Prestimulus Interhemispheric Coupling of Brain Rhythms Predicts Cognitive–Motor Performance in Healthy Humans

2014 ◽  
Vol 26 (9) ◽  
pp. 1883-1890 ◽  
Author(s):  
Fabrizio Vecchio ◽  
Giordano Lacidogna ◽  
Francesca Miraglia ◽  
Placido Bramanti ◽  
Florinda Ferreri ◽  
...  

Physiological and neuroimaging studies suggest that human actions are characterized by time-varying engagement of functional distributed networks within the brain. In this study, we investigated whether specific prestimulus interhemispheric connectivity, as a measure of synchronized network between the two hemispheres, could lead to a better performance (as revealed by RT) in a simple visuomotor task. Eighteen healthy adults underwent EEG recording during a visual go/no-go task. In the go/no-go task, a central fixation stimulus was followed by a green (50% of probability) or red visual stimulus. Participants had to press the mouse button after the green stimuli (go trials). Interhemispheric coupling was evaluated by the spectral coherence among all the electrodes covering one hemisphere and matched with those on the other. The frequency bands of interest were delta (2–4 Hz), theta (4–8 Hz), alpha 1 (8–10.5 Hz), alpha 2 (10.5–13 Hz), beta 1 (13–20 Hz), beta 2 (20–30 Hz), and gamma (30–40 Hz). The task-related results showed that interhemispheric connectivity decreased in delta and increased in alpha band. Furthermore, we observed positive delta and negative alpha correlations with the RT; namely, the faster the RT, the lower delta and the higher alpha connection between the two hemispheres. These results suggested that the best performance is anticipated by the better functional coupling of cortical circuits involved during the processing of the sensorimotor information, occurring between the two hemispheres pending cognitive go/no-go task.

2021 ◽  
Author(s):  
Aymen Sadaka ◽  
Ana Ozuna ◽  
Richard Ortiz ◽  
Praveen Kulkarni ◽  
Clare Johnson ◽  
...  

Abstract Background: The phytocannabinoid cannabidiol (CBD) is a potential treatment for post-traumatic stress disorders. How does CBD interact with the brain to alter behavior? We hypothesized that CBD would produce a dose-dependent reduction in brain activity and functional coupling in neural circuitry associated with fear and defense. Methods: During the scanning session awake mice were given vehicle or CBD (3, 10, or 30 mg/kg I.P.) and imaged for 10 min post treatment. Mice were also treated with the 10 mg/kg dose of CBD and imaged one hr later for resting state BOLD functional connectivity (rsFC). Imaging data were registered to a 3D MRI mouse atlas providing site-specific information on 138 different brain areas. Blood samples were collected for CBD measurements.Results: CBD produced a dose-dependent polarization of activation along the rostral-caudal axis of the brain. The olfactory bulb and prefrontal cortex showed an increase in positive BOLD whereas the brainstem and cerebellum showed a decrease in BOLD signal. This negative BOLD affected many areas connected to the ascending reticular activating system (ARAS). The ARAS was decoupled to much of the brain but was hyperconnected to the olfactory system and prefrontal cortex. The pattern of ARAS connectivity closely overlapped with brain areas showing high levels N-acyl-phosphatidylethanolamines-specific phospholipase D (NAPE-PLD) messenger RNA.Conclusion: The CBD-induced decrease in ARAS activity is consistent with an emerging literature suggesting that CBD reduces autonomic arousal under conditions of emotional and physical stress. The putative target and mechanism of action is NAPE-PLD the enzyme responsible for the biosynthesis of lipid signaling molecules like anandamide.


2008 ◽  
Vol 294 (1) ◽  
pp. R12-R16 ◽  
Author(s):  
Kerstin M. Oltmanns ◽  
Uwe H. Melchert ◽  
Harald G. Scholand-Engler ◽  
Maria C. Howitz ◽  
Bernd Schultes ◽  
...  

The brain regulates all metabolic processes within the organism, and therefore, its energy supply is preserved even during fasting. However, the underlying mechanism is unknown. Here, it is shown, using 31P-magnetic resonance spectroscopy that during short periods of hypoglycemia and hyperglycemia, the brain can rapidly increase its high-energy phosphate content, whereas there is no change in skeletal muscle. We investigated the key metabolites of high-energy phosphate metabolism as rapidly available energy stores by 31P MRS in brain and skeletal muscle of 17 healthy men. Measurements were performed at baseline and during dextrose or insulin-induced hyperglycemia and hypoglycemia. During hyperglycemia, phosphocreatine (PCr) concentrations increased significantly in the brain ( P = 0.013), while there was a similar trend in the hypopglycemic condition ( P = 0.055). Skeletal muscle content remained constant in both conditions ( P > 0.1). ANOVA analyses comparing changes from baseline to the respective glycemic plateau in brain (up to +15%) vs. muscle (up to −4%) revealed clear divergent effects in both conditions ( P < 0.05). These effects were reflected by PCr/Pi ratio ( P < 0.05). Total ATP concentrations revealed the observed divergency only during hyperglycemia ( P = 0.018). These data suggest that the brain, in contrast to peripheral organs, can activate some specific mechanisms to modulate its energy status during variations in glucose supply. A disturbance of these mechanisms may have far-reaching implications for metabolic dysregulation associated with obesity or diabetes mellitus.


2021 ◽  
Vol 11 ◽  
Author(s):  
Orestis Stylianou ◽  
Frigyes Samuel Racz ◽  
Andras Eke ◽  
Peter Mukli

While most connectivity studies investigate functional connectivity (FC) in a scale-dependent manner, coupled neural processes may also exhibit broadband dynamics, manifesting as power-law scaling of their measures of interdependence. Here we introduce the bivariate focus-based multifractal (BFMF) analysis as a robust tool for capturing such scale-free relations and use resting-state electroencephalography (EEG) recordings of 12 subjects to demonstrate its performance in reconstructing physiological networks. BFMF was employed to characterize broadband FC between 62 cortical regions in a pairwise manner, with all investigated connections being tested for true bivariate multifractality. EEG channels were also grouped to represent the activity of six resting-state networks (RSNs) in the brain, thus allowing for the analysis of within- and between- RSNs connectivity, separately. Most connections featured true bivariate multifractality, which could be attributed to the genuine scale-free coupling of neural dynamics. Bivariate multifractality showed a characteristic topology over the cortex that was highly concordant among subjects. Long-term autocorrelation was higher in within-RSNs, while the degree of multifractality was generally found stronger in between-RSNs connections. These results offer statistical evidence of the bivariate multifractal nature of functional coupling in the brain and validate BFMF as a robust method to capture such scale-independent coupled dynamics.


Author(s):  
MAHESWARI REDDY B ◽  
DHANAPAL CK ◽  
LAKSHMI BVS

Objective: The current study evaluates anti-Parkinson’s activity of aqueous extracts of leaves of Murraya koenigii (MK) (AEMK) against paraquat (PQ)-induced Parkinsonism in rats. Methods: In this study, effects of MK (100, 200, and 400 mg/kg, p.o.) were studied using in vivo behavioral parameters such as catalepsy, muscle rigidity, and locomotor activity and its effects on neurochemical parameters malondialdehyde, catalase (CAT), glutathione (GSH) reductase, GSH peroxidase, and GSH in rats. Results: Parkinson’s disease was induced by administering PQ 10 mg/kg b.w/i.p once in a week for 4 weeks. The increased cataleptic scores were significantly (p<0.001) found to be reduced, with the AEMK in a dose-dependent manner. Chronic administration of PQ significantly induced motor dysfunction (muscle rigidity and hypolocomotion), showed a significant increase in lipid peroxidation level, and depleted the levels of GSH, CAT, and reduced GSH. Daily administration of AEMK significantly improved motor performance and also significantly attenuated oxidative damage. Conclusion: The study proved that MK treatment significantly attenuated motor defects and also protected the brain from oxidative stress.


2019 ◽  
Vol 116 (17) ◽  
pp. 8370-8379 ◽  
Author(s):  
Hao Zuo ◽  
Ian Glaaser ◽  
Yulin Zhao ◽  
Igor Kurinov ◽  
Lidia Mosyak ◽  
...  

Metabotropic GABABreceptors mediate a significant fraction of inhibitory neurotransmission in the brain. Native GABABreceptor complexes contain the principal subunits GABAB1and GABAB2, which form an obligate heterodimer, and auxiliary subunits, known as potassium channel tetramerization domain-containing proteins (KCTDs). KCTDs interact with GABABreceptors and modify the kinetics of GABABreceptor signaling. Little is known about the molecular mechanism governing the direct association and functional coupling of GABABreceptors with these auxiliary proteins. Here, we describe the high-resolution structure of the KCTD16 oligomerization domain in complex with part of the GABAB2receptor. A single GABAB2C-terminal peptide is bound to the interior of an open pentamer formed by the oligomerization domain of five KCTD16 subunits. Mutation of specific amino acids identified in the structure of the GABAB2–KCTD16 interface disrupted both the biochemical association and functional modulation of GABABreceptors and G protein-activated inwardly rectifying K+channel (GIRK) channels. These interfacial residues are conserved among KCTDs, suggesting a common mode of KCTD interaction with GABABreceptors. Defining the binding interface of GABABreceptor and KCTD reveals a potential regulatory site for modulating GABAB-receptor function in the brain.


2016 ◽  
Vol 33 (S1) ◽  
pp. S41-S41
Author(s):  
P. Falkai

Schizophrenia is a severe brain disorder characterised by positive, negative, affective and cognitive symptoms and can be viewed as a disorder of impaired neural plasticity. Aerobic exercise has a profound impact on the plasticity of the brain of both rodents and humans such as inducing the proliferation and differentiation of neural progenitor cells of the hippocampus in mice and rats. Aerobic exercise enhances LTP and leads to a better performance in hippocampus related memory tasks, eventually by increasing metabolic and synaptic plasticity related proteins in the hippocampus. In healthy humans, regular aerobic exercise increases hippocampal volume and seems to diminish processes of ageing like brain atrophy and cognitive decline.Disclosure of interestThe author has not supplied his declaration of competing interest.


1955 ◽  
Vol 9 (2) ◽  
pp. 121-134
Author(s):  
Naosaburo Yoshii ◽  
Yoshihiko Koyasu ◽  
Kin-ichi Okazalci ◽  
Yoshiharu Hasegawa

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bastiaan H. A. Urbanus ◽  
Saša Peter ◽  
Simon E. Fisher ◽  
Chris I. De Zeeuw

AbstractFOXP2 has been identified as a gene related to speech in humans, based on rare mutations that yield significant impairments in speech at the level of both motor performance and language comprehension. Disruptions of the murine orthologue Foxp2 in mouse pups have been shown to interfere with production of ultrasonic vocalizations (USVs). However, it remains unclear which structures are responsible for these deficits. Here, we show that conditional knockout mice with selective Foxp2 deletions targeting the cerebral cortex, striatum or cerebellum, three key sites of motor control with robust neural gene expression, do not recapture the profile of pup USV deficits observed in mice with global disruptions of this gene. Moreover, we observed that global Foxp2 knockout pups show substantive reductions in USV production as well as an overproduction of short broadband noise “clicks”, which was not present in the brain region-specific knockouts. These data indicate that deficits of Foxp2 expression in the cortex, striatum or cerebellum cannot solely explain the disrupted vocalization behaviours in global Foxp2 knockouts. Our findings raise the possibility that the impact of Foxp2 disruption on USV is mediated at least in part by effects of this gene on the anatomical prerequisites for vocalizing.


2015 ◽  
Vol 126 (1) ◽  
pp. e2-e3 ◽  
Author(s):  
F. Miraglia ◽  
F. Vecchio ◽  
G. Lacidogna ◽  
F. Ferreri ◽  
P.M. Rossini

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