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At least 595 records · Page 33Linked to original sources
PubMed2004

Cytoplasmic dynein mediates adenovirus binding to microtubules.

During infection, adenovirus (Ad) capsids undergo microtubule-dependent retrograde transport as part of a program of vectorial transport of the viral genome to the nucleus. The microtubule-associated molecular motor, cytoplasmic dynein, has been implicated in the retrograde movement of Ad. We hypothesized that cytoplasmic dynein constituted the primary mode of association of Ad with microtubules. To evaluate this hypothesis, an Ad-microtubule binding assay was established in which microtubules were polymerized with taxol, combined with Ad in the presence or absence of microtubule-associated proteins (MAPs), and centrifuged through a glycerol cushion. The addition of purified bovine brain MAPs increased the fraction of Ad in the microtubule pellet from 17.3% +/- 3.5% to 80.7% +/- 3.8% (P < 0.01). In the absence of tubulin polymerization or in the presence of high salt, no Ad was found in the pellet. Ad binding to microtubules was not enhanced by bovine brain MAPs enriched for tau protein or by the addition of bovine serum albumin. Enhanced Ad-microtubule binding was also observed by using a fraction of MAPs purified from lung A549 epithelial cell lysate which contained cytoplasmic dynein. Ad-microtubule interaction was sensitive to the addition of ATP, a hallmark of cytoplasmic dynein-dependent microtubule interactions. Immunodepletion of cytoplasmic dynein from the A549 cell lysate abolished the MAP-enhanced Ad-microtubule binding. The interaction of Ad with both dynein and dynactin complexes was demonstrated by coimmunoprecipitation. Partially uncoated capsids isolated from cells 40 min after infection also exhibited microtubule binding. In summary, the primary mode of Ad attachment to microtubules occurs though cytoplasmic dynein-mediated binding.

Adenosine Triphosphate↗
PubMed2002

Longitudinal PET Evaluation of Cerebral Metabolic Decline in Dementia: A Potential Outcome Measure in Alzheimer's Disease Treatment Studies.

OBJECTIVE: It is well established that regional cerebral metabolic rates for glucose assessed by [(18)F]fluorodeoxyglucose (FDG) positron emission tomography (PET) in patients with Alzheimer's disease in the mental resting state (eyes and ears covered) provide a sensitive, in vivo metabolic index of Alzheimer's disease dementia. Few studies, however, have evaluated longitudinal declines in regional cerebral glucose metabolism in patients with dementia caused by Alzheimer's disease. In addition, the available studies have not used recently developed brain mapping algorithms to characterize the progression of Alzheimer's disease throughout the brain, and none considered the statistical power of regional cerebral glucose metabolism in testing the ability of treatments to attenuate the progression of dementia. METHOD: The authors used FDG PET and a brain mapping algorithm to investigate cross-sectional reductions in regional cerebral glucose metabolism, longitudinal decline in regional cerebral glucose metabolism after a 1-year follow-up, and the power of this method to evaluate treatments for Alzheimer's disease in patients with mild to moderate dementia. PET scans were initially acquired in 14 patients with Alzheimer's disease and 34 healthy comparison subjects of similar age and sex. Repeat scans were obtained in the patients 1 year later. Power analyses for voxels showing maximal decline over the 1-year period in regional cerebral glucose metabolism (mg/100 g per minute) were computed to estimate the sample sizes needed to detect a significant treatment response in a 1-year, double-blind, placebo-controlled treatment study. RESULTS: The patients with Alzheimer's disease had significantly lower glucose metabolism than healthy comparison subjects in parietal, temporal, occipital, frontal, and posterior cingulate cortices. One year later, the patients with Alzheimer's disease had significant declines in glucose metabolism in parietal, temporal, frontal, and posterior cingulate cortices. Using maximal glucose metabolism reductions in the left frontal cortex, we estimated that as few as 36 patients per group would be needed to detect a 33% treatment response with one-tailed significance of p</=0.005 and 80% power in a 1-year, double-blind, placebo-controlled treatment study. CONCLUSIONS: These findings indicate that brain metabolism as assessed by FDG PET during mental rest is a sensitive marker of disease progression in Alzheimer's disease over a 1-year period. These findings also support the feasibility of using FDG PET as an outcome measure to test the ability of treatments to attenuate the progression of Alzheimer's disease.

Aged↗
PubMed2003

Architectonic subdivision of the human orbital and medial prefrontal cortex.

The structure of the human orbital and medial prefrontal cortex (OMPFC) was investigated using five histological and immunohistochemical stains and was correlated with a previous analysis in macaque monkeys [Carmichael and Price (1994) J. Comp. Neurol. 346:366-402]. A cortical area was recognized if it was distinct with at least two stains and was found in similar locations in different brains. All of the areas recognized in the macaque OMPFC have counterparts in humans. Areas 11, 13, and 14 were subdivided into areas 11m, 11l, 13a, 13b, 13m, 13l, 14r, and 14c. Within area 10, the region corresponding to area 10m in monkeys was divided into 10m and 10r, and area 10o (orbital) was renamed area 10p (polar). Areas 47/12r, 47/12m, 47/12l, and 47/12s occupy the lateral orbital cortex, corresponding to monkey areas 12r, 12m, 12l, and 12o. The agranular insula (areas Iam, Iapm, Iai, and Ial) extends onto the caudal orbital surface and into the horizontal ramus of the lateral sulcus. The growth of the frontal pole in humans has pushed area 25 and area 32pl, which corresponds to the prelimbic area 32 in Brodmann's monkey brain map, caudal and ventral to the genu of the corpus callosum. Anterior cingulate areas 24a and 24b also extend ventral to the genu of the corpus callosum. Area 32ac, corresponding to the dorsal anterior cingulate area 32 in Brodmann's human brain map, is anterior and dorsal to the genu. The parallel organization of the OMPFC in monkeys and humans allows experimental data from monkeys to be applied to studies of the human cortex.

Acetylcholinesterase↗
PubMed1994

Dopamine D2 receptors mapped in rat brain with [3H](+)PHNO.

Previous work with membrane preparations had demonstrated that the agonist (+)-4-propyl-9-hydroxynaphthoxazine (PHNO) labels the high-affinity state of dopamine D2 receptors with 67-fold selectivity over D1 sites. In this study, quantitative autoradiography was used to examine the binding of [3H](+)PHNO to rat brain sections. Highest binding densities were found in caudate-putamen, accumbens, and olfactory tubercles, as expected, and also in specific layers of the olfactory bulb. In addition, a second group of brain regions, including lateral septum, entorhinal cortex, molecular layer of hippocampus, and several brainstem structures showed low but consistent levels of binding. In all brain regions [3H](+)PHNO binding (2 nM) was completely displaced by 10 microM sulpiride (> 99%). Addition of 150 microM guanilylimidodiphosphate, which normally converts D2 receptors from high to low affinity states, abolished [3H](+)PHNO binding in all brain regions (> 99%), except for the islands of Callejas. This is likely to reflect binding to D3 sites in this area. Omission of preincubation in binding assays decreased [3H](+)PHNO binding in a regionally dependent manner, with strongest effects (22%) seen in high-density areas. These preincubation results confirm that (+)PHNO may have limitations for in vivo imaging studies. On the other hand, [3H](+)PHNO's negligible levels of non-specific binding compared to other agonists and overall selectivity would make it an excellent tool for in vitro autoradiographic monitoring of the high affinity state of D2 receptors.

Animals↗
PubMed1979

Mapping study of brain dopamine- and epinephrine-sensitive sites which cause feeding suppression in the rat.

Central injections of dopamine (DA) or epinephrine (EPI) have been found to suppress feeding behavior in hungry rats. In the present study, 24 different brain areas, in 299 animals, were examined to localize the precise region of catecholamine (CA) sensitivity. Essentially all sites outside the hypothalamus, as well as in the medial portion of the hypothalamus, were relatively or totally unresponsive to DA or EPI. The area of greatest sensitivity for both agonists (where they yielded a 50--70% suppression of feeding) was found to be the perifornical region of the lateral hypothalamus, extending from the caudal aspect of the paraventricular nucleus to the caudal aspect of the ventromedial nucleus. Dorsal, lateral, or ventrolateral movement of the injection site away from the fornix and into the zona incerta or the lateral hypothalamic medial forebrain bundle area caused a dramatic reduction in the effectiveness of the CA. These findings are consistent with histochemical studies, which have shown the fornix to be surrounded by CA varicosities, and pharmacological studies, which have shown the perifornical region to be most sensitive to the anorexic effect of centrally injected amphetamine, which releases endogenous CA. It is suggested that the perifornical hypothalamus plays a role in the process of inhibiting food consumption in response to increased dopaminergic and adrenergic activity.

Amphetamine↗
PubMed1996

Satietin: Fos mapping of putative brain sites of action.

A purified extract of a blood-borne satiety factor, called satietin, was injected into the cerebral ventricles of rats that were either fed ad libitum or were food deprived. The animals were killed 2 h after injection and their brains subsequently sectioned and stained for Fos-like immunoreactivity (Fos-IR) to determine the putative sites of action for satietin in the brain. Fos-IR was induced in only a few locations, the most prominent sites being the bed nucleus of the stria terminalis, the central nucleus of the amygdala, and the parvocellular division of the paraventricular nucleus of the hypothalamus. Each of these areas has previously been implicated in the control of feeding behavior. Sites in the hindbrain that are associated with nausea were devoid of satietin-induced Fos-IR. Finally, these sites of action of satietin show some differences from sites that are prominently activated by other classes of anorectic agents.

Amygdala↗
PubMed2005

Mapping postnatal mouse brain development with diffusion tensor microimaging.

While mouse brain development has been extensively studied using histology, quantitative characterization of morphological changes is still a challenging task. This paper presents how developing brain structures can be quantitatively characterized with magnetic resonance diffusion tensor microimaging coupled with techniques of computational anatomy. High resolution diffusion tensor images of ex vivo postnatal mouse brains provide excellent contrasts to reveal the evolutions of mouse forebrain structures. Using anatomical landmarks defined on diffusion tensor images, tissue level growth patterns of mouse brains were quantified. The results demonstrate the use of these techniques to three-dimensionally and quantitatively characterize brain growth.

Algorithms↗
PubMed1997

A non-thalamic pathway contributes to a whole body map in the brain of the budgerigar.

Nucleus basalis (Bas) of the budgerigar contains an ordered, but distorted, somatotopic representation of the whole body, as does the primary somatosensory cortex (SI) of mammals. Unlike SI, however, the beak and body regions of Bas receive their sensory input via disynaptic pathways relaying in the pons. That to the body parts originates in a previously undescribed nucleus that receives its inputs from primary afferents via a novel, ipsilateral somatosensory pathway.

Animals↗
PubMed2003

DTI mapping of human brain connectivity: statistical fibre tracking and virtual dissection.

Several approaches have been used to trace axonal trajectories from diffusion MRI data. If such techniques were first developed in a deterministic framework reducing the diffusion information to one single main direction, more recent approaches emerged that were statistical in nature and that took into account the whole diffusion information. Based on diffusion tensor MRI data coming from normal brains, this paper presents how brain connectivity could be modelled globally by means of a random walk algorithm. The mass of connections thus generated was then virtually dissected to uncover different tracts. Corticospinal, corticobulbar, and corticothalamic tracts, the corpus callosum, the limbic system, several cortical association bundles, the cerebellar peduncles, and the medial lemniscus were all investigated. The results were then displayed in the form of an in vivo brain connectivity atlas. The connectivity pattern and the individual fibre tracts were then compared to known anatomical data; a good matching was found.

Algorithms↗
PubMed1988

G protein mRNA mapped in rat brain by in situ hybridization.

Guanine nucleotide-binding regulatory proteins (G proteins) mediate many receptor-coupled signal transduction events. We have localized in rat brain by in situ hybridization the mRNA for the G protein subunits--G alpha s, G alpha o, and G beta. Oligonucleotide probes were radiolabeled by a technique that resulted in a probe of defined specific activity and uniform length. mRNA species encoding G alpha s and G beta occur in high densities heterogeneously throughout the brain, especially in large neuronal cell bodies--e.g., hippocampal pyramidal cells, granule cells of the dentate gyrus, hypothalamic nuclei, and neurons of brainstem nuclei and the reticular formation. G alpha o mRNA has a more limited distribution and abundance, being detectable in the claustrum, endopiriform nucleus, habenula, hippocampal pyramidal cells, granule cells of the dentate gyrus, and cerebellar Purkinje cells.

Animals↗
PubMed1985

Effect upon mitogenic stimulation of calcium-dependent phosphorylation of cytoskeleton-associated 350,000- and 80,000-mol-wt polypeptides in quiescent 3Y1 cells.

Rabbit antiserum raised against highest molecular weight microtubule-associated protein (MAP-1) of brain immunoprecipitated 350,000-, 300,000-, and 80,000-mol-wt phosphoproteins of rat embryo fibroblasts (3Y1-B). The 350,000-mol-wt protein was sensitive to heat as was brain MAP-1, but the 300,000- and 80,000-mol-wt proteins were not. These polypeptides were hardly phosphorylated in cells in the quiescent G0 phase but were rapidly phosphorylated after addition of serum, epidermal growth factor, phorbol ester, insulin, or transferrin in the presence of calcium ions. All these agents also induced incorporation of [3H]-thymidine into DNA. These polypeptides were detected in isolated microtubules and cold-resistant filaments by immunoblotting. Since the 350,000-mol-wt polypeptide was detected in the membrane, the cytoskeletons, and the nucleus, and has been suggested to function as a linker, its rapid phosphorylation might represent an early process in transduction of the signal of mitogenic stimulation to the nucleus.

Animals↗
PubMed1999

Mapping variation in brain structure and function: implications for rehabilitation.

The recognition of structural and functional variability of the human brain promoted the development of a system to organize and analyze the rapidly growing body of knowledge acquired among diverse disciplines. The Human Brain Project (HBP) was initiated and has evolved as a means of establishing an information infrastructure through tools related to the emerging science of neuroinformatics. This article will briefly describe the implications that such an endeavor has for the field of traumatic brain injury (TBI) rehabilitation.

Brain↗