bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of competition in the refinement of the projections of sympathetic neurons to the rat eye during development
Authors: Hill Caryl E. , Vidovic Maria 
Published: April 2003

AbstractWithin the iris, the extent of the nerve plexuses derived from the sympathetic neurons of the superior cervical ganglion (SCG) and the sensory, substance P (SP) neurons of the trigeminal ganglion depend on competition for target tissue derived growth factors. During the postnatal period when these plexuses are initially established, many sympathetic neurons are known to extend transient collateral projections to various targets within the eye. We have investigated the role of neuronal competition in the withdrawal of these transient projections by removing the sensory SP fibres using neonatal capsaicin treatment (50 mg/kg) on days 2, 10 and 17, or day 2 only. At 2, 4 and 7 weeks, fast blue was injected into the anterior chamber or posteriorly into the vitreous to retrogradely label sympathetic neurons in the SCG. Capsaicin treatment resulted in a transient retention of the projections of supernumerary neurons to the eye early during development and a maintenance of the collaterals of some of these sympathetic neurons to adulthood, but only when rats received multiple capsaicin injections. The retention of collaterals in these animals was reflected in an increase in the density of the sympathetic nerve plexus within targets such as the iris. Immunohistochemistry for SP showed that a single injection of capsaicin was less effective than multiple injections in removing the SP‐containing nerve fibres from the iris and in causing long‐lasting changes to the sympathetic projections. We conclude that some form of interaction between different neuronal populations within the eye plays an important role in the refinement of collateral projections of sympathetic neurons, but has no long‐term effect in influencing the final number of neurons which project to the eye.
Evaluation of the effects of inhibition of monoamine oxidase and senescence on methamphetamine‐induced neuronal damage
Authors: Wagner George C. , Walsh Sharon L. 
Published: April 2003

AbstractThe administration of high doses of methamphetamine causes long lasting damage to central dopaminergic and serotonergic neurons through a mechanism known to involve presynaptic, cytoplasmic stores of those transmitters and thought to be dependent upon a free radical reaction. The following studies were designed to determine if differential inhibition of the subtypes of monoamine oxidase would alter the magnitude of the methamphetamine induced neuronal damage. In addition, since monoamine oxidase type B increases with age, the effects of high dose administration of methamphetamine were evaluated in sensescent mice. It was observed that inhibition of monoamine oxidase type A, and to a lesser degree, type B, increased the magnitude of methamphetamine‐induced neuronal damage and that aged mice were more sensitive to the toxic action of methamphetamine. These results are interpreted with respect to the use of monoamine oxidase inhibitors in the treatment of Parkinson's disease.
In vitro screening for anticonvulsant‐induced teratogenesis: Drug alteration of cell adhesivity
Authors: Maguire C. , Regan C.M. 
Published: April 2003

AbstractAnticonvulsant‐induced alteration in C6 glioma cell adhesivity has been evaluated in two independent in vitro assay systems. A centrifugal shear assay was employed to determine drug‐induced change in cell‐substratum adhesivity. Valproate and clonazepam were found to significantly increase cell‐substratum adhesivity when cells were cultured at concentrations which were within twice their therapeutic plasma level. A second assay evaluated change in affinity for concanavalin A lectin coated surfaces to determine change in cell surface glycoconjugate expression. Valproate and clonazepam and, to a lesser extent, diazepam significantly decreased drug‐exposed C6 glioma cell affinity for concanavalin A lectin coated surfaces. Valproate and clonazepam had approximate IC50 values of 0.75 mM and 75 μM, respectively. These findings are compared and discussed in relation to those obtained with an anti‐proliferative assay which has been suggested to predict teratogen potential.
Short‐ and long‐term effects of combined pre‐ and postnatal ethanol exposure (three trimester equivalency) on the development of myelin and axons in rat optic nerve
Authors: Phillips D.E. , Krueger S.K. , Rydquist J.E. 
Published: April 2003

AbstractThis study evaluated the effects of a combined gestational and 10 day postnatal alcohol exposure (human three trimester equivalency) on the development of myelin and axons in rat optic nerve. Rats were exposed during gestation via liquid diet, then their artificially reared pups were further exposed for 10 postnatal days via an ethanol‐containing diet fed by gastrostomy. Control animals from pair‐fed dams were artificially reared for 10 days on pair‐fed isocaloric diets. Anesthetized animals were perfused with fixative on gestational days (G) 15 and 20 and postnatal days (P) 5, 10, 15, 20, and 90, then optic nerve tissues prepared for electron microscopy. Optic nerve cross‐sectional areas were generally less from G20 through P90 in ethanol exposed animals. Counts of the number of myelinated nerve fibers per unit area and of the numbers of fibers in different stages of myelin development revealed that alcohol exposure caused a delay in myelin acquisition at 10 and 15 days that was compensated for at 20 and 90 days. Myelin thickness as a function of axon diameter was decreased in the alcohol exposed animals from 10 through 90 days, indicating a permanent reduction in the relative thickness of myelin.These results show that alcohol exposure for all of gestation and 10 postnatal days in the rat (human three trimester equivalency) causes a permanent reduction in myelin thickness along with a delay in myelin acquisition in the optic nerve. Such alterations in developing and adult myelin could help to explain some of the neurological and visual dysfunctions associated with developmental alcohol exposures.
Ontogeny of MAP2 and GFAP antigens in primary cultures of embryonic chick brain. Effect of substratum, oxygen tension, serum and Ara‐C
Authors: Bruinink A. , Reiser P. 
Published: April 2003

AbstractBrain cells from embryonic chick (stage 28–29) were cultivated for 16 days under serum‐free conditions. Nerve cells were found to mature during the first 7 days in culture, as indicated by the presence and developmental pattern of the relative amount of dendritic‐specific microtubule‐associated protein type 2 (MAP2). Maximal amounts of MAP2 antigen were found to be directly correlated with the number of cells plated out. Astroglia cell proliferation and differentiation, as measured by the amounts of glial fibrillary acidic protein (GFAP), were found to stabilize after a certain astrocyte cell density was reached. Variation in culture plate coating procedure, oxygen tension and addition of serum or of the cytostatic drug Ara‐C were found to differently affect viability and maturation processes of astroglia and of nerve cells. Moreover, optimal culture conditions for long‐term brain cell cultures are described.
Neurotransmitter amino acid levels in rat thalamus and cerebral cortex after cerebellectomy
Authors: Cicirata F. , Meli C. , Castorina C. , Serapide M.F. , Sorrenti V. , Di Giacomo C. , Gambera G. , Vanella A. 
Published: April 2003

AbstractGlutamate, aspartate, GABA, glycine and taurine levels have been measured in rat thalamus and in cerebral cortex at different time intervals (3rd, 7th, 15th, 30th day) after cerebellectomy. A decrease in glutamate, aspartate and GABA was detected at the 7th day after cerebellectomy in the thalamus and at the 15th day in the cerebral cortex; at the 30th day after cerebellectomy the levels of these amino acids in the thalamus and in the cerebral cortex were observed to have recovered to control values. No statistically significant difference in glycine and taurine levels in the thalamus and in the cerebral cortex after cerebellectomy could be seen. These results show that the functional recovery process after cerebellar injury is associated with a complex modification of amino acid levels in thalamus and in cerebral cortex.
Corpus callosum: Demasculinization via perinatal anti‐androgen
Authors: Fitch Roslyn H. , Cowell Patricia E. , Schrott Lisa M. , Denenberg Victor H. 
Published: April 2003

AbstractThe male rat's corpus callosum is significantly larger than the female's. This dimorphism depends in part on the early presence of testosterone, since postnatal administration of testosterone to female pups enlarges their callosa in adulthood to the size of males. However, castrating males on day 1 is ineffective in reducing (demasculinizing) the size of their callosa as adults. We then addressed the question as to whether testosterone acts prior to day 1 to enlarge the callosa of males. To investigate this hypothesis pregnant rats were administered a non‐steroidal androgen blocker, flutamide, during the last 5 days of pregnancy, while controls received vehicle only. Male pups from flutamide litters were castrated on day 3 to prevent postnatal recovery following clearance of flutamide, while others received sham surgery. Callosal sex differences were found between males and females of control litters, but not between males and females from flutamide litters. The absence of sex effects among flutamide litters was a consequence of small callosal size in flutamide‐castrated males as compared to control males. We concluded that the prenatal production of testosterone in the male rat pup contributes to sexual dimorphism in the callosa of adult rats.
Development of the sensory innervation of muscle spindles in the kitten
Authors: Patak A. , Proske U. , Turner H. , Gregory J.E. 
Published: April 2003

AbstractThis is a report of the changes observed in the pattern of sensory innervation of muscle spindles in hindlimb muscles of kittens during the first four weeks of life. The structural analysis, made on teased, silver‐stained preparations, was complemented by a series of recordings of afferent responses of kitten spindles during ramp‐and‐hold stretches of the muscle. The primary endings of spindles from newborn animals showed a large degree of variability in their branching pattern and branches formed a network across the intrafusal fibres. In older animals there was less variability and lateral branches of stem axons began to encircle the intrafusal fibres. The process of maturation was characterized by a more uniform shape of the endings and more complete, evenly spaced, annulospiral terminals. Recordings of the responses of primary endings of spindles during muscle stretch showed that several features of the adult response were already present in the newborn, although the overall rate of discharge was very much lower. It was concluded that the changes observed in the structure of the sensory endings of kitten spindles did not have clearly identifiable physiological correlates. It appears that an annulospiral shape of the sensory terminals is not a necessary prerequisite for the generation of stretch responses. The predominant factor which appears to determine the responses of spindles to stretch is the maturity of the intrafusal fibres, in particular, the bag2 fibre.
Neuron‐enriched cultures derived from spinal cord of 10‐day‐old chick embryos: Influence of neuropeptides on neuronal survival, proliferation and cholinergic expression
Authors: Kentroti Susan , Vernadakis Antonia 
Published: April 2003

AbstractThe developmental regulation of cell proliferation, survival and cholinergic expression by growth hormone‐releasing hormone (GHRH) and somatostatin (SRIF) was investigated in neuronenriched cultures derived from 10‐day‐old embryonic chick spinal cord. In this study, 3H‐thymidine incorporation into DNA was assessed, using two different applications, in order to determine both cellular proliferation and survival. The rate of neuroblast proliferation in both control and neuropeptide‐treated cultures increased or remained the same up to day 6. However, in neuropeptide‐treated cultures the magnitude of cell proliferation remained at levels higher than those observed in controls through day 6 and was most significant in SRIF‐treated cultures at C4. In all groups, proliferation markedly declined by day 8. Survival of neuronal cells labelled at C4 remained high up to day 12 in all three groups, then drastically declined by day 17. Neuronal survival in the neuropeptide‐treated cultures was also higher than in controls. Cholinergic expression, as assessed by activity of choline acetyltransferase (ChAT), responded differentially to neuropeptide treatment. Cultures treated with GHRH (100 nM) exhibited a long term significant enhancement in ChAT activity throughout the culture period, whereas those treated with SRIF (50 nM) expressed a transient decline in ChAT activity. Videometric analysis showed that both neuropeptides enhanced neuronal aggregation, neuritic arborization and neuritic length. These findings lead us to suggest that GHRH and SRIF may provide neurotrophic signals important not only for neuronal proliferation and survival but also for cholinergic neuronal expression. Furthermore, we propose that GHRH possesses specific cholinotrophic properties, whereas SRIF may act as a general neurotrophic factor.
Effects of polyamine synthesis blockade on neuronal loss and astroglial reaction after transient forebrain ischemia
Authors: Zoli Michele , Zini Isabella , Grimaldi Roberta , Biagini Giuseppe , Agnati Luigi F. 
Published: April 2003

AbstractPolyamines and ornithine decarboxylase, the polyamine biosynthetic enzyme, have been demonstrated to increase in the early phase of several types of brain lesion. However, their role in the pathogenesis of tissue damage is still debated. In the present paper the effects of treatments with α‐difluoromethylornithine, a suicide inhibitor of ornithine decarboxylase, have been investigated in a model of transient forebrain ischemia. Three treatment schedules were used: α‐difluoromethylornithine treatment was either started 3 hr before and repeated 1 hr after the insult, or started at the time of the insult and continued for 3 or 7 days after post‐ischemic reperfusion. The rats were sacrificed 4 hr, 7 or 40 days after reperfusion, respectively. The acute experiment demonstrated that α‐difluoromethylornithine can reduce the increase of glial fibrillary acidic protein immunoreactivity, an early marker of astroglial reaction, in ischemic striatum. Subchronic and chronic α‐difluoromethylornithine treatments induced a worsening of the morphological outcome of the ischemic lesion. In caudate‐putamen a trend for an increase of the area of neuronal loss was present after both treatments. In the hippocampal formation, a significant increase in the severity of neuronal lesion was observed in the mildly lesioned CA3 field. In addition, other alterations of lesioned tissue were observed in α‐difluoromethylornithine‐treated animals, including increases of non‐neuronal cells at 7 and especially 40 days post‐lesion in striatum and CA3 hippocampal field. In conclusion, present data indicate that ornithine decarboxylase activation after ischemic lesion is a crucial factor for survival of mildly lesioned neurons and proper tissue reaction to the ischemic lesion. The experiment on acute α‐difluoromethylornithine treatment suggests that these effects may be, at least in part, related to putrescine‐induced activation of astroglial cells in the early post‐lesion period.
Gene expression in astrocytes is affected by subculture
Authors: Passaquin Anne‐Catherine , Schreier Wayne A. , de Vellis Jean 
Published: April 2003

AbstractWe have investigated the effects of cell passaging and time in culture on astrocyte morphology, transferrin expression and the expression of two main astrocyte markers, glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS; EC 6.3.1.2). When primary astrocytes were subcultured, giving rise to secondary and tertiary cultures, their morphology changed, regardless of the split ratio used to passage the cells. Correlating with this morphological change, a dramatic increase in the accumulation of GFAP and GS mRNAs was observed after cells had been passaged. This effect was in marked contrast to the moderate increase in the levels of GFAP and GS mRNAs observed over several weeks in primary culture. Hydrocortisone induction of GS gene expression was not affected by cell passage. Transferrin mRNA, which is not normally found in astrocytes in vivo, was expressed at a high level in primary cultures of astrocytes. However, transferring mRNA almost completely disappeared after the second passage. Astrocyte‐conditioned media, or co‐cultures with oligodendrocytes, modified transferrin gene expression. Taken together, these results show that subculturing of primary rat astrocytes leads to a dramatic change in the genetic expression of several proteins and provides a new approach to modify astrocyte differentiation in vitro.
Lifetime symptoms of depression in Alzheimer's disease
Authors: Reinhard Heun , Kockler Martin , Ptok Ursula 
Published: April 2003

AbstractIntroductionDepression is common in Alzheimer's disease (AD). The symptomatology of depression in dementia may differ from depression alone. Consequently, the reports on lifetime depressive symptoms were compared in AD patients and age-matched non-demented participants.MethodsSeventy-six AD patients, 109 elderly from the general population and their 189 siblings were examined using the Composite International Diagnostic Interview (CIDI). The presence of individual lifetime depressive symptoms was compared between 76 AD patients, 29 AD patients with comorbid depression, and different control groups using χ2 statistics and logistic regression analysis.ResultsLifetime depressive symptoms were significantly more frequent in 76 AD patients than in 109 age-matched elderly from the general population. These 76 AD patients complained more about thinking and concentration disturbances, and less about depressed mood or appetite disturbance than the 298 non-demented participants matched for the lifetime presence of major depression (MD). In agreement, the 29 patients comorbid for lifetime diagnoses of AD and MD reported less about depressed mood than the 114 age-matched elderly with MD only. Feelings of worthlessness and suicidal ideas were related to the severity of cognitive decline.ConclusionsAD influences the reports on lifetime depressive symptoms. This may be caused by additional neurodegeneration, by an overlap of symptoms of depression and dementia or by an altered perception of mood disturbances in AD. Further studies should investigate these alternatives.
Relationship between body-mass index and depressive symptoms in patients with major depression
Authors: Berlin Ivan , Lavergne Francis 
Published: April 2003

AbstractBackgroundAppetite and weight changes are commonly occurring symptoms of depressive illness. The occurrence of these symptoms may not only be related to depressive mood but may also be related to body weight.AimTo examine the relationship between symptoms of depression and body weight.MethodsSymptoms of depression were assessed by the Montgomery-Asberg depression rating scale (MADRS) in 1694 patients seeking medical help and fulfilling DSM-IV criteria for a major depressive episode. The level of anxiety was evaluated by Covi’s anxiety scale. Body weight was expressed as body-mass index (BMI, kg/m2) and treated both categorically and continuously.ResultsThe total MADRS score was not statistically different across the four BMI categories (underweight: 32.3 ± 0.6, normal weight: 30.9 ± 0.2, grade 1: 30.6 ± 0.3, and 2 overweight: 30.6 ± 0.6, P = 0.053 (NS)). In women with BMI ≤ 18.5 kg/m2 MADRS was significantly higher than that in other BMI categories (underweight: 32.4 ± 0.6, normal weight: 30.6 ± 0.2, grade 1: 30.6 ± 0.4, and 2 overweight: 30.6 ± 0.6: P = 0.036). Increasing BMI was related to a linear decrease in symptoms “Reduced appetite” (P < 0.0001) and “Pessimistic thoughts” (P < 0.003). The presence of melancholic or atypical features was not associated with lower or higher BMI, respectively.ConclusionsIn patients with major depression higher body weight is likely to be associated with less reduction in appetite and less pessimistic thoughts.
Basal and exercise‐induced neuroendocrine activation in patients with heart failure and in normal subjects
Authors: Kjær Andreas , Appel Jon , Hildebrandt Per , Petersen Claus Leth 
Published: April 2003

AbstractBackground:Neuroendocrine activation is a pathophysiological response and an important prognostic marker in patients with chronic heart failure (CHF). Although chronic activation is well described, data on the responsiveness of the hormone systems are more limited. Most previous studies have looked at activation during maximal exercise, whereas we believe that activation at a submaximal level might be more pathophysiologically relevant.Aim:To compare exercise‐induced neurohormonal activation between CHF patients and normal subjects using the same relative and submaximal workload.Subjects:Twenty‐three newly‐diagnosed CHF patients and 18 age‐ and gender‐matched healthy subjects were exercised at two workloads, which were calculated to correspond to 50 and 75% of each individual's heart rate response.Results:In CHF patients, baseline levels of ANP, BNP, AVP, PRA and ET‐1 were elevated compared to healthy subjects. Exercise induced an increase in ANP, A and NA in both CHF patients and in normal subjects, however BNP was only increased in CHF patients and not in normal subjects.Conclusion:When CHF patients exercise at the same relative and submaximal level as age‐matched healthy subjects, the relative increases in ANP, A and NA were similar, however, BNP levels only increased in the CHF group.
Energy‐dependent degradation: Linkage between ClpX‐catalyzed nucleotide hydrolysis and protein‐substrate processing
Authors: Burton Randall E. , Baker Tania A. , Sauer Robert T. 
Published: April 2003

AbstractClpX requires ATP to unfold protein substrates and translocate them into the proteolytic chamber of ClpP for degradation. The steady‐state parameters for hydrolysis of ATP and ATPγS by ClpX were measured with different protein partners and the kinetics of degradation of ssrA‐tagged substrates were determined with both nucleotides. ClpX hydrolyzed ATPγS to ADP and thiophosphate at a rate (6/min) significantly slower than ATP hydrolysis (140/min), but the hydrolysis of both nucleotides was increased by ssrA‐tagged substrates and decreased by ClpP. KM and kcat for hydrolysis of ATP and ATPγS were linearly correlated over a 200‐fold range, suggesting that protein partners largely affect kcat rather than nucleotide binding, indicating that most bound ATP leaves the enzyme by hydrolysis rather than dissociation, and placing an upper limit of ≈15 μM on KD for both nucleotides. Competition studies with ClpX and fluorescently labeled ADP gave inhibition constants for ATPγS (≈2 μM) and ADP (≈3 μM) under the reaction conditions used for steady‐state kinetics. In the absence of Mg2+, where hydrolysis does not occur, the inhibition constant for ATP (≈55 μM) was weaker but very similar to the value for ATPγS (≈45 μM). Compared with ATP, ATPγS supported slow but roughly comparable rates of ClpXP degradation for two Arc‐ssrA substrates and denatured GFP‐ssrA, but not of native GFP‐ssrA. These results show that the processing of protein substrates by ClpX is closely coupled to the maximum rate of nucleotide hydrolysis.