DOMINANT AWN INHIBITOR Encodes the ALOG Protein Originating from Gene Duplication and Inhibits AWN Elongation by Suppressing Cell Proliferation and Elongation in Sorghum.

The awn, a needle-like structure extending from the tip of the lemma in grass species, plays a role in environmental adaptation and fitness. In some crops, awns appear to have been eliminated during domestication. Although numerous genes involved in awn development have been identified, several dominant genes that eliminate awns are also known to exist. For example, in sorghum (Sorghum bicolor), the dominant awn-inhibiting gene has been known since 1921; however, its molecular features remain uncharacterized. In this study, we conducted quantitative trait locus analysis and a genome-wide association study of awn-related traits in sorghum and identified DOMINANT AWN INHIBITOR (DAI), which encodes the ALOG family protein on chromosome 3. DAI appeared to be present in most awnless sorghum cultivars, likely because of its effectiveness. Detailed analysis of the ALOG protein family in cereals revealed that DAI originated from a duplication of its twin paralog (DAIori) on chromosome 10. Observations of immature awns in near-isogenic lines revealed that DAI inhibits awn elongation by suppressing both cell proliferation and elongation. We also found that only DAI gained a novel function to inhibit awn elongation through an awn-specific expression pattern distinct from that of DAIori. Interestingly, heterologous expression of DAI with its own promoter in rice inhibited awn elongation in the awned cultivar Kasalath. We found that DAI originated from gene duplication, providing an interesting example of gain-of-function that occurs only in sorghum but shares its functionality with rice and sorghum.

Atypical Sensory Processing Profiles and Their Associations With Motor Problems In Preschoolers With Developmental Coordination Disorder.

The aims of this study were to identify sensory processing profiles specific to preschoolers with DCD in a community sample and examine the association of sensory processing problems with motor coordination difficulties in these children. Sixty-three 5-year-old children with DCD and without other neurodevelopmental disorders and 106 age-matched typically developing children participated in this study. Sensory processing problems were assessed using the Sensory Profile. Our results demonstrated problems in wide sensory processing patterns (low registration, sensitivity and avoiding) and areas (auditory, vestibular, touch and oral) in children with DCD compared with typically developing children. Additionally, the association of problems in sensory processing patterns (sensitivity and avoiding) and areas (touch and auditory) with motor coordination difficulties were identified in children with DCD alone. Our findings indicate that sensory processing abnormalities may contribute to the pathophysiology of DCD, suggesting the importance of assessing sensory processing functions in children with DCD.

Ultrasound irradiation before high-load exercise reduces muscle rigidity associated with delayed-onset muscle soreness.

[Purpose] We investigated the occurrence of delayed-onset muscle soreness and the suppression of muscle rigidity by ultrasound irradiation before high-load exercise. [Participants and Methods] The study was a randomized crossover controlled trial. The participants were 28 healthy university students (12 males, 16 females). Delayed-onset muscle soreness was induced in the biceps brachii muscle; ultrasound (3 MHz, 1.5 W/cm2, 10 min) was applied before high-load exercise. Pain during elbow motion was evaluated on a visual analog scale. Muscle rigidity was evaluated using a muscle rigidity meter. [Results] After exercise on the second day, the ultrasound group showed significantly less muscle rigidity. [Conclusion] The heat stimulus of ultrasound therapy before high-load exercise reduces muscle rigidity.

Propofol Anesthesia Is Reduced in Phospholipase C-Related Inactive Protein Type-1 Knockout Mice.

The GABA type A receptor (GABAA-R) is a major target of intravenous anesthetics. Phospholipase C-related inactive protein type-1 (PRIP-1) is important in GABAA-R phosphorylation and membrane trafficking. In this study, we investigated the role of PRIP-1 in general anesthetic action. The anesthetic effects of propofol, etomidate, and pentobarbital were evaluated in wild-type and PRIP-1 knockout (PRIP-1 KO) mice by measuring the latency and duration of loss of righting reflex (LORR) and loss of tail-pinch withdrawal response (LTWR). The effect of pretreatment with okadaic acid (OA), a protein phosphatase 1/2A inhibitor, on propofol- and etomidate-induced LORR was also examined. PRIP-1 deficiency provided the reduction of LORR and LTWR induced by propofol but not by etomidate or pentobarbital, indicating that PRIP-1 could determine the potency of the anesthetic action of propofol. Pretreatment with OA recovered the anesthetic potency induced by propofol in PRIP-1 KO mice. OA injection enhanced phosphorylation of cortical the GABAA-R ß3 subunit in PRIP-1 KO mice. These results suggest that PRIP-1-mediated GABAA-R ß3 subunit phosphorylation might be involved in the general anesthetic action induced by propofol but not by etomidate or pentobarbital.

HSP90 Regulation of P2X7 Receptor Function Requires an Intact Cytoplasmic C-Terminus.

P2X7 receptors (P2X7Rs) are ATP-gated ion channels that display the unusual property of current facilitation during long applications of agonists. Here we show that facilitation disappears in chimeric P2X7Rs containing the C-terminus of the P2X2 receptor (P2X2R), and in a truncated P2X7R missing the cysteine-rich domain of the C-terminus. The chimeric and truncated receptors also show an apparent decreased permeability to N-methyl-d-glucamine(+) (NMDG(+)). The effects of genetic modification of the C-terminus on NMDG(+) permeability were mimicked by preapplication of the HSP90 antagonist geldanamycin to the wild-type receptor. Further, the geldanamycin decreased the shift in the reversal potential of the ATP-gated current measured under bi-ionic NMDG(+)/Na(+) condition without affecting the ability of the long application of agonist to facilitate current amplitude. Taken together, the results suggest that HSP90 may be essential for stabilization and function of P2X7Rs through an action on the cysteine-rich domain of the cytoplasmic the C-terminus.

Morphological and electrophysiological changes in intratelencephalic-type pyramidal neurons in the motor cortex of a rat model of levodopa-induced dyskinesia.

Levodopa-induced dyskinesia (LID) is a major complication of long-term dopamine replacement therapy for Parkinson's disease, and becomes increasingly problematic in the advanced stage of the disease. Although the cause of LID still remains unclear, there is accumulating evidence from animal experiments that it results from maladaptive plasticity, resulting in supersensitive excitatory transmission at corticostriatal synapses. Recent work using transcranial magnetic stimulation suggests that the motor cortex displays the same supersensitivity in Parkinson's disease patients with LID. To date, the cellular mechanisms underlying the abnormal cortical plasticity have not been examined. The morphology of the dendritic spines has a strong relationship to synaptic plasticity. Therefore, we explored the spine morphology of pyramidal neurons in the motor cortex in a rat model of LID. We used control rats, 6-hydroxydopamine-lesioned rats (a model of Parkinson's disease), 6-hydroxydopamine-lesioned rats chronically treated with levodopa (a model of LID), and control rats chronically treated with levodopa. Because the direct pathway of the basal ganglia plays a central role in the development of LID, we quantified the density and size of dendritic spines in intratelencephalic (IT)-type pyramidal neurons in M1 cortex that project to the striatal medium spiny neurons in the direct pathway. The spine density was not different among the four groups. In contrast, spine size became enlarged in the Parkinson's disease and LID rat models. The enlargement was significantly greater in the LID model than in the Parkinson's disease model. This enlargement of the spines suggests that IT-type pyramidal neurons acquire supersensitivity to excitatory stimuli. To confirm this possibility, we monitored miniature excitatory postsynaptic currents (mEPSCs) in the IT-type pyramidal neurons in M1 cortex using whole-cell patch clamp. The amplitude of the mEPSCs was significantly increased in the LID model compared with the control. This indicates that the IT-type pyramidal neurons become hyperexcited in the LID model, paralleling the enlargement of spines. Thus, spine enlargement and the resultant hyperexcitability of IT-type pyramidal neurons in M1 cortex might contribute to the abnormal cortical neuronal plasticity in LID.

Morphologic changes of dendritic spines of striatal neurons in the levodopa-induced dyskinesia model.

Maladaptive plasticity at corticostriatal synapses plays an important role in the development of levodopa-induced dyskinesia. Recently, it has been shown that synaptic plasticity is closely linked to morphologic changes of dendritic spines. To evaluate morphologic changes of dendritic spines of two types of striatal medium spiny neurons, which project to the internal segment of globus pallidus or the external segment of globus pallidus, in the levodopa-induced dyskinesia model, we used 6-hydroxydopamine-lesioned rats chronically treated with levodopa. Dendritic spines were decreased and became enlarged in the direct pathway neurons of the model of levodopa-induced dyskinesia. The same levodopa treatment to normal rats, in which no dyskinesia was observed, also induced enlargement of dendritic spines, but not a decrease in density of spines in the direct pathway neurons. These results suggest that a loss and enlargement of dendritic spines in the direct pathway neurons plays important roles in the development of levodopa-induced dyskinesia.

Cl⁻ homeodynamics in gap junction-coupled astrocytic networks on activation of GABAergic synapses.

The electrophysiological properties and functional role of GABAergic signal transmission from neurons to the gap junction-coupled astrocytic network are still unclear. GABA-induced astrocytic Cl⁻ flux has been hypothesized to affect the driving force for GABAergic transmission by modulating [Cl⁻]o. Thus, revealing the properties of GABA-mediated astrocytic responses will deepen our understanding of GABAergic signal transmission. Here, we analysed the Cl⁻ dynamics of neurons and astrocytes in CA1 hippocampal GABAergic tripartite synapses, using Cl⁻ imaging during GABA application, and whole cell recordings from interneuron-astrocyte pairs in the stratum lacunosum-moleculare. Astrocytic [Cl⁻]i was adjusted to physiological conditions (40 mm). Although GABA application evoked bidirectional Cl⁻ flux via GABAA receptors and mouse GABA transporter 4 (mGAT4) in CA1 astrocytes, a train of interneuron firing induced only GABAA receptor-mediated inward currents in an adjacent astrocyte. A GAT1 inhibitor increased the interneuron firing-induced currents and induced bicuculline-insensitive, mGAT4 inhibitor-sensitive currents, suggesting that synaptic spillover of GABA predominantly induced the astrocytic Cl⁻ efflux because GABAA receptors are localized near the synaptic clefts. This GABA-induced Cl⁻ efflux was accompanied by Cl⁻ siphoning via the gap junctions of the astrocytic network because gap junction inhibitors significantly reduced the interneuron firing-induced currents. Thus, Cl⁻ efflux from astrocytes is homeostatically maintained within astrocytic networks. A gap junction inhibitor enhanced the activity-dependent depolarizing shifts of reversal potential of neuronal IPSCs evoked by repetitive stimulation to GABAergic synapses. These results suggest that Cl⁻ conductance within the astrocytic network may contribute to maintaining GABAergic synaptic transmission by regulating [Cl⁻]o.

Taurine inhibits K+-Cl- cotransporter KCC2 to regulate embryonic Cl- homeostasis via with-no-lysine (WNK) protein kinase signaling pathway.

GABA inhibits mature neurons and conversely excites immature neurons due to lower K(+)-Cl(-) cotransporter 2 (KCC2) expression. We observed that ectopically expressed KCC2 in embryonic cerebral cortices was not active; however, KCC2 functioned in newborns. In vitro studies revealed that taurine increased KCC2 inactivation in a phosphorylation-dependent manner. When Thr-906 and Thr-1007 residues in KCC2 were substituted with Ala (KCC2T906A/T1007A), KCC2 activity was facilitated, and the inhibitory effect of taurine was not observed. Exogenous taurine activated the with-no-lysine protein kinase 1 (WNK1) and downstream STE20/SPS1-related proline/alanine-rich kinase (SPAK)/oxidative stress response 1 (OSR1), and overexpression of active WNK1 resulted in KCC2 inhibition in the absence of taurine. Phosphorylation of SPAK was consistently higher in embryonic brains compared with that of neonatal brains and down-regulated by a taurine transporter inhibitor in vivo. Furthermore, cerebral radial migration was perturbed by a taurine-insensitive form of KCC2, KCC2T906A/T1007A, which may be regulated by WNK-SPAK/OSR1 signaling. Thus, taurine and WNK-SPAK/OSR1 signaling may contribute to embryonic neuronal Cl(-) homeostasis, which is required for normal brain development.

Properties of a novel GABAA receptor γ2 subunit mutation associated with seizures.

We recently identified a novel missense mutation of the γ(2) subunit at position 40 with serine (N40S) of the GABA(A) receptor from a patient with epilepsy. Here, we report properties of the mutant receptor using the whole cell patch clamp technique. The Hill coefficient for the N40S receptor was greater than for the wild-type (WT) receptor, while the EC50 and kinetics did not differ. Furthermore, the effects of diazepam, Zn(2+), bicuculline, and pH were indistinguishable between WT and N40S receptors. These results suggest that the changes in the steepness of the concentration-response relationship for GABA in the N40S receptor may trigger epilepsy.

Drebrin immunoreactivity in the striatum of a rat model of levodopa-induced dyskinesia.

Levodopa-induced dyskinesia has been suggested to result from maladaptive plasticity at corticostriatal synapses. Synaptic plasticity is based upon morphologic changes of dendritic spines. To elucidate whether the morphologic changes of spines occur in the striatum of rat models of levodopa-induced dyskinesia, we examined immunoreactivity of drebrin, an actin-binding protein localized in dendritic spines of excitatory synapses, using 6-hydroxydopamine-lesioned rats repeatedly treated with levodopa. The cross-sectional area of drebrin-immunoreactive organelles, putative spines, in the dopamine-denervated striatum of the levodopa-induced dyskinesia model was greater than that of the Parkinson's disease model. Immunoelectron microscopic examinations confirmed that drebrin-immunoreactive spines became enlarged in the dopamine-denervated striatum of the levodopa-induced dyskinesia model, but not in the Parkinson's disease model. These results suggest that the development of levodopa-induced dyskinesia is associated with enlargement of dendritic spines at corticostriatal excitatory synapses.

Trajectories of emotional and behavioral problems in school-age children with coordination difficulties and their relationships to ASD/ADHD traits.

BACKGROUND: Although research has demonstrated associations between motor coordination difficulties and psychological problems in school-age children, including emotional and behavioral problems, longitudinal changes in these problems in children with motor coordination difficulties are not fully understood. AIMS: The current study aimed to identify patterns in the trajectory of emotional and behavioral problems in school-age children with motor coordination difficulties, and to elucidate the effect of co-existing neurodevelopmental traits on the occurrence and course of these problems. METHODS AND PROCEDURES: Using the Developmental Coordination Disorder Questionnaire, 773 children were defined as cases with motor coordination difficulties and followed for 4 years, from 6 to 10 years of age. Emotional and behavioral problems were assessed using the Strengths and Difficulties Questionnaire completed by children's parents or guardians. OUTCOMES AND RESULTS: We identified four trajectory patterns of emotional and behavioral problems. Children with higher autism spectrum disorder and attention deficit hyperactivity disorder traits were more likely to be assigned to poor prognostic trajectory patterns. CONCLUSIONS AND IMPLICATIONS: Our findings emphasize the importance of assessing emotional and behavioral problems and co-existing neurodevelopmental traits in children with motor coordination difficulties in early elementary school.

Dysfunction of extrasynaptic GABAergic transmission in phospholipase C-related, but catalytically inactive protein 1 knockout mice is associated with an epilepsy phenotype.

Phospholipase C-related, but catalytically inactive protein (PRIP) was first identified as a novel inositol 1,4,5-triphosphate binding protein. The PRIP-1 subtype is expressed predominantly in the central nervous system and binds directly to the GABA type A receptor (GABA(A)-R) ß-subunit and several other proteins involved in the trafficking of GABA(A)-Rs to the plasma membrane. We found that the PRIP-1 knockout mouse showed an epileptic phenotype, confirmed by electroencephalogram. These ictal seizures were completely suppressed by diazepam (DZP), but the interictal discharges could not be abolished. We studied the electrophysiological properties of GABAergic transmission in hippocampal CA1 pyramidal neurons, using a slice patch-clamp technique. There was no difference in the effect of up to 1 µM DZP on the amplitude and frequency of miniature inhibitory postsynaptic currents between PRIP-1 knockout neurons versus wild-type neurons. In contrast, the amplitude of the tonic GABA current in PRIP-1 knockout neurons was markedly reduced compared with that in wild-type neurons. Consequently, the effect of DZP on PRIP-1 knockout mice was reduced. Dysfunction of extrasynaptic GABAergic transmission probably is involved in the epileptic phenotype of PRIP-1 knockout mice.

Early abdominal pregnancy complicated by parasitic dermoid cyst: diagnosis by diffusion-weighted magnetic resonance imaging and management by laparoendoscopic single-site surgery.

A 26-year-old primigravida patient was referred with suspicion of ectopic pregnancy 39 days after her last menstrual period. Her serum ß-human chorionic gonadotropin value was 3812 mIU/mL. As we suspected the existence of ectopic pregnancy with bilateral dermoid cysts, laparoendoscopic single-site surgery was performed. After dissection of dense pelvic adhesion, cystectomy was performed for a left ovarian dermoid cyst. Although there was a right ovary at the correct position, a parasitic dermoid cyst firmly attached to the peritoneal surface of cul-de-sac was identified. After excision of the parasitic dermoid cyst, early abdominal pregnancy tissue implanted in the peritoneal hollow of right deep pararectal space was identified under the guidance of diffusion-weighted magnetic resonance imaging and was excised. With systemic administration of methotorexate, the postoperative course was uneventful.

Association between relational mobility, brain structure, and prosociality in adolescents.

Trust plays a vital role in human society. Previous studies have suggested that trust comprises general trust and caution. General trust is a belief that others, in general, are trustworthy, and caution is a belief in the importance of vigilance in dealing with others. Adolescence is a critical period for establishing these psychological traits. It is a period of physical and mental development, and the social environment during this period influences adolescents' psychology, including their brain structures. In this study, we focus on relational mobility as a socio-environmental factor that influences the development of adolescents' psychology and the brain. Relational mobility refers to the degree of freedom to choose and replace social relationships and consists of two subfactors (the degree of freedom to choose and replace social relationships and the number of opportunities to meet new people). Accordingly, we analyzed each subfactor separately. Results showed that the degree of freedom to choose and replace social relationships was only negatively associated with caution and left posterior superior temporal gyrus (pSTG) volume in adolescents. Furthermore, the effect of the freedom to choose and replace social relationships on caution was significantly relevant to the left pSTG volume. In contrast, the degree of opportunities to meet new people was associated with neither general trust nor caution, whereas it was positively associated with the right supramarginal gyrus volume. This study suggests that the social environment during adolescence influences brain structures related to prosociality.

Is oxytocin a trust hormone? Salivary oxytocin is associated with caution but not with general trust.

Studies on the association between trust and oxytocin, a neuropeptide of the central nervous system, have not reached a consensus, thereby challenging the possibility of a direct association between the two. However, previous studies have not examined how oxytocin is correlated with trust, based on its categorization into different factors in the field of social science. For instance, based on Yamagishi's trust theory, trust can be categorized into two factors: general trust and caution. General trust refers to beliefs about the trustworthiness of others, whereas caution refers to the belief that caution is needed when dealing with high social uncertainty. In this study, to examine the relationship between these two factors and oxytocin, we analyzed data of 197 adults (men = 98, women = 99; mean age = 41.7 years; standard deviation for age = 10.4 years) and examined the relationships between these two factors of trust and endogenous salivary oxytocin levels. We found that oxytocin was positively correlated with caution rather than with general trust thereby suggesting that oxytocin plays a role in regulating caution rather than general trust among the components of trust. The present study demonstrated that salivary oxytocin level can act as a biomarker that partially predicts one's trust, especially as reflected by caution.

Collaboration among psychological researchers, the government, and non-profit organizations for "Konkatsu" (marriage hunting) in Japan.

In contemporary Japanese society, it is difficult to find a marriage partner, and therefore, "Konkatsu," the search for a marriage partner, has become a socially accepted activity in Japan. In response to this social challenge, in addition to private companies, governments and non-profit organizations are supporting individuals in their search for a marriage partner. This paper reviews statistical information related to marriage hunting published in Japan. In addition, some of the authors' collaborative activities and academic publications based on these activities are reviewed. Subsequently, the paper discusses and highlights the importance of helping individuals have confidence in their physical attractiveness.

Association between salivary oxytocin levels and the amygdala and hippocampal volumes.

Salivary oxytocin levels have been widely measured and studied in relation to social behavior because of procedural simplicity and noninvasiveness. Although the relationship between oxytocin levels in the blood and the hippocampus and amygdala is now becoming clear with reliable blood oxytocin studies, few studies have examined the relationship between salivary oxytocin and the brain function and structure. This study aimed to investigate whether the salivary oxytocin level is associated with the volume of the amygdala and hippocampus in 178 adults (92 women and 86 men) in their third to seventh decade of life. We performed volumetric analysis of the amygdala and hippocampus using FreeSurfer and measured salivary oxytocin levels using enzyme-linked immunosorbent assay. The results showed contradictory effects of the salivary oxytocin level on the amygdala volume by sex and no significant effect on the hippocampal volume. Specifically, men showed a positive correlation between the salivary oxytocin level and amygdala volume, whereas women showed a negative correlation between the salivary oxytocin level and amygdala volume. The present study's finding of sex differences in the association between salivary oxytocin and brain structure supports previous findings that there are sex differences in the oxytocin system.

Phenotypes of pain behavior in phospholipase C-related but catalytically inactive protein type 1 knockout mice.

Phospholipase C-related inactive protein (PRIP) plays important roles in trafficking to the plasma membrane of GABA(A) receptor, which is involved in the dominant inhibitory neurotransmission in the spinal cord and plays an important role in nociceptive transmission. However, the role of PRIP in pain sensation remains unknown. In this study, we investigated the phenotypes of pain behaviors in PRIP type 1 knockout (PRIP-1 (-/-)) mice. The mutant mice showed hyperalgesic responses in the second phase of the formalin test and the von Frey test as compared with those in wild-type mice. In situ hybridization studies of GABA(A) receptors revealed significantly decreased expression of γ2 subunit mRNA in the dorsal and ventral horns of the spinal cord in PRIP-1 (-/-) mice, but no difference in α1 subunit mRNA expression. ß2 subunit mRNA expression was significantly higher in PRIP-1 (-/-) mice than in wild-type mice in all areas of the spinal cord. On the other hand, the slow decay time constant for the spontaneous inhibitory current was significantly increased by treatment with diazepam in wild-type mice, but not in PRIP-1 (-/-) mice. These results suggest that PRIP-1 (-/-) mice exhibit the changes of the function and subunits expression of GABA(A) receptor in the spinal cord, which may be responsible for abnormal pain sensation in these mice.

Uterus-like mass of ovarian ligament: Image diagnosis and management by laparoendoscopic single-site surgery.

Uterus-like mass composed of a cavity lined by mucosa resembling endometrium and surrounding smooth muscle layer simulating myometrium is an extremely rare disease entity of which the histogenesis is presently unknown. A 39-year-old, gravida 2, para 2, woman presented with sudden onset of lower abdominal pain and was found to have left adnexal mass with unusual image diagnostic appearance. The adnexal mass arising from the left ovarian ligament was excised by laparoendoscopic single-site surgery. Histopathological diagnosis was uterus-like mass of ovarian ligament.