The effect of subchronic supplementation with folic acid and l-arginine on homocysteine-induced seizures

2016 ◽  
Vol 94 (10) ◽  
pp. 1083-1089 ◽  
Author(s):  
A. Rasic-Markovic ◽  
D. Hrncic ◽  
D. Krstic ◽  
M. Colovic ◽  
E. Djuric ◽  
...  

The aim of the present study was to examine the effect of subchronic co-administration of folic acid (F) and l-arginine (A) on behavioural and electroencephalographic (EEG) characteristics of dl homocysteine thiolactone (H) induced seizures in adult rats. The activity of membrane ATPases in different brain regions were also investigated. Rats were treated with F, A, or vehicle for 15 days (regimen: F 5 mg/kg + A 500 mg/kg (F5A500); F 10 mg/kg + A 300 mg/kg (F10A300)). Seizures were elicited by convulsive dose of H (H, F5A500H, F10A300H) Subchronic supplementation with F and A did not affect seizure incidence, number of seizure episodes, and severity in F5A500H and F10A300H groups vs. H group. However, a tendency to increase latency and decrease the number of seizure episodes was noticed in the F10A300H group. EEG mean spectral power densities during ictal periods were significantly lower in F10A300H vs. H group. The activity of Na+/K+-ATPase and Mg2+-ATPase was significantly increased in almost all examined structures in rats treated with F and A. We can conclude that subchronic supplementation with folic acid and l-arginine has an antiepileptic effect in dl homocysteine thiolactone induced epilepsy.

2016 ◽  
pp. 4014-4017
Author(s):  
Michael A Persinger

                The value for the Lorentz contraction to produce a discrepancy for a hypothetical number that reflects a property (21.3π4) of sub-matter space was calculated. When applied to time the contraction would be ~35 min. The difference in mass-equivalent energy for an electron at c (the velocity of light in a vacuum) and the required v was ~2 ·10-20 J which has emerged as a significant quantity that may permeate from the force at Planck’s Length when applied across the wavelength of the neutral hydrogen line. Two separate types of photomultiplier instruments (digital and analogue) measuring with different sampling rates for background photon quantities over 50 randomly selected days demonstrated averaged conspicuous inflections of standardized spectral power densities around 35 min. This is the same basic interval where microvariations in the value of the gravitational constant (G) approached a limit at which white noise dominated.  The possibility is considered that this value for temporal inflections in photon power spectral densities may reflect the intrinsic nature of space-time contractions that relate gravity and photons.


2012 ◽  
Vol 8 (1) ◽  
pp. 59-64 ◽  
Author(s):  
Dragan Hrncic ◽  
Aleksandra Rasic- Markovic ◽  
Danijela Krstic ◽  
Djuro Macut ◽  
Veselinka Susic ◽  
...  

1985 ◽  
Vol 5 (3) ◽  
pp. 401-412 ◽  
Author(s):  
Vincent A. Murphy ◽  
Conrad E. Johanson

Acute hypertension induced by adrenergic agents opens up the blood–CSF barrier (choroid plexus) to nonelectrolyte and protein tracers. Sprague-Dawley adult rats anesthetized with ketamine were given an intravenous bolus of either epinephrine (10 μg/kg), phenylephrine (100 μg/kg), isoproterenol (10 μg/kg), or d,l-amphetamine (2 mg/kg). Tracers were injected simultaneously with test agents, and the animals killed 10 min later. Epinephrine raised MABP by 57 mm Hg, to a peak pressure of 160 mm Hg; and it increased the volume of distribution ( Vd) of urea, mannitol, and 125I-bovine serum albumin in CSF by 1.5-, 2.7-, and 30-fold, respectively. There was enhanced uptake by lateral and fourth ventricle choroid plexuses, cerebral cortex, cerebellum, medulla, and thalamus. Phenylephrine also elevated MABP to 160 mm Hg, but it increased permeation of tracers into CSF (and several brain regions) to a lesser extent than epinephrine, attributable to protective vasoconstriction associated with α-agonist activity. Ratio analysis of Vd data provides evidence that augmented permeation of nonelectrolyte tracers in acute hypertension occurs predominantly by diffusion rather than vesicular transport. It is postulated that elevated MABP distends the central cores of choroid plexus villi and cerebral capillaries, with resultant stretching and opening of tight junctions in both barrier systems; with less hindrance to diffusion, urea and mannitol are cleared at rates closer to free diffusion. Neither isoproterenol (decreased MABP by 40 mm Hg) nor amphetamine (did not alter MABP) significantly opened the choroid plexus or blood–brain barrier to tracers.


2020 ◽  
Vol 2 (4) ◽  
pp. 536-556
Author(s):  
Alejandra Mondino ◽  
Matías Cavelli ◽  
Joaquín González ◽  
Lucía Osorio ◽  
Santiago Castro-Zaballa ◽  
...  

The sleep-wake cycle is constituted by three behavioral states: wakefulness (W), non-REM (NREM) and REM sleep. These states are associated with drastic changes in cognitive capacities, mostly determined by the function of the thalamo-cortical system, whose activity can be examined by means of intra-cranial electroencephalogram (iEEG). With the purpose to study in depth the basal activity of the iEEG in adult rats, we analyzed the spectral power and coherence of the iEEG during W and sleep in the paleocortex (olfactory bulb), and in neocortical areas. We also analyzed the laterality of the signals, as well as the influence of the light and dark phases. We found that the iEEG power and coherence of the whole spectrum were largely affected by behavioral states and highly dependent on the cortical areas recorded. We also determined that there are night/day differences in power and coherence during sleep, but not in W. Finally, we observed that, during REM sleep, intra-hemispheric coherence differs between right and left hemispheres. We conclude that the iEEG dynamics are highly dependent on the cortical area and behavioral states. Moreover, there are light/dark phases disparities in the iEEG during sleep, and intra-hemispheric connectivity differs between both hemispheres during REM sleep.


2015 ◽  
Vol 8 (4) ◽  
pp. 730-741 ◽  
Author(s):  
L.J. Bour ◽  
M.A.J. Lourens ◽  
R. Verhagen ◽  
R.M.A. de Bie ◽  
P. van den Munckhof ◽  
...  

2013 ◽  
Vol 33 (8) ◽  
pp. 1307-1311 ◽  
Author(s):  
Yifan Zhang ◽  
Youzhi Kuang ◽  
Kui Xu ◽  
Donald Harris ◽  
Zhenghong Lee ◽  
...  

The brain is dependent on glucose as a primary energy substrate, but is capable of utilizing ketones such as β-hydroxybutyrate and acetoacetate, as occurs with fasting, starvation, or chronic feeding of a ketogenic diet. The relationship between changes in cerebral metabolic rates of glucose (CMRglc) and degree or duration of ketosis remains uncertain. To investigate if CMRglc decreases with chronic ketosis, 2-[18F]fluoro-2-deoxy-D-glucose in combination with positron emission tomography, was applied in anesthetized young adult rats fed 3 weeks of either standard or ketogenic diets. Cerebral metabolic rates of glucose (μmol/min per 100 g) was determined in the cerebral cortex and cerebellum using Gjedde-Patlak analysis. The average CMRglc significantly decreased in the cerebral cortex (23.0 ±4.9 versus 32.9 ±4.7) and cerebellum (29.3 ± 8.6 versus 41.2 ±6.4) with increased plasma ketone bodies in the ketotic rats compared with standard diet group. The reduction of CMRg|c in both brain regions correlates linearly by ∼9% for each 1 mmol/L increase of total plasma ketone bodies (0.3 to 6.3 mmol/L). Together with our meta-analysis, these data revealed that the degree and duration of ketosis has a major role in determining the corresponding change in CMRglc with ketosis.


2011 ◽  
Vol 105 (9) ◽  
pp. 1294-1302 ◽  
Author(s):  
Ta-Fu Chen ◽  
Ming-Jang Chiu ◽  
Chou-Tz Huang ◽  
Ming-Chi Tang ◽  
Sue-Jane Wang ◽  
...  

Accumulating evidence suggests that changes in dietary folate intake may modulate the risks of Alzheimer's disease (AD) through as yet unknown mechanisms. The aims of the present study were to investigate how dietary folate affects the brain folate distribution, levels of oxidised lipid and DNA damage in the absence/presence of β-amyloid(25–35)(Aβ) peptide challenge, a pathogenic hallmark of AD. Male Wistar rats were assigned to diets with folic acid at 0 (folate deprivation; FD), 8 (moderate folate; MF) and 8 mg folic acid/kg diet+0·003 % in drinking-water (folate supplementation; FS) for 4 weeks. A single injection of Aβ peptide (1 mg/ml) or the vehicle solution was intracerebroventricularly (icv) administrated to rats a week before killing. Brain folate, a marker of oxidative injury, and neuronal death were assayed. In the absence of an Aβ injection, FD rats showed reduced folate levels, and increased 2-thiobarbituric acid-reactive substances and a mitochondrial (mt)DNA 4834 bp large deletion (mtDNA4834deletion) in the hippocampus compared with the counterpart brains of control rats (P < 0·05). A single icv injection of Aβ peptide potentiated lipid peroxidation in the medulla of FD rats, which was ameliorated by feeding FD rats with the MF and FS diets (P < 0·05). Feeding the FS diet to Aβ-injected rats enriched brain folate levels and reduced mtDNA4834deletion in the hippocampal and medullary regions compared with corresponding tissues of Aβ+FD rats (P < 0·05). Aβ+FS rats had reduced rates of neuronal death in the frontal cortex compared with Aβ+FD rats (P < 0·05). Taken together, our data revealed that folate deprivation differentially depleted brain folate levels, and increased lipid peroxidation and mtDNA4834deletions, particularly, in the hippocampus. Upon Aβ challenge, the FS diet may protect various brain regions against lipid peroxidation, mitochondrial genotoxicity and neural death associated with folate deprivation.


2000 ◽  
Vol 20 (8) ◽  
pp. 1166-1173 ◽  
Author(s):  
WeiGang Gu ◽  
Thomas Brännström ◽  
Per Wester

Neurogenesis occurs throughout life in the dentate gyrus of hippocampus and subventricular zone, but this phenomenon has rarely been observed in other brain regions of adult mammals. The aim of the current study was to investigate the cell proliferation process in the ischemically challenged region-at-risk after focal cerebral ischemia in the adult rat brain. A reversible photothrombotic ring stroke model was used, which features sustained hypoperfusion followed by late spontaneous reperfusion and a remarkable morphologic tissue recovery in the anatomically well defined somatosensory cortical region-at-risk. Twelve-week-old male Wistar rats received repeated intraperitoneal injections of the cell proliferation specific marker 5-bromodeoxyuridine (BrdU) after stroke induction. Immunocytochemistry of coronal brain sections revealed that the majority of BrdU-positive cells were of glial, macrophage, and endothelial origin, whereas 3% to 6% of the BrdU-positive cells were double-labeled by BrdU and the neuron-specific marker Map-2 at 7 and 100 days after stroke onset in the region-at-risk. They were distributed randomly in cortical layers II-VI. Three-dimensional confocal analyses of BrdU and the neuronal-specific marker Neu N by double immunofluorescence confirmed their colocalization within the same cells at 72 hours and 30 days after stroke induction. This study suggests that, as a potential pathway for brain repair, new neurons can be generated in the cerebral cortex of adult rats after sublethal focal cerebral ischemia.


2010 ◽  
Vol 121 (4) ◽  
pp. e7-e8
Author(s):  
A. Rašić – Marković ◽  
D. Hrnčić ◽  
D. Djurić ◽  
O. Stanojlović

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