scholarly journals The concentration of ascorbic acid in the cerebral cortex and internal organs of rats in chronic and acute hyperglycemia

1998 ◽  
Vol 44 (1) ◽  
pp. 40-42
Author(s):  
I. P. Grigoriev
Keyword(s):  
Ascorbic Acid ◽  
Brain Cortex ◽  
Mental Disease ◽  
Streptozotocin Diabetes ◽  
Causative Role ◽  
Internal Organs ◽  
Acute Hyperglycemia ◽  
Acute Hypoglycemia ◽  
The Brain

The author hypothesizes a probable causative role of alteration of ascorbic acid concentration in the brain in the development of mental disease in diabetics. In order to verify this hypothesis, ascorbic acid was measured in the brain cortex of rats 21 days after induction of streptozotocin diabetes or 1 h after intraperitoneal injection of glucose in a dose of 5 g/kg. Ascorbic acid level was increased both in diabetes (456+26 yg/g tissue versus 415+37 \vg/g in the control, p<0.01) and in acute hyperglycemia (475+54 \tg/g versus 406+65 \xg/g in the control, p<0.001). This confirmed that changed concentration of ascorbic acid in the brain can promote the development of a mental disease in diabetics. In the liver the concentration of ascorbic acid was decreased in streptozotocin diabetes (by 17%), p<0.001) and increased in acute hypoglycemia (by 24%, p<0.01). The findings permit us to hypothesize that hypoglycemia inhibits the production of ascorbic acid from the liver to the blood in rats and impedes the transport of ascorbic acid through the gut wall into the blood in humans.

Recent progress on the role of GABAergic neurotransmission in the pathogenesis of Alzheimer’s disease

2016 ◽  
Vol 27 (4) ◽  
pp. 449-455 ◽  
Author(s):  
Ghulam Abbas ◽  
Wajahat Mahmood ◽  
Nurul Kabir
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gaba Receptor ◽  
Amyloid Β ◽  
Receptor Subtypes ◽  
Causative Role ◽  
Gabaergic Neurotransmission ◽  
Promising Target ◽  
The Brain

AbstractDespite their possible causative role, targeting amyloidosis, tau phosphorylation, acetylcholine esterase, glutamate, oxidative stress and mitochondrial metabolism have not yet led to the development of drugs to cure Alzheimer’s disease (AD). Recent preclinical and clinical reports exhibit a surge in interest in the role of GABAergic neurotransmission in the pathogenesis of AD. The interaction among GABAergic signaling, amyloid-β and acetylcholine is shown to affect the homeostasis between excitation (glutamate) and inhibition (GABA) in the brain. As a consequence, over-excitation leads to neurodegeneration (excitotoxicity) and impairment in the higher level functions. Previously, the glutamate arm of this balance received the most attention. Recent literature suggests that over-excitation is primarily mediated by dysfunctional GABA signaling and can possibly be restored by rectifying anomalous metabolism observed in the GABAergic neurons during AD. Additionally, neurogenesis and synaptogenesis have also been linked with GABAergic signaling. This association may provide a basis for the needed repair mechanism. Furthermore, several preclinical interventional studies revealed that targeting various GABA receptor subtypes holds potential in overcoming the memory deficits associated with AD. In conclusion, the recent scientific literature suggests that GABAergic signaling presents itself as a promising target for anti-AD drug development.

The Pathology of Milkiness, Thickening, and Opacity of the Pia-arachnoid in the Insane

1895 ◽  
Vol 41 (175) ◽  
pp. 622-635
Author(s):  
W. F. Robertson
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Structural Changes ◽  
Brain Cortex ◽  
Mental Disease ◽  
Waste Products ◽  
The Central Nervous System ◽  
The Subject ◽  
The Brain

There is at the present time great need of more complete and definite knowledge as to the pathology of the very marked structural changes that so commonly affect the pia-arachnoid in the insane. The subject is one of much importance to all of us as medical psychologists, for not only is the condition in question one of the most conspicuous lesions associated with mental disease, but it implicates a structure of primary importance in the economy of the central nervous system. It is by way of vessels that course through this membrane that nutriment is conveyed to the brain cortex, and the waste products resulting from metabolism in the cerebral tissues are mainly conveyed away in the fluid that circulates in its lymph spaces. Therefore it is evident that these morbid changes may very seriously interfere with the functions both of nutrition and excretion in the brain.

scholarly journals Cerebral glycogen in humans following acute and recurrent hypoglycemia: Implications on a role in hypoglycemia unawareness

2016 ◽  
Vol 37 (8) ◽  
pp. 2883-2893 ◽  
Author(s):  
Gülin Öz ◽  
Mauro DiNuzzo ◽  
Anjali Kumar ◽  
Amir Moheet ◽  
Ameer Khowaja ◽  
...  
Keyword(s):  
Occipital Lobe ◽  
Biophysical Model ◽  
Resonance Spectroscopy ◽  
Hypoglycemic Episode ◽  
Hypoglycemia Unawareness ◽  
Brain Glycogen ◽  
Acute Hypoglycemia ◽  
The Brain ◽  
Recurrent Hypoglycemia

Supercompensated brain glycogen levels may contribute to the development of hypoglycemia-associated autonomic failure (HAAF) following recurrent hypoglycemia (RH) by providing energy for the brain during subsequent periods of hypoglycemia. To assess the role of glycogen supercompensation in the generation of HAAF, we estimated the level of brain glycogen following RH and acute hypoglycemia (AH). After undergoing 3 hyperinsulinemic, euglycemic and 3 hyperinsulinemic, hypoglycemic clamps (RH) on separate occasions at least 1 month apart, five healthy volunteers received [1-13C]glucose intravenously over 80+ h while maintaining euglycemia. 13C-glycogen levels in the occipital lobe were measured by 13C magnetic resonance spectroscopy at ∼8, 20, 32, 44, 56, 68 and 80 h at 4 T and glycogen levels estimated by fitting the data with a biophysical model that takes into account the tiered glycogen structure. Similarly, prior 13C-glycogen data obtained following a single hypoglycemic episode (AH) were fitted with the same model. Glycogen levels did not significantly increase after RH relative to after euglycemia, while they increased by ∼16% after AH relative to after euglycemia. These data suggest that glycogen supercompensation may be blunted with repeated hypoglycemic episodes. A causal relationship between glycogen supercompensation and generation of HAAF remains to be established.

Abstract 9180: Importance of Preventing Decreased Levels of Lysophosphatidylcholine—DHA in Brain and Plasma for Attenuating Brain Injury After Cardiac Arrest

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Mitsuaki Nishikimi ◽  
Muhammad Shoaib ◽  
Tomoaki Aoki ◽  
Rishabh Choudhary ◽  
Santiago J Miyara ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Brain Injury ◽  
Brain Damage ◽  
Cell Cultures ◽  
Brain Function ◽  
Causative Role ◽  
Metabolic Alterations ◽  
Neurological Outcomes ◽  
The Brain

Introduction: Lysophosphatidylcholine (LPC) was found to be decreased in plasma in the early phase of resuscitation after cardiac arrest (CA), including a species containing docosahexaenoic acid (LPC-DHA). Supplementing this deficiency of plasma LPC-DHA post-CA significantly attenuated brain dysfunction implicating a causative role of plasma decreased LPC-DHA for brain injury. Previous studies showed the importance of LPC-DHA as a carrier of DHA to maintain proper brain function. However, the role of LPC-DHA for brain function has not been fully understood. Objective: This study is aimed at determining the importance of maintaining proper brain LPC-DHA level via plasma supplementation to prevent brain damage after CA using human patients, animal model, and in-vitro cell studies. Methods and Results: We first evaluated associations between the plasma LPC-DHA levels and neurological outcomes using 45 post-CA patients. We then measured LPC-DHA levels and histological, biochemical, metabolic alterations in the plasma and brain after 10 min CA rat model and examined how these alterations were attenuated by supplementing LPC-DHA. Finally, we further investigated the beneficial effect of LPC-DHA using cell cultures. We found that the decreased plasma LPC-DHA was strongly associated with neurological outcomes and disappearance of difference between gray and white matter in the brain after CA in human patients. In rats, the decreased plasma LPC-DHA was associated with decreased level of brain LPC-DHA after CA, and supplementing plasma LPC-DHA normalized the brain levels of LPC-DHA and alleviated neuronal cell death, activation of astrocyte, and expression of various inflammatory and mitochondrial dysfunction genes. We also found normalized overall metabolic alterations from the untargeted metabolomics analysis. Furthermore, LPC treatment showed a similar protective effect for neurons and astrocytes in mixed primary brain cell cultures. Conclusion: The attenuation of biochemical and physiologic alterations, and the normalization of decreased brain LPC-DHA post-CA with LPC-DHA supplementation demonstrate plasma LPC-DHA is important for the maintenance of proper brain LPC-DHA levels, which is essential for preventing brain damage post-CA.

scholarly journals Complementary Role of Oxytocin and Vasopressin in Cardiovascular Regulation

2021 ◽  
Vol 22 (21) ◽  
pp. 11465
Author(s):  
Ewa Szczepanska-Sadowska ◽  
Agnieszka Wsol ◽  
Agnieszka Cudnoch-Jedrzejewska ◽  
Tymoteusz Żera
Keyword(s):  
Brain Cortex ◽  
Adrenal Glands ◽  
Cardiovascular Regulation ◽  
Peripheral Organs ◽  
Carotid Bodies ◽  
Complementary Role ◽  
Vasopressin Secretion ◽  
Volume Blood ◽  
The Brain

The neurons secreting oxytocin (OXY) and vasopressin (AVP) are located mainly in the supraoptic, paraventricular, and suprachiasmatic nucleus of the brain. Oxytocinergic and vasopressinergic projections reach several regions of the brain and the spinal cord. Both peptides are released from axons, soma, and dendrites and modulate the excitability of other neuroregulatory pathways. The synthesis and action of OXY and AVP in the peripheral organs (eye, heart, gastrointestinal system) is being investigated. The secretion of OXY and AVP is influenced by changes in body fluid osmolality, blood volume, blood pressure, hypoxia, and stress. Vasopressin interacts with three subtypes of receptors: V1aR, V1bR, and V2R whereas oxytocin activates its own OXTR and V1aR receptors. AVP and OXY receptors are present in several regions of the brain (cortex, hypothalamus, pons, medulla, and cerebellum) and in the peripheral organs (heart, lungs, carotid bodies, kidneys, adrenal glands, pancreas, gastrointestinal tract, ovaries, uterus, thymus). Hypertension, myocardial infarction, and coexisting factors, such as pain and stress, have a significant impact on the secretion of oxytocin and vasopressin and on the expression of their receptors. The inappropriate regulation of oxytocin and vasopressin secretion during ischemia, hypoxia/hypercapnia, inflammation, pain, and stress may play a significant role in the pathogenesis of cardiovascular diseases.

The Role of Mitochondria in the Genesis of Neuroaxonal Dystrophy in the Brains of Aging Mice

1975 ◽  
Vol 33 ◽  
pp. 372-373
Author(s):  
J.E. Johnson
Keyword(s):  
Electron Microscopy ◽  
Present Report ◽  
Light And Electron Microscopy ◽  
Dorsal Column ◽  
Neuroaxonal Dystrophy ◽  
Nucleus Gracilis ◽  
Dystrophic Axons ◽  
The Brain ◽  
Nucleus Cuneatus

Although neuroaxonal dystrophy (NAD) has been examined by light and electron microscopy for years, the nature of the components in the dystrophic axons is not well understood. The present report examines nucleus gracilis and cuneatus (the dorsal column nuclei) in the brain stem of aging mice.Mice (C57BL/6J) were sacrificed by aldehyde perfusion at ages ranging from 3 months to 23 months. Several brain areas and parts of other organs were processed for electron microscopy.At 3 months of age, very little evidence of NAD can be discerned by light microscopy. At the EM level, a few axons are found to contain dystrophic material. By 23 months of age, the entire nucleus gracilis is filled with dystrophic axons. Much less NAD is seen in nucleus cuneatus by comparison. The most recurrent pattern of NAD is an enlarged profile, in the center of which is a mass of reticulated material (reticulated portion; or RP).

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