Effects of brain extracts on activity of the trigeminal motor and hypoglossal nuclei

1961 ◽  
Vol 201 (2) ◽  
pp. 341-346
Author(s):  
Yojiro Kawamura ◽  
Masaya Funakoshi ◽  
Mitsuru Takata
Keyword(s):  
Brain Tissue ◽  
Ethanol Extract ◽  
Tris Buffer ◽  
Brain Extract ◽  
Cortical Tissue ◽  
Saline Extract ◽  
Tissue Extracts ◽  
Lower Jaw ◽  
Brain Extracts ◽  
The Brain

Alterations in trigeminal motor and hypoglossal nuclei discharges were noted following microinjections of ethanol and saline brain tissue extracts, ACh and γ-aminobutyric acid (GABA). Background activities of these nuclei were not affected by microinjection of 0.9% saline solution or tris buffer [tris (hydroxymethyl) amino methane] of pH 7.2. Solutions of pH 8.5 (tris buffer) or pH 5.8 (glycine buffer) gradually inhibited these discharges. Spontaneous discharges of the trigeminal motor nuclei were accelerated by the saline extract of the brain tissue and ACh, and they were inhibited by the ethanol extract of the brain tissue and GABA. Discharge of this nucleus accelerated by lower jaw depression was also inhibited by the ethanol brain extract and GABA. Background activity of the hypoglossal nuclei was mildly accelerated by the saline brain extracts and ACh, greatly accelerated by the ethanol brain extracts, and strongly inhibited by GABA. The saline extract of the brain tissue extracted from brain stem had a stronger activator than that extracted from cortical tissue.

An immunological study on the effect of brain extract on the developing nervous tissue in the chick embryo

Development ◽  
1964 ◽  
Vol 12 (1) ◽  
pp. 77-88
Author(s):  
D. J. McCallion ◽  
J. Langman
Keyword(s):  
Nervous Tissue ◽  
Brain Extract ◽  
Immunological Study ◽  
Chick Brain ◽  
Adult Chicken ◽  
Saline Extract ◽  
Chicken Brain ◽  
Tissue Extracts ◽  
Organ Systems ◽  
The Brain

In recent experiments 24–32 hr. chick embryos were treated with saline extract of adult chicken brain, which was injected into the yolk, into the sub-blastodermal space, or deposited over the blastoderm. After an additional 60-hr, incubation period, 30 to 40 per cent of the surviving embryos showed defects of the brain, spinal cord and eye, such as anencephalus, microcephalus, abnormal shape of the brain vesicles, rachischisis, anophthalmia and microphthalmia (Lenicque, 1959; Clarke & McCallion, 1959; Braverman, 1961). In addition, a number of embryos showed abnormal proliferation in the walls of the brain vesicles. When other tissue extracts were examined it was found that the abovementioned abnormalities could be produced only by saline extracts of chick brain and nervous retina, and not by extracts prepared from liver, spleen and skeletal muscle. The latter extracts do sometimes affect brain development, but then always in association with defects in other organ systems.

scholarly journals Synapsin I: an actin-bundling protein under phosphorylation control.

1987 ◽  
Vol 105 (3) ◽  
pp. 1355-1363 ◽  
Author(s):  
T C Petrucci ◽  
J S Morrow
Keyword(s):  
Actin Filaments ◽  
Binding Activity ◽  
Brain Extract ◽  
Synapsin I ◽  
Peptide Fragments ◽  
Molecular Weights ◽  
Brain Extracts ◽  
The Brain ◽  
Precise Role

Synapsin I is a neuronal phosphoprotein comprised of two closely related polypeptides with apparent molecular weights of 78,000 and 76,000. It is found in association with the small vesicles clustered at the presynaptic junction. Its precise role is unknown, although it probably participates in vesicle clustering and/or release. Synapsin I is known to associate with vesicle membranes, microtubules, and neurofilaments. We have examined the interaction of purified phosphorylated and unphosphorylated bovine and human synapsin I with tubulin and actin filaments, using cosedimentation, viscometric, electrophoretic, and morphologic assays. As purified from brain homogenates, synapsin I decreases the steady-state viscosity of solutions containing F-actin, enhances the sedimentation of actin, and bundles actin filaments. Phosphorylation by cAMP-dependent kinase has minimal effect on this interaction, while phosphorylation by brain extracts or by purified calcium- and calmodulin-dependent kinase II reduces its actin-bundling and -binding activity. Synapsin's microtubule-binding activity, conversely, is stimulated after phosphorylation by the brain extract. Two complementary peptide fragments of synapsin generated by 2-nitro-5-thiocyanobenzoic cleavage and which map to opposite ends of the molecule participate in the bundling process, either by binding directly to actin or by binding to other synapsin I molecules. 2-Nitro-5-thiocyanobenzoic peptides arising from the central portion of the molecule demonstrate neither activity. In vivo, synapsin I may link small synaptic vesicles to the actin-based cortical cytoskeleton, and coordinate their availability for release in a Ca++-dependent fashion.

Simultaneous Automated Estimation of Noradrenaline and Dopamine in Brain Tissue

1974 ◽  
Vol 20 (1) ◽  
pp. 81-83 ◽  
Author(s):  
P Waldmeier ◽  
P De Herdt ◽  
L Maitre
Keyword(s):  
Brain Tissue ◽  
Slight Modification ◽  
Brain Extract ◽  
Automated Method ◽  
Brain Extracts ◽  
Related Compounds

Abstract A method is described for the simultaneous automated fluorometric estimation of noradrenaline and dopamine in brain extracts. It is based on a slight modification of the automated method for dopamine published recently. Interference of noradrenaline in the estimation of dopamine, and vice versa, is low (0.8 and 1.4%, respectively). Interferences of other catechols and related compounds have also been studied. Samples can be processed at a rate of 30 per hour, and the limit of sensitivity for both amines is about 2 ng/ml of brain extract.

UPTAKE OF INTRAVENOUSLY ADMINISTERED PROGESTERONE, PREGNANEDIONE AND PREGNANOLONE BY THE RAT BRAIN

1968 ◽  
Vol 57 (3) ◽  
pp. 395-404 ◽  
Author(s):  
K. H. Raisinghani ◽  
R. I. Dorfman ◽  
E. Forchielli ◽  
L. Gyermek ◽  
G. Genther
Keyword(s):  
Liquid Chromatography ◽  
Thin Layer ◽  
Rat Brain ◽  
Brain Tissue ◽  
Gas Liquid Chromatography ◽  
Radioactive Tracers ◽  
Tissue Extracts ◽  
Layer Chromatography ◽  
The Brain ◽  
Entire Procedure

ABSTRACT A method has been developed for the detection, isolation and quantitation of progesterone, pregnanolone and pregnanedione in brain tissue of rats receiving pharmacological hypnotic doses of these three substances. Prior to extraction radioactive tracers were added to brain tissue obtained from animals receiving these agents and the brain tissue extracts were purified by paper and thin layer chromatography. The material administered as well as some of the major metabolites were quantitated by gas liquid chromatography, and corrections for losses throughout the entire procedure and up to injection into GLC were based on recovery of added radioactive markers. The possible significance of the conversion of progesterone into hypnotically more potent metabolites is discussed.

scholarly journals ACUTE DISSEMINATED ENCEPHALOMYELITIS FOLLOWING IMMUNIZATION WITH HOMOLOGOUS BRAIN EXTRACTS

1950 ◽  
Vol 92 (2) ◽  
pp. 133-152 ◽  
Author(s):  
Lewis Thomas ◽  
Philip Y. Paterson ◽  
Betty Smithwick
Keyword(s):  
Brain Tissue ◽  
Complement Fixation ◽  
Mammalian Species ◽  
Acute Disseminated Encephalomyelitis ◽  
Adult Brain ◽  
Unsaponifiable Fraction ◽  
Whole Brain ◽  
Brain Lipids ◽  
Brain Extracts ◽  
The Brain

1. A severe demyelinating condition characterized by ataxia and paralysis, in some instances leading to death, was produced in thirty-five of a total of fifty-five dogs following immunization with homologous brain tissue combined with Freund's adjuvants. In more than 30 per cent of instances paralysis did not occur until immunization was continued for 6 or more months. Only eight dogs became paralyzed after a single injection of antigen. The condition appeared between 6 and 15 days after the last injection in all animals, irrespective of the total number of injections or the duration of immunization. 2. An antibody which reacted in complement fixation tests with aqueous and alcoholic extracts of homologous brain tissue was demonstrable in the majority of immunized dogs, whether or not the animals became paralyzed. It appeared during or after the 3rd week of immunization, and its occurrence or titer could not be correlated with the incidence of the encephalomyelitis. In general, there were fewer dogs with demonstrable antibody in the paralyzed group than in the non-paralyzed group. 3. A flocculation reaction with alcohol extracts of homologous brain was demonstrated in the serum of immunized dogs. The antigen and antibody involved were apparently identical with those responsible for the complement fixation reactions. 4. The brain tissue component which reacted as antigen in the complement fixation test was present in adult brain from several mammalian species, and peripheral nerve. It was not present in the brain of newborn dogs nor in other unrelated organs. It was demonstrable in brain tissue which had been allowed to autolyze, or treated with 10 per cent formalin. It was not impaired by boiling, or by acid hydrolysis, and was contained in the unsaponifiable fraction of brain lipids. It was separable from cholesterol by digitonin precipitation of the latter. 5. Immunization of dogs with the unsaponifiable fraction of homologous brain, in adjuvants, caused the appearance of antibrain antibody similar to that in animals injected with whole brain. Encephalomyelitis was not observed during a 2 month period of immunization with this fraction. 6. In guinea pigs, an injection of the unsaponifiable fraction of brain, in adjuvants, was followed by fatal meningoencephalitis, but the identity of the state with that caused by whole brain antigens was not established.

scholarly journals Exogenous Aβ seeds induce Aβ depositions in the blood vessels rather than the brain parenchyma, independently of Aβ strain-specific information

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Tsuyoshi Hamaguchi ◽  
Jee Hee Kim ◽  
Akane Hasegawa ◽  
Ritsuko Goto ◽  
Kenji Sakai ◽  
...  
Keyword(s):  
Human Brain ◽  
Blood Vessels ◽  
Brain Homogenate ◽  
Brain Parenchyma ◽  
Brain Extract ◽  
Amyloid Angiopathy ◽  
Specific Information ◽  
Brain Extracts ◽  
Iatrogenic Transmission ◽  
The Brain

AbstractLittle is known about the effects of parenchymal or vascular amyloid β peptide (Aβ) deposition in the brain. We hypothesized that Aβ strain-specific information defines whether Aβ deposits on the brain parenchyma or blood vessels. We investigated 12 autopsied patients with different severities of Aβ plaques and cerebral amyloid angiopathy (CAA), and performed a seeding study using an Alzheimer’s disease (AD) mouse model in which brain homogenates derived from the autopsied patients were injected intracerebrally. Based on the predominant pathological features, we classified the autopsied patients into four groups: AD, CAA, AD + CAA, and less Aβ. One year after the injection, the pathological and biochemical features of Aβ in the autopsied human brains were not preserved in the human brain extract-injected mice. The CAA counts in the mice injected with all four types of human brain extracts were significantly higher than those in mice injected with PBS. Interestingly, parenchymal and vascular Aβ depositions were observed in the mice that were injected with the human brain homogenate from the less Aβ group. The Aβ and CAA seeding activities, which had significant positive correlations with the Aβ oligomer ratio in the human brain extracts, were significantly higher in the human brain homogenate from the less Aβ group than in the other three groups. These results indicate that exogenous Aβ seeds from different Aβ pathologies induced Aβ deposition in the blood vessels rather than the brain parenchyma without being influenced by Aβ strain-specific information, which might be why CAA is a predominant feature of Aβ pathology in iatrogenic transmission cases. Furthermore, our results suggest that iatrogenic transmission of Aβ pathology might occur due to contamination of brain tissues from patients with little Aβ pathology, and the development of inactivation methods for Aβ seeding activity to prevent iatrogenic transmission is urgently required.

Liquid Chromatography Analysis of Clozapine in Rat Brain Tissue, Using its Molecularly Imprinted Polymer after Administration of Toxic Dose of Drug and Lipid Emulsion Therapy

2019 ◽  
Vol 15 (3) ◽  
pp. 251-257
Author(s):  
Bahareh Sadat Yousefsani ◽  
Seyed Ahmad Mohajeri ◽  
Mohammad Moshiri ◽  
Hossein Hosseinzadeh
Keyword(s):  
Rat Brain ◽  
Brain Tissue ◽  
Molecularly Imprinted Polymer ◽  
Lipid Emulsion ◽  
Limit Of Detection ◽  
Imprinted Polymer ◽  
Toxic Dose ◽  
Molecularly Imprinted ◽  
The Brain ◽  
Rat Brain Tissue

Background:Molecularly imprinted polymers (MIPs) are synthetic polymers that have a selective site for a given analyte, or a group of structurally related compounds, that make them ideal polymers to be used in separation processes.Objective:An optimized molecularly imprinted polymer was selected and applied for selective extraction and analysis of clozapine in rat brain tissue.Methods:A molecularly imprinted solid-phase extraction (MISPE) method was developed for preconcentration and cleanup of clozapine in rat brain samples before HPLC-UV analysis. The extraction and analytical process was calibrated in the range of 0.025-100 ppm. Clozapine recovery in this MISPE process was calculated between 99.40 and 102.96%. The limit of detection (LOD) and the limit of quantification (LOQ) of the assay were 0.003 and 0.025 ppm, respectively. Intra-day precision values for clozapine concentrations of 0.125 and 0.025 ppm were 5.30 and 3.55%, whereas inter-day precision values of these concentrations were 9.23 and 6.15%, respectively. In this study, the effect of lipid emulsion infusion in reducing the brain concentration of drug was also evaluated.Results:The data indicated that calibrated method was successfully applied for the analysis of clozapine in the real rat brain samples after administration of a toxic dose to animal. Finally, the efficacy of lipid emulsion therapy in reducing the brain tissue concentration of clozapine after toxic administration of drug was determined.Conclusion:The proposed MISPE method could be applied in the extraction and preconcentration before HPLC-UV analysis of clozapine in rat brain tissue.

scholarly journals Safety profile of the transcription factor EB (TFEB)-based gene therapy through intracranial injection in mice

2020 ◽  
Vol 11 (1) ◽  
pp. 241-250
Author(s):  
Zhenyu Li ◽  
Guangqian Ding ◽  
Yudi Wang ◽  
Zelong Zheng ◽  
Jianping Lv
Keyword(s):  
Gene Therapy ◽  
Transcription Factor ◽  
Neurodegenerative Diseases ◽  
Brain Tissue ◽  
Inflammatory Responses ◽  
Tissue Samples ◽  
Protein Levels ◽  
Virus Serotype ◽  
Transcription Factor Eb ◽  
The Brain

AbstractTranscription factor EB (TFEB)-based gene therapy is a promising therapeutic strategy in treating neurodegenerative diseases by promoting autophagy/lysosome-mediated degradation and clearance of misfolded proteins that contribute to the pathogenesis of these diseases. However, recent findings have shown that TFEB has proinflammatory properties, raising the safety concerns about its clinical application. To investigate whether TFEB induces significant inflammatory responses in the brain, male C57BL/6 mice were injected with phosphate-buffered saline (PBS), adeno-associated virus serotype 8 (AAV8) vectors overexpressing mouse TFEB (pAAV8-CMV-mTFEB), or AAV8 vectors expressing green fluorescent proteins (GFPs) in the barrel cortex. The brain tissue samples were collected at 2 months after injection. Western blotting and immunofluorescence staining showed that mTFEB protein levels were significantly increased in the brain tissue samples of mice injected with mTFEB-overexpressing vectors compared with those injected with PBS or GFP-overexpressing vectors. pAAV8-CMV-mTFEB injection resulted in significant elevations in the mRNA and protein levels of lysosomal biogenesis indicators in the brain tissue samples. No significant changes were observed in the expressions of GFAP, Iba1, and proinflammation mediators in the pAAV8-CMV-mTFEB-injected brain compared with those in the control groups. Collectively, our results suggest that AAV8 successfully mediates mTFEB overexpression in the mouse brain without inducing apparent local inflammation, supporting the safety of TFEB-based gene therapy in treating neurodegenerative diseases.

scholarly journals High-fat diet-induced obesity and impairment of brain neurotransmitter pool

2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Obese Group ◽  
Control Group ◽  
High Fat ◽  
Brain Neurotransmitter ◽  
The Brain ◽  
Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

scholarly journals Effect of Xenon Treatment on Gene Expression in Brain Tissue after Traumatic Brain Injury in Rats

2021 ◽  
Vol 11 (7) ◽  
pp. 889
Author(s):  
Anton D. Filev ◽  
Denis N. Silachev ◽  
Ivan A. Ryzhkov ◽  
Konstantin N. Lapin ◽  
Anastasiya S. Babkina ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Target Genes ◽  
Neural Function ◽  
Stress Genes ◽  
Expression Of Genes ◽  
Delayed Recovery ◽  
The Brain ◽  
Lower Expression

The overactivation of inflammatory pathways and/or a deficiency of neuroplasticity may result in the delayed recovery of neural function in traumatic brain injury (TBI). A promising approach to protecting the brain tissue in TBI is xenon (Xe) treatment. However, xenon’s mechanisms of action remain poorly clarified. In this study, the early-onset expression of 91 target genes was investigated in the damaged and in the contralateral brain areas (sensorimotor cortex region) 6 and 24 h after injury in a TBI rat model. The expression of genes involved in inflammation, oxidation, antioxidation, neurogenesis and neuroplasticity, apoptosis, DNA repair, autophagy, and mitophagy was assessed. The animals inhaled a gas mixture containing xenon and oxygen (ϕXe = 70%; ϕO2 25–30% 60 min) 15–30 min after TBI. The data showed that, in the contralateral area, xenon treatment induced the expression of stress genes (Irf1, Hmox1, S100A8, and S100A9). In the damaged area, a trend towards lower expression of the inflammatory gene Irf1 was observed. Thus, our results suggest that xenon exerts a mild stressor effect in healthy brain tissue and has a tendency to decrease the inflammation following damage, which might contribute to reducing the damage and activating the early compensatory processes in the brain post-TBI.

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