR) groups from gestation day 12 to parturition. After parturition, dams were fed AD chow. After weaning, the pups were also fed AD into adulthood. At adulthood (aged 8-9 weeks), we carried out sleep recordings. Although offspring mice displayed a significantly reduced body weight at birth, their weights recovered three days after birth. Enhancement of electroencephalogram (EEG) slow wave activity (SWA) during non-rapid eye movement (NREM) sleep was observed in the DR mice over a 24-hour period without changing the diurnal pattern or amounts of wake, NREM, or rapid eye movement (REM) sleep. In addition, DR mice also displayed an enhancement of EEG-SWA rebound after a 6-hour sleep deprivation and a higher threshold for waking in the face of external stimuli. DR adult offspring mice exhibited small but significant increases in the expression of hypothalamic peroxisome proliferator-activated receptor (Ppar) and brain-specific carnitine palmitoyltransferase 1 (Cpt1c) mRNA, two genes involved in lipid metabolism. Undernutrition during pregnancy may influence sleep homeostasis, with offspring exhibiting greater sleep pressure.


Chronic exposure to an extremely low-frequency magnetic field induces depression-like behavior and corticosterone secretion without enhancement of the hypothalamicpituitaryadrenal axis in mice

An extremely low-frequency magnetic field (ELF-MF) is generated by power lines and household electrical devices. Many studies have suggested an association between chronic ELF-MF exposure and anxiety and/or depression. The mechanism of these effects is assumed to be a stress response induced by ELF-MF exposure. However, this mechanism remains controversial. In the present study, we investigated whether chronic ELF-MF exposure (intensity, 1.5 mT; [corrected] total exposure, 200 h) affected emotional behavior and corticosterone synthesis in mice. ELF-MF-treated mice showed a significant increase in total immobility time in a forced swim test and showed latency to enter the light box in a light-dark transition test, compared with sham-treated (control) mice. Corticosterone secretion was significantly high in the ELF-MF-exposed mice; however, no changes were observed in the amount of the adrenocorticotropic hormone and the expression of genes related to stress response. Quantification of the mRNA levels of adrenal corticosteroid synthesis enzymes revealed a significant reduction in Cyp17a1 mRNA in the ELF-MF-exposed mice. Our findings suggest the possibility that high intensity and chronic exposure to ELF-MF induces an increase in corticosterone secretion, along with depression- and/or anxiety-like behavior, without enhancement of the hypothalamic-pituitary-adrenal axis.


Retinoic acid receptor antagonist LE540 attenuates wakefulness via the dopamine D1 receptor in mice

Vitamin A is a common lipophilic vitamin, and its function is mainly mediated by the binding of its metabolite retinoic acid to retinoic acid receptors (RARs) and retinoid X receptors. Recently, it was reported that the expression of the RARb (an RAR subtype) gene determines the contribution of the delta oscillation in the sleep electroencephalogram (EEG) patterns in mice. We also reported that 4-week dietary deficiency of vitamin A (VAD) causes the attenuation of delta power in sleep and spontaneous activity in mice. However, our previous study could not clarify whether the attenuation of delta power by VAD is attributed to the suppression of RARs. To address this problem, we investigated whether the chronic administration of LE540 (30mg/kg/day), an antagonist of RARs, for 1 or 4weeks attenuated EEG delta power during sleep in mice. Consequently, 4-week LE540 administration induced a significant attenuation of wakefulness and delta power in non-rapid eye movement sleep. Western blot analysis revealed a significant decrease in the expression of dopamine D1 receptor (D1DR) in the striatum and tyrosine hydroxylase in the midbrain of mice that were administered LE540 for 4weeks. High-performance liquid chromatography analysis of striatal tissue revealed a significant decrease in the homovanillic acid/dopamine ratio. Meanwhile, dopamine levels did not change in these mice. Our results suggest that the 4-week antagonism of RARs induces the attenuation of delta power. However, the attenuation of delta power may be elicited indirectly by the decrease of wakefulness followed by the hypo-expression of dopamine receptors especially D1DR.


Refeeding after a 24-hour fasting deepens NREM sleep in a time-dependent manner.

Sleep/wake cycle is regulated by a variety of neuropeptides in the hypothalamus, a brain region that also regulates energy homeostasis and feeding behavior. Since circadian rhythms are affected by energy metabolism and feeding condition, we investigated whether changes in feeding regimen would influence sleep/wake parameters and body temperature. We monitored sleep and body temperature across three days of baseline (day 1), fasting (day 2), and refeeding (day 3) conditions under ordinary ambient temperature and employed different refeeding schedules. Refeeding at ZT1 following the 24-h fasting enhanced EEG delta power in NREM sleep. However, when the time of refeeding was set at either ZT7 or ZT12, the enhancement of EEG delta power was attenuated. The amount of NREM sleep was not largely affected by a 24-h fasting started at ZT1, although fasting that started at ZT12 changed the temporal distribution of NREM sleep. Hypothalamic nNOS mRNA level was increased both before and after refeeding at ZT1 compared with control condition, while there was no significant change in mice refed at ZT7. Level of NPY mRNA in the arcuate nucleus was increased before the refeeding only at ZT1. These results suggest that refeeding after a 24-h fasting makes NREM sleep deeper in a time-dependent manner.


Feed-forward changes in carotid blood flow velocity during active standing.

Orthostatic changes induce temporary loss of circulatory regulation. Feedback systems react to cardiovascular alterations to compensate for the instability. To clarify the existence of anticipatory cardiovascular regulation during active standing, we continuously recorded blood flow velocity (BFV) in the common carotid artery and cerebral blood volume (CBV) in healthy men. The maximum BFV value decreased significantly before standing in the reaction-time condition. The decrease significantly correlated with the change in systolic blood pressure that accompanies upright standing from a supine position. The anticipatory BFV decrease disappeared during self-paced standing, and all BFV parameters significantly declined after the self-paced standing. The CBV recording showed a significant increase in oxyhemoglobin levels before standing in the reaction-time condition. Our study suggests that some feed-forward cardiovascular regulation triggered by central command could be activated before standing, and it may play a functional role in the maintenance of cerebral perfusion during standing.


Impaired olfactory function in mice with allergic rhinitis.

OBJECTIVE: It has been reported that olfactory function is impaired in patients with allergic rhinitis. However, the mechanism of olfactory dysfunction in allergic rhinitis remains poorly understood. Because of difficulties in obtaining and analyzing human olfactory mucosa due to both technical and ethical issues, an animal model needs to be established to clarify the mechanism of olfactory dysfunction in allergic rhinitis. The purpose of this study was to study olfactory function and changes in olfactory mucosa using allergic rhinitis mice. METHODS: A model of allergic rhinitis mice with olfactory dysfunction was developed by sensitizing with ovalbumin (OVA), and intranasally challenging with the same allergen. Olfactory function of mice with or without allergic rhinitis was assessed by odor detection ability test with cycloheximide and local field potential (LFP) with 1-octanal. We also evaluated histological changes in the olfactory mucosa of allergic rhinitis mice by both light and electron microscopy. RESULTS: Both of odor detection ability test and LFP showed that olfactory function was impaired in mice with allergic rhinitis, but not in mice without allergic rhinitis. Histopathological findings showed prominent infiltration of eosinophils, plasma cells, neutrophils, mast cells, and macrophages in lamina propria of olfactory mucosa of mice with allergic rhinitis, although infiltration of these cells was not seen in control mice. Allergic rhinitis also increased the number and size of glands in olfactory mucosa, suggesting an elevated amount of mucin in olfactory mucosa. CONCLUSION: This study showed for the first time that mice with allergic rhinitis have impaired olfactory function, increased size and number of olfactory glands, and infiltration of eosinophils, neutrophils, mast cells, plasma cells, and macrophages in the olfactory mucosa. This suggests that allergic reactions are seen in olfactory mucosa of mice with allergic rhinitis, and that greater olfactory gland activity is associated with olfactory dysfunction. Also, this mouse model could provide an expedient system for analyzing mechanisms of olfactory dysfunction.


Disturbance of rapid eye movement sleep in senescence-accelerated mouse prone/8 mice is improved by retinoic acid receptor agonist Am80 (Tamibarotene).

Senescence-accelerated mouse prone/8 (SAMP8) mice are known to exhibit age-related deterioration in sleep-wake architecture compared with senescence-accelerated mouse resistant/1 (SAMR1) mice. We investigated whether treatment with Am80 (Tamibarotene), a retinoic acid receptor agonist, would improve sleep in 9-10-month-old SAMP8 mice. One week of Am80 administration improved the decrease in rapid eye movement (REM) sleep shown by SAMP8 mice. Real-time RT-PCR analysis demonstrated an impairment in the hippocampal retinoid cascade (retinoic acid receptor alpha and transthyretin) in SAMP8 in comparison to SAMR1 mice. Am80 treatment induced an increase in mRNA expression in the vesicular acetylcholine transporter in the brainstem and transthyretin in the hippocampus. Furthermore, decreased cortical acetylcholine content in SAMP8 was improved by Am80 administration. Decreased non-REM sleep and delta oscillation were also observed in SAMP8 mice; however, this was not improved by Am80 administration. These results partially support the hypothesis that the effects of aging on sleep-wake architecture are improved by the activation of retinoic acid receptors. The improvement may be induced by the activation of the cholinergic pathway.


Central AMPK contributes to sleep homeostasis in mice

AMP-activated protein kinase (AMPK) is an energy-sensing molecular signal involved in glucose and lipid metabolism. The known interaction of sleep with energy metabolism led us to investigate the role of central AMPK in sleep homeostasis. Sleep deprivation (SD) for 6 h increased p-AMPK protein in the hypothalamus and also increased the mRNA level of Ca(2+)/calmodulin (CaM)-dependent protein kinase kinase beta (CaMKK2), an activator of AMPK, and carnitine palmitoyltransferase 1 (CPT1), a downstream signaling factor of AMPK. Central injection of compound C (CC), an inhibitor of AMPK, suppressed EEG delta power during NREM sleep, while 5-aminoimidazole-4-carboxamide riboside (AICAR), an activator of AMPK, enhanced EEG delta power. The treatment of both CC and AICAR attenuated rebound responses of delta power in NREM sleep after SD. These results indicate that central AMPK is involved in the regulation of sleep depth and sleep homeostasis.


Fermented ginseng improves the first-night effect in humans

The goal of this study was to clarify whether ginseng fermented by lactic acid bacteria (fermented ginseng, FG), can improve the first-night effect (FNE) in humans. Behavioral tests and quantification of mRNA expression related to GABAergic neurotransmission in brain (glutamic acid decarboxylase 1, gamma-aminobutyrate aminotransferase [Abat], gamma-aminobutyric acid transporter 1 [GAT1], gamma-aminobutyric acid transporter 4, gamma-aminobutyric acid A receptor subunit alpha 1 and gamma-aminobutyric acid A receptor subunit alpha 2) were carried out in FG-treated mice. We also performed double-blind sleep recordings of human subjects given FG or placebo. A university-based sleep laboratory. Sixteen healthy male volunteers (aged 20.69 +/- 0.44 years) were observed in the human study. At the end of administration, 2 consecutive all-night polysomnography recordings were performed. Subjects also completed psychological questionnaires, and urine and saliva samples were taken to analyze stress-sensitive markers. The light-dark transition test demonstrated that FG had some anxiolytic effect in mice, but other anxiety measures were unaffected. The hippocampal mRNA expression showed a decrease of Abat and GAT1 suggesting an increase of GABA. Other regions (amygdala and cerebellum) showed no differences. Furthermore, there was some evidence (using simple pairwise comparisons but not supported in the full ANOVA model) that administration of FG tended to diminish decreases in total sleep time and sleep efficiency (seen as first night effects in the placebo group) without affecting sleep architecture. Our results suggest the administration of FG could improve the FNE in humans. The improvement may be related to an anxiolytic effect of FG which acts via GABAergic modification.


Bezafibrate, a PPARs agonist, decreases body temperature and enhances EEG delta oscillation during sleep in mice.

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belonging to the nuclear receptor family. PPARs play a critical role in lipid and glucose metabolism. We examined whether chronic treatment with bezafibrate, a PPAR agonist, would alter sleep and body temperature (BT). Mice fed with a control diet were monitored for BT, electroencephalogram (EEG), and electromyogram for 48 h under light-dark conditions. After obtaining the baseline recording, the mice were provided with bezafibrate-supplemented food for 2 wk, after which the same recordings were performed. Two-week feeding of bezafibrate decreased BT, especially during the latter half of the dark period. BT rhythm and sleep/wake rhythm were phase advanced about 2-3 h by bezafibrate treatment. Bezafibrate treatment also increased the EEG delta-power in nonrapid eye movement sleep compared with the control diet attenuating its daily amplitude. Furthermore, bezafibrate-treated mice showed no rebound of EEG delta-power in nonrapid eye movement sleep after 6 h sleep deprivation, whereas values in control mice largely increased relative to baseline. DNA microarray, and real-time RT-PCR analysis showed that bezafibrate treatment increased levels of Neuropeptide Y mRNA in the hypothalamus at both Zeitgeber time (ZT) 10 and ZT22, and decreased proopiomelanocortin-alpha mRNA in the hypothalamus at ZT10. These findings demonstrate that PPARs participate in the control of both BT and sleep regulation, which accompanied changes in gene expression in the hypothalamus. Activation of PPARs may enhance deep sleep and improve resistance to sleep loss.


Diurnal amplitudes of arterial pressure and heart rate are dampened in Clock mutant mice and adrenalectomized mice.

Arterial pressure (AP), heart rate (HR), and cardiovascular diseases, including ischemic heart attack and cerebrovascular accident, show diurnal variation. Evidence that circadian-related genes contribute to cardiovascular control has been accumulated. In this study, we measured the AP and HR of Clock mutant mice on the Jcl/ICR background to determine the role of the Clock gene in cardiovascular function. Mice with mutated Clock genes had a dampened diurnal rhythm of AP and HR, compared with wild-type control mice, and this difference disappeared after adrenalectomy. The diurnal acrophase in both mean arterial pressure and HR was delayed significantly in Clock mutant mice, compared with wild-type mice, and this difference remained after adrenalectomy. Clock mutant mice had a lower concentration of plasma aldosterone, compared with wild-type mice. Our data suggest that the adrenal gland is involved in the diurnal amplitude, but not the acrophase, of AP and HR, and that the function of the Clock gene may be related to the nondipping type of AP elevation.


Vitamin A deficiency induces a decrease in EEG delta power during sleep in mice

Recent report (Maret, S., Franken, P., Dauvilliers, Y., Ghyselinck, N.B., Chambon, P., Tafti, M., 2005. Retinoic acid signaling affects cortical synchrony during sleep. Science 310, 111-113.) has suggested that vitamin A (retinol and its derivatives) is genetically involved in the electroencephalogram (EEG) delta oscillation during sleep. However, this finding has not yet been confirmed by other studies. In this study, we attempted to record the sleep EEG and behavior, and to quantify striatal monoamines in mice fed a vitamin A-deficient (VAD) diet for 4 weeks, in order to clarify the linkage between the delta oscillation and vitamin A. VAD mice demonstrated a significant decrease in the delta power of the EEG. However, 6-h sleep deprivation caused the recovery of the delta power in VAD mice to a level similar to that of the control. VAD also caused the decrease of spontaneous activity throughout 24-h period. Furthermore, dihydroxyphenylacetic acid, a metabolite of dopamine, was decreased significantly in the striatal tissue of VAD mice. Our present results suggest that the deficiency of vitamin A causes the attenuation of delta power in NREM sleep and spontaneous activity. These attenuations may be related to the alteration of striatal dopaminergic function.


Anxiolytic effect of music depends on ovarian steroid in female mice.

Music is known to be able to elicit emotional changes, including anxiolytic effects. The gonadal steroid hormones estradiol and progesterone have also been reported to play important roles in the modulation of anxiety. In the present study, we examined whether the effect of music on anxiety is related to ovarian steroid in female mice. Behavioral paradigms measuring anxiety were tested in gonadally intact (SHAM) and ovariectomized (OVX) female mice chronically treated with either placebo (OVX/Placebo), 17β-estradiol (OVX/E), or progesterone (OVX/P). In the elevated plus maze, light-dark transition, and marble burying tests, SHAM and OVX/P mice exposed to music showed less anxiety than those exposed to white noise or silence while OVX/placebo mice did not show these effects at all. OVX/E mice showed the anxiolytic effect of music only in the marble burying test. Furthermore, pretreatment with progesterone's metabolite inhibitor completely prevented the anxiolytic effect of music in behavioral tests, while pretreatment with a progesterone receptor blocker did not prevent the anxiolytic effect of music. These results suggest that exposure to music reduces anxiety levels, and ovarian steroids, mainly progesterone, may be involved in the anxiolytic effect of music observed in female mice.


Exposure to music in the perinatal period enhances learning performance and alters BDNF/TrkB signaling in mice as adults.

Music has been suggested to have a beneficial effect on various types of performance in humans. However, the physiological and molecular mechanism of this effect remains unclear. We examined the effect of music exposure during the perinatal period on learning behavior in adult mice, and measured the levels of brain-derived neurotrophic factor (BDNF) and its receptor, tyrosine kinase receptor B (TrkB), which play critical roles in synaptic plasticity. In addition, we measured the levels of 3-phosphoinositide-dependent protein kinase-1 (PDK1) and mitogen-activated protein kinase (MAPK), downstream targets of two main pathways in BDNF/TrkB signaling. Music-exposed mice completed a maze learning task with fewer errors than the white noise-exposed mice and had lower levels of BDNF and higher levels of TrkB and PDK1 in the cortex. MAPK levels were unchanged. Furthermore, TrkB and PDK1 protein levels in the cortex showed a significant negative correlation with the number of errors on the maze. These results suggest that perinatal exposure of mice to music has an influence on BDNF/TrkB signaling and its intracellular signaling pathway targets, including PDK1, and thus may induce improved learning and memory functions.


Effect of repetitive transcranial magnetic stimulation applied over the premotor cortex on somatosensory-evoked potentials and regional cerebral blood flow.

Somatosensory-evoked potentials (SEPs) are attenuated by movement. This phenomenon of 'gating' reflects sensorimotor integration for motor control. The frontal N30 component after median nerve stimulation was shown to be reduced in amplitude prior to hand movement. To investigate the mechanism of this sensory gating, we recorded median SEPs immediately before and after application of monophasic very low-frequency (0.2 Hz) repetitive transcranial magnetic stimulation (rTMS) of 250 stimuli over motor cortex (MC), premotor cortex (PMC), or supplementary motor area (SMA) in 9 healthy volunteers. The stimulus intensity for MC or PMC was set 85% of the resting motor threshold for the hand muscle, and that for SMA was at the active motor threshold for the leg muscle. SEPs showed significant increases in amplitudes of the frontal N30 component after PMC stimulation, but not after SMA or MC stimulation. Low-frequency (1 Hz) biphasic stimulation over PMC showed no significant N30 changes in 6 out of 9 subjects tested, indicating the effect being specific for 0.2 Hz monophasic stimulation. To examine the functional anatomy of the N30 change, single photon emission computed tomography was performed immediately before and after monophasic 0.2 Hz rTMS over PMC in all the 9 subjects. Regional cerebral blood flow showed significant increases mainly in PMC and prefrontal cortex, indicating the involvement of these cortical areas in sensory input gating for motor control.


Effect of mood state on anticipatory postural adjustments.

Static postural control has been demonstrated to link with psychological state. However, the effect of psychological state on dynamic postural control remains unclear. In this study, we examined the effect of mood state on anticipatory postural adjustment (APA), one of the most important functions for dynamic postural control. Fourteen healthy male subjects performed unilateral arm elevation tasks after completing a Profile of Mood States (POMS) questionnaire. Mood state measured by POMS and the latency or amplitude of the APA in the ventral muscles (rectus femoris, tibialis anterior) of the lower limb showed significant negative correlations. The correlation between the mood state and APA amplitude in the soleus was found to be significantly positive. There were significant negative correlations between the mood state and reaction-time. These findings suggest that it is possible that dynamic postural control is affected by mood state.