scholarly journals Transcranial Focal Electrical Stimulation Modifies Biogenic Amines’ Alterations Induced by 6-Hydroxydopamine in Rat Brain

2021 ◽  
Vol 14 (8) ◽  
pp. 706
Author(s):  
Cesar Emmanuel Santana-Gómez ◽  
Daniel Pérez-Pérez ◽  
Daniel Fonseca-Barriendos ◽  
Oscar Arias-Carrión ◽  
Walter Besio ◽  
...  
Keyword(s):  
Biogenic Amines ◽  
Therapeutic Strategy ◽  
Nigrostriatal System ◽  
Brain Areas ◽  
Neuroprotective Effects ◽  
Non Invasive ◽  
Tissue Content ◽  
6 Hydroxydopamine ◽  
The Brain ◽  
Intrastriatal Injection

Transcranial focal stimulation (TFS) is a non-invasive neuromodulation strategy with neuroprotective effects. On the other hand, 6-hidroxidopamine (6-OHDA) induces neurodegeneration of the nigrostriatal system producing modifications in the dopaminergic, serotoninergic, and histaminergic systems. The present study was conducted to test whether repetitive application of TFS avoids the biogenic amines’ changes induced by the intrastriatal injection of 6-OHDA. Experiments were designed to determine the tissue content of dopamine, serotonin, and histamine in the brain of animals injected with 6-OHDA and then receiving daily TFS for 21 days. Tissue content of biogenic amines was evaluated in the cerebral cortex, hippocampus, amygdala, and striatum, ipsi- and contralateral to the side of 6-OHDA injection. Results obtained were compared to animals with 6-OHDA, TFS alone, and a Sham group. The present study revealed that TFS did not avoid the changes in the tissue content of dopamine in striatum. However, TFS was able to avoid several of the changes induced by 6-OHDA in the tissue content of dopamine, serotonin, and histamine in the different brain areas evaluated. Interestingly, TFS alone did not induce significant changes in the different brain areas evaluated. The present study showed that repetitive TFS avoids the biogenic amines’ changes induced by 6-OHDA. TFS can represent a new therapeutic strategy to avoid the neurotoxicity induced by 6-OHDA.

scholarly journals Shocking the brain to regain motor function : a non-invasive therapy for stroke patients

2018 ◽  
Vol 1 ◽  
pp. 20-22
Author(s):  
Michael Min Wah Leung
Keyword(s):  
Direct Current ◽  
Transcranial Direct Current Stimulation ◽  
Invasive Technique ◽  
Stroke Patients ◽  
Interhemispheric Inhibition ◽  
Brain Areas ◽  
Sensory Deficits ◽  
Direct Current Stimulation ◽  
Non Invasive ◽  
The Brain

Invasive treatments and its associated risks are important factors of concern when the conditions are affecting the nervous system. Transcranial direct current stimulation (tDCS) is a non-invasive technique that stimulates brain areas through the scalp and has excitatory or inhibitory neuromodulatory effects. In the context of stroke patients, recovery is often impaired from the increased inhibition of the damaged area from the unaffected hemisphere. Fujimoto et al. uses dual-hemisphere transcranial direct current stimulation to address this interhemispheric inhibition and demonstrates that stroke patients were able to periodically restore sensory deficits. 

scholarly journals Variance in cortical depth across the brain surface

2020 ◽  
Author(s):  
Nick J. Davis
Keyword(s):  
Grey Matter ◽  
Brain Area ◽  
Cortical Surface ◽  
Brain Areas ◽  
Brain Images ◽  
Non Invasive ◽  
Brain Surface ◽  
Key Factor ◽  
Anatomical Mri ◽  
The Brain

AbstractThe distance between the surface of the scalp and the surface of the grey matter of the brain is a key factor in determining the effective dose of non-invasive brain stimulation for an individual person. The highly folded nature of the cortical surface means that the depth of a particular brain area is likely to vary between individuals. The question addressed here is: what is the variability of this measure of cortical depth? 94 anatomical MRI images were taken from the OASIS database. For each image, the minimum distance from each point in the grey matter to the scalp surface was determined. Transforming these estimates into standard space meant that the coefficient of variation could be determined across the sample. The results indicated that depth variability is high across the cortical surface, even when taking sulcal depth into account. This was true even for the primary visual and motor areas, which are often used in setting TMS dosage. The correlation of the depth of these areas and the depth of other brain areas was low. The results suggest that dose-setting of TMS based on visual or evoked potentials may offer poor reliability, and that individual brain images should be used when targeting non-primary brain areas.

scholarly journals Parkinson’s Disease and Autophagy

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Ana María Sánchez-Pérez ◽  
Berta Claramonte-Clausell ◽  
Juan Vicente Sánchez-Andrés ◽  
María Trinidad Herrero
Keyword(s):  
Cell Death ◽  
Animal Models ◽  
Neurodegenerative Disease ◽  
Causal Relationship ◽  
Neurodegenerative Disorders ◽  
Therapeutic Strategy ◽  
Neuroprotective Effects ◽  
Autophagy Induction ◽  
Effective Therapeutic Strategy ◽  
The Brain

It is generally accepted that a correlation between neurodegenerative disease and protein aggregation in the brain exists; however, a causal relationship has not been elucidated. In neurons, failure of autophagy may result in the accumulation of aggregate-prone proteins and subsequent neurodegeneration. Thus, pharmacological induction of autophagy to enhance the clearance of intracytoplasmic aggregate-prone proteins has been considered as a therapeutic strategy to ameliorate pathology in cell and animal models of neurodegenerative disorders. However, autophagy has also been found to be a factor in the onset of these diseases, which raises the question of whether autophagy induction is an effective therapeutic strategy, or, on the contrary, can result in cell death. In this paper, we will first describe the autophagic machinery, and we will consider the literature to discuss the neuroprotective effects of autophagy.

Effects of chlordiazepoxide administration on biogenic amines in cat brain

1983 ◽  
Vol 61 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Luc Vachon ◽  
Andree G. Roberge
Keyword(s):  
Central Nervous System ◽  
Biogenic Amines ◽  
Low Doses ◽  
Brain Areas ◽  
Cat Brain ◽  
Hydroxyindoleacetic Acid ◽  
The Central Nervous System ◽  
High Doses ◽  
The Brain ◽  
Chlordiazepoxide Hydrochloride

Cats underwent treatment with chlordiazepoxide hydrochloride (0.4, 10.0, and 20.0 mg/kg per os), for 7 consecutive days, and were killed 18 h after the last administration. The endogenous levels of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), noradrenaline (NA), and dopamine (DA) were assayed in 12 brain areas. Few effects on 5-HT, 5-HIAA, and NA content and on the 5-HT:5-HIAA ratio were observed with a 0.4 mg/kg treatment. These changes were localized in the piriform lobe (amygdala), hippocampus, mesencephalon, and mesencephalon raphe nuclei. Moreover, the DA concentration was not affected. The changes produced by 10.0 and 20.0 mg/kg chlordiazepoxide treatments were extended to many more structures, including the limbic system, brainstem, diencephalon, and neostriatum with respect to 5-HT, 5-HIAA, and NA content and also to DA levels. The changes observed after the three doses generally included an increased 5-HT content, a decreased 5-HIAA level, a high 5-HT:5-HIAA ratio, and increased NA and DA concentrations. However, in some structures, a decreased NA content and an increased 5-HIAA level were found. The present results suggest that administration of chlordiazepoxide for 7 consecutive days in cats produces regional changes in the content of endogenous biogenic amines in the central nervous system (CNS) at low doses; much more extended effects are produced at high doses. These findings are in agreement with a reducing effect of benzodiazepines on the turnover and release of biogenic amines in the CNS, but also suggest that certain discrete areas are more involved in these changes, thus dissociating them from the rest of the brain.

scholarly journals Probiotic Supplementation Facilitates Recovery of 6-OHDA-Induced Motor Deficit via Improving Mitochondrial Function and Energy Metabolism

2021 ◽  
Vol 13 ◽  
Author(s):  
Bira Arumndari Nurrahma ◽  
Shu-Ping Tsao ◽  
Chieh-Hsi Wu ◽  
Tu-Hsueh Yeh ◽  
Pei-Shan Hsieh ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Mitochondrial Function ◽  
Motor Deficit ◽  
Potential Candidate ◽  
Neuroprotective Effects ◽  
Motor Functions ◽  
Overwhelming Evidence ◽  
6 Hydroxydopamine ◽  
Aging People ◽  
The Brain

Parkinson’s disease (PD) is a neurodegenerative disease associated with progressive impairment of motor and non-motor functions in aging people. Overwhelming evidence indicate that mitochondrial dysfunction is a central factor in PD pathophysiology, which impairs energy metabolism. While, several other studies have shown probiotic supplementations to improve host energy metabolism, alleviate the disease progression, prevent gut microbiota dysbiosis and alter commensal bacterial metabolites. But, whether probiotic and/or prebiotic supplementation can affect energy metabolism and cause the impediment of PD progression remains poorly characterized. Therefore, we investigated 8-weeks supplementation effects of probiotic [Lactobacillus salivarius subsp. salicinius AP-32 (AP-32)], residual medium (RM) obtained from the AP-32 culture medium, and combination of AP-32 and RM (A-RM) on unilateral 6-hydroxydopamine (6-OHDA)-induced PD rats. We found that AP-32, RM and A-RM supplementation induced neuroprotective effects on dopaminergic neurons along with improved motor functions in PD rats. These effects were accompanied by significant increases in mitochondrial activities in the brain and muscle, antioxidative enzymes level in serum, and altered SCFAs profile in fecal samples. Importantly, the AP-32 supplement restored muscle mass along with improved motor function in PD rats, and produced the best results among the supplements. Our results demonstrate that probiotic AP-32 and A-RM supplementations can recover energy metabolism via increasing SCFAs producing and mitochondria function. This restoring of mitochondrial function in the brain and muscles with improved energy metabolism might additionally be potentiated by ROS suppression by the elevated generation of antioxidants, and which finally leads to facilitated recovery of 6-OHDA-induced motor deficit. Taken together, this work demonstrates that probiotic AP-32 supplementation could be a potential candidate for alternate treatment strategy to avert PD progression.

scholarly journals Alterations in aminergic system of rat brain by the opioid analgesic tramadol in the absence of pain-induction

2017 ◽  
Vol 6 (12) ◽  
pp. 2774 ◽  
Author(s):  
Sahitya C. Panadanabiona
Keyword(s):  
Biogenic Amines ◽  
Severe Pain ◽  
Wistar Rats ◽  
Opioid Analgesic ◽  
Brain Areas ◽  
Male Adult ◽  
Tissue Responses ◽  
Hydroxyindoleacetic Acid ◽  
The Brain ◽  
Differential Tissue

Background: Tramadol is an opioid analgesic used for treating moderate to severe pain. No research is available on pharmacology of tramadol without induction of pain. This study examines the effect of administration of tramadol on the levels of biogenic amines and their metabolites in the brain areas of male adult Wistar rats, without inducing pain.Methods: Tramadol was injected subcutaneously at 0, 24, and 48 hours, and changes in the levels of epinephrine (EP), norepinephrine (NE), dopamine (DA) and serotonin (5-HT), 5-hydroxyindoleacetic acid (HIAA) and homovanillic acid (HVA) were examined in cerebral cortex, cerebellum, pons-medulla, hippocampus and thalamus. The changes were recorded in the select brain areas at 3, 6, 12, 24 hours after the first injection, as well as at 24 hours after the second and third injections, respectively.Results: Administration of tramadol at 0 hours elevated the levels of DA, 5-HT and HVA in all brain areas. Changes in levels of EP, NE, and HIAA varied across the four brain areas surveyed. All parameters showed maximal changes at 3 or 6 hours following the first administration at 0 hours. For the second and third doses of tramadol at 24 and 48 hours respectively, the parameters showed variations at 48 and 72 hours that generally fluctuated around the control.Conclusions: The results indicate differential tissue responses to administered tramadol in different areas of the brain. The results suggest that the alterations in biogenic amines for the administration of tramadol are similar under both pain and no-pain conditions.

scholarly journals PLGA-Based Nanoparticles for Neuroprotective Drug Delivery in Neurodegenerative Diseases

Pharmaceutics ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1042
Author(s):  
Anthony Cunha ◽  
Alexandra Gaubert ◽  
Laurent Latxague ◽  
Benjamin Dehay
Keyword(s):  
Drug Delivery ◽  
Neurodegenerative Diseases ◽  
Therapeutic Strategy ◽  
Enzymatic Digestion ◽  
Drug Solubility ◽  
Crucial Point ◽  
Disease Treatment ◽  
Non Invasive ◽  
Disorder Treatment ◽  
The Brain

Treatment of neurodegenerative diseases has become one of the most challenging topics of the last decades due to their prevalence and increasing societal cost. The crucial point of the non-invasive therapeutic strategy for neurological disorder treatment relies on the drugs’ passage through the blood-brain barrier (BBB). Indeed, this biological barrier is involved in cerebral vascular homeostasis by its tight junctions, for example. One way to overcome this limit and deliver neuroprotective substances in the brain relies on nanotechnology-based approaches. Poly(lactic-co-glycolic acid) nanoparticles (PLGA NPs) are biocompatible, non-toxic, and provide many benefits, including improved drug solubility, protection against enzymatic digestion, increased targeting efficiency, and enhanced cellular internalization. This review will present an overview of the latest findings and advances in the PLGA NP-based approach for neuroprotective drug delivery in the case of neurodegenerative disease treatment (i.e., Alzheimer’s, Parkinson’s, Huntington’s diseases, Amyotrophic Lateral, and Multiple Sclerosis).

NON-INVASIVE BCI METHOD: EEG - ELECTROENCEPHALOGRAPHY

2019 ◽  
pp. 139-145
Author(s):  
Selma Büyükgöze
Keyword(s):  
Brain Computer Interface ◽  
Computer Interface ◽  
Electrode Placement ◽  
Eeg Signals ◽  
Non Invasive ◽  
Brain Signals ◽  
Brain States ◽  
The Brain

Brain Computer Interface consists of hardware and software that convert brain signals into action. It changes the nerves, muscles, and movements they produce with electro-physiological signs. The BCI cannot read the brain and decipher the thought in general. The BCI can only identify and classify specific patterns of activity in ongoing brain signals associated with specific tasks or events. EEG is the most commonly used non-invasive BCI method as it can be obtained easily compared to other methods. In this study; It will be given how EEG signals are obtained from the scalp, with which waves these frequencies are named and in which brain states these waves occur. 10-20 electrode placement plan for EEG to be placed on the scalp will be shown.

Aetiologies and anatomy of confabulation

2017 ◽  
Author(s):  
Armin Schnider
Keyword(s):  
Brain Damage ◽  
Limbic Encephalitis ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Brain Areas ◽  
Anatomical Basis ◽  
Korsakoff Syndrome ◽  
Hypoxic Brain ◽  
Degenerative Dementia ◽  
The Brain

What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.

scholarly journals The Potential Effects of Phytoestrogens: The Role in Neuroprotection

Molecules ◽  
2021 ◽  
Vol 26 (10) ◽  
pp. 2954
Author(s):  
Justyna Gorzkiewicz ◽  
Grzegorz Bartosz ◽  
Izabela Sadowska-Bartosz
Keyword(s):  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Estrogen Therapy ◽  
Neuroprotective Effects ◽  
Potential Health ◽  
Naturally Occurring ◽  
Epigenetic Effects ◽  
Estrogen Synthesis ◽  
Health Promoting ◽  
The Brain

Phytoestrogens are naturally occurring non-steroidal phenolic plant compounds. Their structure is similar to 17-β-estradiol, the main female sex hormone. This review offers a concise summary of the current literature on several potential health benefits of phytoestrogens, mainly their neuroprotective effect. Phytoestrogens lower the risk of menopausal symptoms and osteoporosis, as well as cardiovascular disease. They also reduce the risk of brain disease. The effects of phytoestrogens and their derivatives on cancer are mainly due to the inhibition of estrogen synthesis and metabolism, leading to antiangiogenic, antimetastatic, and epigenetic effects. The brain controls the secretion of estrogen (hypothalamus-pituitary-gonads axis). However, it has not been unequivocally established whether estrogen therapy has a neuroprotective effect on brain function. The neuroprotective effects of phytoestrogens seem to be related to both their antioxidant properties and interaction with the estrogen receptor. The possible effects of phytoestrogens on the thyroid cause some concern; nevertheless, generally, no serious side effects have been reported, and these compounds can be recommended as health-promoting food components or supplements.

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