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At least 793 records · Page 44Linked to original sources
PubMed1981

[Effect of L-DOPA on brain serotonin metabolism related to tryptophan concentrations in plasma and brain of rats].

Changes in tryptophan (Trp) concentrations in the peripheral and brain tissues and their influences on brain serotonin (5-HT) metabolism were investigated after i.p. administrations of L-DOPA alone and in combination with Ro4-4602 in male Wistar rats. L-DOPA alone elicited marked increases of both plasma free and liver Trp levels, and a slight increase of brain Trp level. Concomitant application of L-DOPA and Ro4-4602 did not change peripheral Trp concentrations but did reduce brain Trp level. Brain 5-HT levels were reduced in proportion to the increase of dopamine (DA) level by L-DOPA alone and Ro4-4602 plus L-DOPA. A marked increase of 5-HIAA level was exhibited by L-DOPA alone, while Ro4-4602 plus L-DOPA increased 5-HIAA levels slightly despite a marked decrease in 5-HT levels. The decrease of 5-HT and increase of 5-HIAA levels were also observed after administration of L-DOPA to neonatal rats in which the brain tryptophan hydroxylase was considered to be saturated. These results suggest that changes in 5-HT metabolism after L-DOPA injections are not only caused by DA which displaces 5-HT from vesicular stores, but also by changes in Trp concentrations in the plasma and brain which alter 5-HT synthesis and turnover.

Animals↗
PubMed1978

Over-all accuracy of 99mTc-pertechnetate brain scanning for brain tumours--study of 471 patients.

A 3-year follow-up and re-evaluation of all scans on all patients referred for brain scanning in Iceland during 1 year was performed in order to assess the diagnostic reliability of radioisotope scanning for brain tumours. The study included 471 patients. Of these 25 had primary brain tumours and 7 brain metastases. Scans were positive and correctly interpreted in 68% of the patients with primary brain tumours and in 3 of the 7 patients with metastases. The over-all accuracy of brain scanning for brain tumours defined as the total number of correct positive scans and correct negative scans versus total number of scans examined was 96%, this figure being mainly influenced by the high number of true negative scans.

Angiography↗
PubMed1993

How to run a brain bank: potentials and pitfalls in the use of human post-mortem brain material in research.

Brain banks for neurological diseases serve as a link between the clinician, the neuropathologist and the basic scientist who require brain tissue samples from patients who have undergone a thorough clinical investigation and whose brains have been subjected to detailed neuropathological analysis. In order to provide research groups with post-mortem brain tissue from patients who show clinical signs of dementia such as Alzheimer's disease (AD), senile dementia of Alzheimer type (SDAT), vascular dementia including multi-infarct dementia (MID) and mixed dementia, a brain bank was established at Huddinge University Hospital at the end of 1988. The brain bank provides either rapidly or slowly frozen tissue samples, tissue samples fixed in formalin (short/long fixation time), cerebrospinal fluid (CSF), and blood samples. Average postmortem times are from 3-47 hours. The information available on the cases includes the clinical diagnosis, the premortem clinical investigation with behavioral observations, psychometric and neuropsychological test data, premortem medication, cause of death, agonal state, pH in brain and CSF, and the general anatomic and neuropathologic assessments leading to the final diagnosis.

Autopsy↗
PubMed1977

Modulation of brain tryptophan hydroxylase activity by brain tryptophan content.

Although hydroxylation of tryptophan (TP) is considered to be the rate-limiting step in serotonin synthesis, the mechanism whereby tryptophan hydroxylase (TPH) participates in the regulation of serotonin synthesis is still in question. Since the brain TP concentration is probably near the Km for tryptophan hydroxylase, changes in brain TP content could affect the rate of its hydroxylation. However, it has not been established whether in vivo the activity of TPH and TP in several brain nuclei and other regions of rat brain after treatments known to lower brain TP levels. Chlorimipramine, loading with neutral amino acids and a TP-deficient diet decreased the TP content of some, but not all, brain regions studied. Whenever TP decrease withe TP injections. Several brain nuclei accumulate TP at different rates after a TP load. These data suggest possible mechanisms for regulation of serotonin synthesis in the face of fluctuating plasma levels of TP.

Amino Acids↗
PubMed1998

Discordance between FDG uptake and technetium-99m-HMPAO brain perfusion in acute traumatic brain injury.

A 28-yr-old woman who sustained a mild traumatic brain injury had an 18F-fluorodeoxyglucose (FDG) PET brain study using coincidence imaging performed on a dual-head gamma camera (MCD version; ADAC, Milpitas, CA) followed 24 hr later by 99mTc-hexamethyl propyleneamine oxime SPECT brain perfusion imaging using a triple-head gamma camera (TRIONIX, Twinsburg, OH). The results of the SPECT brain perfusion study demonstrated decreased frontoparietal cortical brain perfusion, whereas 18F-FDG cerebral uptake was normal. Neuropsychological evaluation suggested frontal lobe involvement. This case demonstrates the possibility of discordance between brain perfusion and glucose uptake in acute mild traumatic brain injury.

Adult↗
PubMed2000

p-Chlorophenylalanine, an inhibitor of serotonin synthesis reduces blood-brain barrier permeability, cerebral blood flow, edema formation and cell injury following trauma to the rat brain.

The role of serotonin in trauma induced alterations in blood-brain barrier (BBB) permeability, cerebral blood flow (CBF), brain edema and cell changes were examined in a new model of cortical injury in the rat using a pharmacological approach. A longitudinal incision into the right parietal cerebral cortex (about 3 mm deep and 5 mm long) was associated with a profound increase in the BBB permeability to Evans blue and [131]I-sodium, brain water content, and a reduction in the CBF in both the ipsilateral and contralateral hemispheres 5 h after trauma. Nissl staining showed a profound nerve cell reaction in the parietal cerebral cortex of both hemispheres. The intensity of these pathological changes was most pronounced in the traumatised hemisphere. Pretreatment with p-CPA, a serotonin synthesis inhibitor, significantly attenuated breakdown of the BBB permeability, brain edema and the CBF disturbances. Damaged and distorted nerve cells were markedly less frequent in p-CPA treated rats. This effect of the drug was most pronounced in the contralateral hemisphere. The observations strongly suggest that serotonin is one of the important neurochemical mediators of BBB permeability disturbances and brain edema formation in the trauma induced brain damage.

Animals↗
PubMed1992

The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction.

The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.

Animals↗
PubMed2004

Stroke-prone rats exhibit prolonged behavioral deficits without increased brain injury: an indication of disrupted post-stroke brain recovery of function.

Stroke-prone rat strains exhibit an increased stroke risk and sensitivity, and reduced endogenous mechanisms of ischemic brain tolerance. This experiment provides a comparative, serial evaluation of neurological deficits and brain injury following middle cerebral artery occlusion/permanent focal stroke in this high-risk strain. Stroke-prone spontaneously hypertensive (SHR-SP), spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats were evaluated over 28 days using magnetic resonance imaging (MRI), histopathology, and neurobehavioral testing. T2- and diffusion weighted-MRI was performed after 1, 10 and 28 days to measure the degree of stroke-induced brain injury. Normotensive WKY rats receiving the same stroke and other SHR-SP rats receiving sham surgery were used for control comparisons. Functional deficits were scored after 1, 4, 11, 18 and 28 days. The degree of brain infarction/injury was practically identical in hypertensive and stroke-prone rats. WKY rats exhibited significantly smaller infarcts (P<0.05), with neurological function recovering quickly to normal by day 11 in this strain. Functional deficits persisted longer in hypertensive rats, with function recovering to normal by day 18 (P<0.05). Functional deficits in SHR-SP rats persisted the longest, and were observed even after 28 days (P<0.05). This increased and prolonged neurologic dysfunction exhibited by SHR-SP compared to SHR rats, while exhibiting practically identical degrees of brain injury/infarction, reflects the increased stroke risk and sensitivity of this strain and suggests a reduced SHR-SP brain plasticity following injury. Therefore, the stroke-prone rat provides an enhanced and prolonged functional deficit model that can be used to elucidate those mechanisms/novel targets critical to longitudinal neurobehavioral recovery post-stroke.

Animals↗
PubMed1994

Blood-brain barrier permeability and brain concentration of sodium, potassium, and chloride during focal ischemia.

Brain edema formation during the early stages of focal cerebral ischemia is associated with an increase in both sodium content and blood-brain barrier (BBB) sodium transport. The goals of this study were to determine whether chloride is the principal anion that accumulates in ischemic brain, how the rate of BBB transport of chloride compares with its rate of accumulation, and whether the stimulation seen in BBB sodium transport is also seen with other cations. Focal ischemia was produced by occlusion of the middle cerebral artery (MCAO) in anesthetized rats. Over the first 6 h after MCAO, the amount of brain water in the center of the ischemic cortex increased progressively at a rate of 0.15 +/- 0.02 (SE) g/g dry wt/h. This was accompanied by a net increase in brain sodium (48 +/- 12 mumol/g dry wt/h) and a loss of potassium (34 +/- 7 mumol/g dry wt/h). The net rate of chloride accumulation (16 +/- 1 mumol/g dry wt/h) approximated the net rate of increase of cations. Three hours after MCAO, the BBB permeability to three ions (22Na, 36Cl, and 86Rb) and two passive permeability tracers ([3H]alpha-aminoisobutyric acid ([3H]AIB) and [14C]urea) was determined. Permeability to either passive tracer was not increased, indicating that the BBB was intact. The rate of 36Cl influx was 3 times greater and the rate of 22Na influx 1.8 times greater than their respective net rates of accumulation in ischemic brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Longitudinal brain volume measurement in multiple sclerosis: rate of brain atrophy is independent of the disease subtype.

BACKGROUND: In multiple sclerosis (MS), brain atrophy depicted by magnetic resonance imaging reflects overall tissue loss, including axonal loss. OBJECTIVE: To determine the course of atrophy by studying the rate of development of brain atrophy in patients who have different subtypes of MS. METHODS: Eighty-three patients with MS (42 with relapsing-remitting, 21 with secondary progressive, and 20 with primary progressive) were studied longitudinally, with an interval of 2 to 4 years. Magnetic resonance imaging included T1- and T2-weighted images to obtain 2 brain volume measurements: (1) the parenchymal fraction as a marker of global brain atrophy and (2) the ventricular fraction as a marker of central atrophy. The annualized rate of global and central brain atrophy was compared between those with different subtypes of MS and related to clinical characteristics, including sex, age, disease duration, and disability. RESULTS: There was a significant decrease of the parenchymal fraction (-0.7% per year; SEM, 0.11% per year) and a significant increase of ventricular fraction (3.7% per year; SEM, 0.54% per year) in the total group. Significant tissue loss was also seen in all 3 subtypes of MS; the decrease in parenchymal fraction was not different between subtypes, whereas the increase in ventricular fraction tended to be larger in patients with secondary progressive MS compared with patients with primary progressive MS. Marginal associations were found between clinical determinants and the rate of brain atrophy. Annualized increase in the ventricular fraction was correlated with age (r = -0.26) and duration of symptoms (r = -0.22): younger patients (mainly patients with relapsing-remitting MS who have a limited disability) displayed a larger increase in ventricular fraction compared with older patients. CONCLUSIONS: The rate of development of brain atrophy is largely independent of the course of the disease and other clinical characteristics. The relentless loss of tissue occurring in MS is not restricted to later (progressive) phases of the disease, thereby stressing the need for early neuroprotective treatment in MS.

Adult↗
PubMed1991

Differential immunochemical markers reveal the normal distribution of brain macrophages and microglia in the developing rat brain.

Brain macrophages and microglia play important roles in central nervous system (CNS) development, especially during regressive events in which particular neuronal and glial constituents are eliminated. The purpose of this study is to provide a complete map of brain macrophage and microglia distribution in all regions of the neuraxis from birth to sexual maturity. We have utilized morphology and immunostaining with the specific antibodies OX-42 and ED1 to distinguish between brain macrophages and microglia. Brain macrophages are large, round cells, 10-15 microns in diameter, with few or no cytoplasmic processes; these cells are ED1- and OX-42-immunopositive. Microglia have small cell bodies with numerous, ramified cytoplasmic processes. These cells are OX-42-positive, and ED1-negative. We found a specific pattern of distribution of brain macrophages, targeting specific cortical and subcortical areas transiently, including developing fiber tracts. These cells disappeared completely by the third postnatal week. In contrast, OX-42-positive microglia exhibited a gradual increase in number and were distributed uniformly throughout gray matter and within white matter tracts. These cells remain in the adult CNS, constituting the resident microglia population. We suggest that these two distinct phagocytic cell populations perform unique functions in the developing brain, including remodeling of restricted CNS areas by brain macrophages that is part of a normal morphological process.

Animals↗
PubMed2003

The brain-specific protein MLC1 implicated in megalencephalic leukoencephalopathy with subcortical cysts is expressed in glial cells in the murine brain.

The human MLC1 gene (also known as KIAA0027 and WKL1) and its murine orthologue (Mlc1) encode a putative transmembrane protein expressed primarily in brain. Recessive mutations within human MLC1 cause megalencephalic leukoencephalopathy with subcortical cysts (MLC), whereas a missense mutation resulting in a methionine substitution within a transmembrane leucine string of MLC has been implicated in catatonic schizophrenia in a large pedigree. To gain insight into the function of the MLC protein and to elucidate the pathophysiology of these severe neurodegenerative disorders, information on the cellular and regional distribution of the murine Mlc1, as well as the developmental pattern of Mlc1 expression in brain, is required. Using in situ hybridization (ISH), Mlc1 mRNA was exclusively detected in glial cells of the adult murine brain, such as astrocytes, Bergmann glia, and ependymal cells. ISH, Northern blot analysis, and quantitative real-time polymerase chain reaction (PCR) demonstrated that Mlc1 mRNA is broadly distributed in the adult mouse brain, with highest concentrations of expression in the cerebellum and olfactory bulb. Furthermore, differential expression patterns during brain development were revealed. Overall brain Mlc1 mRNA concentrations exhibited a substantial increase in the perinatal period reaching adult concentrations at postnatal day 5. At the cellular level, highest Mlc1 expression was found during the pre- and perinatal period in multipotential neural precursor cells, especially in the subventricular zone of the lateral ventricle, whereas in adulthood highest Mlc1 mRNA concentrations were revealed in Bergmann glia cells. Because the temporal expression profile of Mlc1 indicates that, in contrast to developing and mature astrocytes, oligodendrocytes are devoid of Mlc1 expression, white matter tract abnormalities observed in these disorders may result from a primary astrocytic defect. Detailed information on Mlc1 expression in brain is likely to lead to a better understanding of Mlc1 involvement in the pathogenesis of both MLC and catatonic schizophrenia.

Age Factors↗
PubMed1986

The beta subunit of the guanine nucleotide regulatory proteins: identification of its location on two-dimensional gels of brain tissue and its regional and subcellular distribution in brain.

The beta subunit of the guanine nucleotide regulatory proteins (also termed G proteins) has been examined in both rat and human brain. Proteins contained within samples of fresh rat and human brain tissue were separated by two-dimensional gel electrophoresis and either stained with silver or reacted with various antisera raised against the G proteins. In both rat and human brain, a single protein of molecular weight 36,000 daltons and pI 5.8 reacted the antisera. This protein also comigrated with one of the proteins present in a purified preparation of bovine brain G proteins. Based upon molecular weight, pI, and reaction with specific antisera, it was concluded that this protein is the beta subunit of the G proteins in brain. Using this information, the regional and subcellular distribution of the G protein beta subunit was studied in rat brain. Of 25 distinct neuroanatomical areas examined, cortical regions were generally found to contain the largest amount of this protein. The subcellular distribution of the G protein beta subunit revealed that large amounts are present in the synaptic membrane, crude synaptic vesicles, and microsomes. These studies serve to identify another protein visible on silver-stained two-dimensional electrophoretograms of rat and human brain. The regional and subcellular distribution of the G protein beta subunit correlate well with the proposed physiological function of this protein.

Animals↗
PubMed2005

The correlation of midline shifts of human brain with large brain haematoma using a finite element approach.

OBJECTIVES: We report on using a computational (finite element) model to simulate a human skull-brain structure to quantify the distortion of brain. METHODS: We simulated various effects of brain haematoma causing the distortion of brain. Midline shifts of the human brain in relation to size and location of haematoma were compared with the theoretical prediction. RESULTS: Prediction of midline shifts in lobar space-occupying lesions was more accurate that in deep-seated ones (such as thalamic lesions). DISCUSSION: More accurate boundary conditions of space-occupying lesions and better knowledge of physical materials properties of brain tissues can improve predictions of brain deformation using mathematical models.

Brain↗
PubMed1999

Unbound plasma concentrations may predict neuroprotective brain concentrations: a brain microdialysis and pharmacokinetic study of enadoline in rats.

A rat brain microdialysis study of enadoline (CI-977), a k-opioid agonist, was conducted in nonanesthetized healthy rats to determine brain extracellular fluid (ECF) concentrations of CI-977 associated with neuroprotective subcutaneous (s.c.) doses. Three groups of 3 to 4 nonanesthetized yet restrained Sprague-Dawley rats with jugular cannulas and implanted brain (striatum) microdialysis probes received single s.c. doses of 0.3, 1.0, or 3.0 mg/kg CI-977. Blood and microdialysate samples were collected over a 12-hour period. Extent of rat plasma protein binding was 77.5%. Unbound plasma concentrations associated with neuroprotection were 10-50 ng eq/mL. At each dose, brain ECF concentration-time profiles (corrected for probe recovery) were nearly coincident with enadoline plasma unbound concentration-time profiles. Consequently, at each dose the ratio of AUCecf/AUCffplasma, (AUC = Area Under the concentration-time Curve; ffplasma = free fraction in plasma = unbound plasma) which represents the distribution of drug between plasma and brain, was determined to be unity within experimental error. These results suggest that unbound plasma concentrations may predict brain ECF concentrations of CI-977. Further, our findings allow us to postulate enadoline unbound brain ECF concentrations necessary for neuroprotection.

Animals↗
PubMed1978

The influence of brain cytosol on RNA synthesis and RNA products of isolated mouse brain nuclei.

The incubation of isolated nuclei obtained from 10-day-old mouse brain in the presence of brain cell cytosol resulted in an increase in the synthesis of RNA. Under conditions of saturating concentrations of nucleoside triphosphates, the influence of cytosol could not be duplicated by the addition of cyclic nucleotides. The stimulatory activity of cytosol on brain nuclear RNA synthesis could not be attributed to either alterations in the permeability of the nuclear envelope or an increased uptake of radioactively-labeled precursors. Sucrose gradient analysis demonstrated that the RNA products synthesized by nuclei isolated from 10-day-old and adult mouse brain were of a relatively low molecular weight. However, the addition of cytosol resulted in a significant increase in the size of the RNA transcripts. In contrast to the observations with 10-day-old and adult brain nuclei, the RNA from 2-day-old mouse brain nuclei was larger in size and relatively unaffected by the presence of cytosol. Although cytosol caused an increase in the amounts of poly[A]-RNA in nuclei of 2-day-old and adult animals, no comparable effect could be measured in nuclei from 10-day-old brain tissue.

Animals↗
PubMed2003

Evaluation of the effects of methylprednisolone pulse therapy in patients with systemic lupus erythematosus with brain involvement by Tc-99m HMPAO brain SPECT.

Methylprednisolone pulse therapy (MPT) was introduced to avoid life-threatening complications in patients with systemic lupus erythematosus (SLE) with brain manifestations; however, the efficacy of MPT in SLE patients with brain involvement is still uncertain and needs to be objectively evaluated. We enrolled 15 female SLE patients with neuropsychiatric manifestations in this study. All patients had normal brain MRI and abnormal brain HMPAO-SPECT findings. Follow-up HMPAO-SPECT studies were conducted 2 weeks after MPT. Serum levels of anticardiolipin antibodies (ACA) and anti-ribosomal P antibodies (anti-P) were measured before and after MPT. Before MPT, 7 patients were positive for ACA and 7 patients were positive for anti-P. After MPT, none of the 15 patients demonstrated positive serologic findings or neuropsychiatric manifestations. Based on the follow up brain HMPAO-SPECT images following MPT, 13 patients showed disappearance of the perfusion defects and 2 patients showed partial recovery of rCBF. Brain HMPAO-SPECT imaging is a logical and objective tool for measuring the effects of MPT in SLE patients with brain involvement by determining of changes in rCBF.

Adult↗
PubMed2016

Gene co-expression analysis identifies brain regions and cell types involved in migraine pathophysiology: a GWAS-based study using the Allen Human Brain Atlas.

Migraine is a common disabling neurovascular brain disorder typically characterised by attacks of severe headache and associated with autonomic and neurological symptoms. Migraine is caused by an interplay of genetic and environmental factors. Genome-wide association studies (GWAS) have identified over a dozen genetic loci associated with migraine. Here, we integrated migraine GWAS data with high-resolution spatial gene expression data of normal adult brains from the Allen Human Brain Atlas to identify specific brain regions and molecular pathways that are possibly involved in migraine pathophysiology. To this end, we used two complementary methods. In GWAS data from 23,285 migraine cases and 95,425 controls, we first studied modules of co-expressed genes that were calculated based on human brain expression data for enrichment of genes that showed association with migraine. Enrichment of a migraine GWAS signal was found for five modules that suggest involvement in migraine pathophysiology of: (i) neurotransmission, protein catabolism and mitochondria in the cortex; (ii) transcription regulation in the cortex and cerebellum; and (iii) oligodendrocytes and mitochondria in subcortical areas. Second, we used the high-confidence genes from the migraine GWAS as a basis to construct local migraine-related co-expression gene networks. Signatures of all brain regions and pathways that were prominent in the first method also surfaced in the second method, thus providing support that these brain regions and pathways are indeed involved in migraine pathophysiology.

Atlases as Topic↗