bluuebunny/crossref_metadata_2025_split huggingface dataset:
Experiential factors in the expression of hypermotility produced by intradentate colchicine: Lack of effect of GM1 ganglioside on colchicine‐induced loss of granule cells and mossy fibers
Authors: Tilson H. A. , Harry G. J. , Nanry K. , Rogers B. , Peterson J. , Jensen K. , Dyer R. 
Published: January 2005

AbstractAdult male Fischer‐344 rats were given bilateral injections of 2.5 μg colchicine or artificial cerebrospinal fluid into caudal and rostra1 sites of the dentate gyrus of the hippocampus. One group of rats received 21 consecutive daily injections of 20 mg/kg GM1 gangliosides, i.p., beginning the day prior to surgery. Another group received saline. Colchicine‐induced hypermotility was not seen in animals repeatedly handled 21 d after surgery, in spite of significant decreases in granule cell number and decreases in the volume of hippocampal mossy fibers. Pretreatment with GM1 had no effect on behavior and it did not protect against the hippocampal damage produced by colchicine. Rats given colchicine, but not handled for 21 d, showed significant hypermotility, which was associated with decreases in hippocampal granule cells. These data underscore the importance of handling in postlesion functional recovery.
Effects of intraocular tetrodotoxin on the postnatal development of the dorsal lateral geniculate nucleus of the rat: A golgi analysis
Authors: Riccio R. V. , Matthews M. A. 
Published: January 2005

AbstractThe postnatal development of the rat dorsal lateral geniculate nucleus (dLGn) during tetrodotoxin (TTX)‐induced monocular impulse blockade was investigated by quantitative Golgi techniquesIntraocular injections of 1 × 10‐4M TTX were repeated every 2 days in rats aged 5–21 days postnatal dpn.
. Beyond 14 days postnatal (dpn), the effectiveness of TTX was monitored by loss of the pupillary light reflex. By 21 dpn, Golgi analysis indicated that TTX had no effect on the pattern of dendritic branching of class A or class B neurons, although the number of dendritic spinous protrusions was reduced. No evidence of any TTX‐induced loss of optic axons or neuronal degeneration in the dLGn was found, despite a 16% decrease in the size of the nucleus, suggesting a reduction in the growth of neuropil. These data indicate that optic impulses are important in mediating the proper growth of postsynaptic specializations in the dLGn during ontogenesis, but that the postnatal development of the dendritic arbor of neurons in the dLGn appears to be independent of retinal impulse activity.
Neural pathways that mediate the effects of afferent stimuli on paraventricular nucleus multiunit activity in freely moving rats
Authors: Mor G. , Saphier D. , Feldman S. 
Published: January 2005

AbstractThe direct involvement of the hypothalamic paraventricular nucleus (PVN) in the control of adrenocortical secretion is now generally accepted. In order to contribute to our understanding of the electrical activity of cells in this region during adrenocortical activation, we have recorded multiunit electrical activity (MUA) in response to acute neural stimuli in freely moving male rats and have examined the pathways involved. Photic, acoustic, olfactory, and sciatic nerve stimulation all increased PVN MUA by between 130% and 250%. These responses were selectively blocked, according to the stimulus modality tested, by radiofrequency lesions of central neural structures. Thus PVN responses to photic stimulation were blocked by lesions of the suprachiasmatic nuclei and reduced by mammillary peduncle lesions but were unaffected by lesions of the bed nuclei of the stria terminalis. Responses to acoustic stimulation were blocked by lesions of the mammillary peduncles but not by those placed in the suprachiasmatic nuclei, the septum, or the bed nuclei of the stria terminalis. Lesions of the septum blocked the response to sciatic nerve stimulation but did not affect the response to olfactory stimulation with amyl acetate fumes, which was blocked by lesions of the bed nuclei of the stria terminalis. The data confirm those obtained in endocrine studies concerning the neural pathways involved in the transmission of neural stimuli that produce adrenocortical activation.
Noradrenergic sympathetic innervation of the spleen: V. Acute drug‐induced depletion of lymphocytes in the target fields of innervation results in redistribution of noradrenergic fibers but maintenance of compartmentation
Authors: Carlson S. L. , Felten D. L. , Livnat S. , Felten S. Y. 
Published: January 2005

AbstractSympathetic noradrenergic fibers follow the vasculature into the white pulp of the spleen and branch from the periarteriolar plexuses into T lymphocyte zones. These lymphocytes, reported to express adrenergic receptors, are contacted directly by norepinephrine (NE) terminals and are putative targets of the locally released NE. Although this splenic innervation has been studied extensively, the functional interdependence of the lymphocytes and the sympathetic innervation is not well understood. To assess the effect of acute lymphocyte loss on the splenic innervation, T and B lymphocytes were depleted through treatment with cyclophosphamide (CY) or hydrocortisone acetate (HC). Despite reductions in spleen weight and cellularity, the total NE content (pmol) per spleen did not change. However, the NE concentration increased in the treated spleens. Although the general compartmental organization of the noradrenergic fibers in the treated spleens was similar to that of controls, the NE fibers redistributed and increased in density around the smaller central arteries in lymphocyte depleted spleens. The accommodation of these NE fibers to the changing environment of the white pulp suggests that the innervation to the spleen remains chemically stable despite a large disruption to the normal splenic milieu, but is capable of plasticity in the face of a shrinking white pulp.
Enkephalins and autoimmunity: Differential effect of methionine‐enkephalin on experimental allergic encephalomyelitis in wistar and lewis rats
Authors: Janković B. D. , Marić D. 
Published: January 2005

AbstractTo evaluate the immunomodulating activity of methionine‐enkephalin (Met‐Enk) and leucine‐enkephalin (Leu‐Enk) in the development of experimental allergic encephalomyelitis (EAE), two strains of rats, one highly susceptible to EAE (Lewis rats) and the other relatively resistant to the disease (Wistar rats) were used. The animals were given daily injections of either a high dose (5 mg/kg b.w.) or a low dose (0.2 mg/kg b.w.) of these opioid peptides, after receiving guinea pig spinal cord in combination with immunological adjuvants. A major conclusion from this study is that Met‐Enk is a potent immunomodulator/regulator of the autoimmune disease, whereas Leu‐Enk does not affect EAE.The high dose of 5 mg/kg b.w. of Met‐Enk completely or significantly inhibited neurological signs and markedly diminished occurrence and intensity of histological lesions in the brain, and cervical, thoracic, and lumbar spinal cord. The loss of body weight, which accompanies EAE, was also prevented by a high dose of Met‐Enk. In contrast, the low dose of 0.2 mg/kg b.w. Met‐Enk potentiated neurological and histopathological features of the disease. Nonimmunized rats injected with enkephalins for a period of 17 consecutive days showed neither neurological nor histological signs of EAE, nor signs of intoxication due to the application of enkephalins. Thus, these data establish a link between methionine‐enkephalin and EAE, and suggest that this opioid pentapeptide might be important in the pathogenesis and prevention of the inflammatory autoimmune disease.
Thymosin fraction 5 stimulates secretion of immunoreactive β‐endorphin in mouse corticotropic tumor cells
Authors: Farah J. M. , Hall N. R. , Bishop J. F. , Goldstein A. L. , O'Donohue T. L. 
Published: January 2005

AbstractIn addition to reconstituting immune competence, the thymus gland preparation, thymosin fraction 5 (TSN‐5), has recently been shown to stimulate secretion of hormones from the hypothalamic‐pituitary adrenal axis in vivo and from pituitary corticotropes in vitro. The purpose of the present study was to investigate the effects of TSN‐5 on secretion of immunoreactive β‐endorphin (iβ‐E) by mouse corticotropic tumor cells. The release of iβ‐E by AtP‐20 pituitary tumor cells was increased in a dose‐dependent manner by concentrations trations of 30–600 pg/ml of TSN‐5, whereas concenconcentrations greater than 1,000 μg/ml were increasingly less effective in stimulating secretion. TSN‐5 (600 μg/ml) significantly stimulated iβ‐E release within 7 min; maximal secretory responses (up to 275% of control release) occurred by 4 hr. The secretory response of AtP‐20 cells to 600 μg/ml TSN‐5 (37.9 ± 2.0 vs. 16.1 ± 1.0 ng iβ‐E/ml/4 hr, mean ± SE) was similar in magnitude to release evoked by 0.1 μM corticotropin‐releasing factor (CRF). Combining TSN‐5 and CRF treatment increased secretion of iβ‐E to nearly 600% of control levels, an effect greater than an additive influence of the two independent treatments. Whereas CRF treatment reduced the levels of iβ‐E in AtP‐20 cell extracts after 24‐hr treatment by 45% (231.8 ± 24.7 vs. 417.2 ± 17.8 ng iβ‐E/mg protein, CRF vs. vehicle treatments, respectively), TSN‐5 did not significantly alter cellular hormone content. Neither TSN‐α1 nor TSN‐β4, two of the component peptides of TSN‐5, affected basal or CRF‐stimulated releast of iβ‐E, indicating that an unidentified constituent(s) is corticotropic. This study demonstrates that TSN‐5 directly stimulates hormone release from AtT‐20 cells and potentiates the secretory actions of CRF. These findings support the concept of interactions between neuroendocrine and immune regulators of the hypothalamic‐pituitary adrenal axis. Additionally, corticotropic tumor cells appear to be a useful model in which to differentiate a hormonally active constitutent(s) of TSN‐5 and evaluate the cellular mechanisms of action of TSN‐5 on corticotropic cells.
Ameboid microglia as effectors of inflammation in the central nervous system
Authors: Giulian D. 
Published: January 2005

AbstractTechniques for selective isolation, labeling, stimulation, and destruction of ameboid microglia allow study of some fundamental questions in neuroimmunology. Examination of surface morphology, proliferative capacity, and cytochemistry suggests that microglia are a class of brain mononuclear phagocytes distinct from blood monocytes, spleen macrophages, or resident peritoneal macrophages. Morover, cultured ameboid microglia isolated from newborn brain can be induced to grow thin cytoplasmic projectios several hundred microns in length; these process‐bearing cells resemble a differentiated form of microglia found in adult brain.Ameboid microglia may contribute to brain inflammation by engulfing debris, by releasing cytotoxins, by killing neighboring cells, and by secreting astroglial growth factors. Importantly, ameboid microglia are closely tied to a network of immunomodulators that include colony‐stimulating factors and Interluekin‐1. The presence of activated microglia during normal embryogenesis and at sites of penetrating brain injury suggests that these cells serve as important effectors linking the immune system with growth and repqir of the CNS.
Interleukin‐3 modulation of mouse bone marrow derived mast cell receptors for somatostatin
Authors: Renold F. K. , Dazin P. , Goetzl E. J. , Payan D. G. 
Published: January 2005

AbstractReceptors for somatostatin (SOM) were identified on mouse bone marrow derived mast cells (MBMMC) and shown to vary in expression with the state of proliferation and differentiation of the MBMMC. Flow cytometric studies of the binding of fluorescein‐labeled SOM and concurrent analyses of the binding of [125I]SOM demonstrated that the population of MBMMC capable of recognizing SOM specifically is that exhibiting a proliferative response to interleukin‐3. The MBMMC that bound SOM reached a maximal number at 72 hr following the addition of interleukin‐3, and were distributed principally in the G2/M phase of the cell cycle. SOM did not influence directly the proliferative responses of MBMMC to interleukin‐3. The level of expression of SOM receptors thus may reflect the state of differentiation of mast cells, as well as determining the funcitonal sensitivity to the inhibitory effects of SOM.
Effects of entorhinal lesions on trophic activities present in rat entorhinal cortex and hippocampus as studied using primary cultures of entorhinal and septal tissues
Authors: Gibbs R. B. , Needels D. L. , Yu J. , Cotman C. W. 
Published: January 2005

AbstractThe present study examined trophic activities in normal and injured brain which affect the survival and growth of central neurons in culture. Adult rats received bilateral lesions through the angular bundle, severing projections between the entorhinal cortex and the hippocampus. Ten days later, extracts were prepared from the entorhinal or hippocampal regions of the injured brains and compared with extract prepared from analogous regions of normal brains for trophic activities in cultures of either entorhinal or septal tissues.At least three activities were observed: (1) a trophic activity which bound to polylysine‐treated wells, which was >10,000 Da in size, heat labile, and sensitive to trypsin, and which supported the survival of both septal and entorhinal neurons in culture; (2) a trophic activity which did not bind to polylysine‐treated wells, which was >10,000 Da in size, heat labile, and sensitive to trypsin, and which, in the presence of polylysine‐bindable material, facilitated the survival and growth of entorhinal cells in culture, and (3) an inhibitory activity which significantly reduced survival in entorhinal cultures when cells were plated in the presence of high concentrations of extract prepared from normal brain. These effects were not due to nonspecific effects of plating the cells in, or treating the wells with, large amounts of protein.A significant injury‐related increase in nonpolylysine‐bindable trophic activity was also observed. Extracts prepared from either the hippocampus or the entorhinal area of the injured brains contained more non‐polylusine‐bindable trophic activity than extract prepared from normal brains. Injury‐related changes in trophic activities were more prominent in entorhinal than in septal cultures. This increase in activity may account for the injury‐related effects on the survival of entorhinal transplants reported previously [Gibbs and Cotman: Neuroscience (in press) 1987], and may represent an endogenous mechanism by which the brain attempts to selectively support the survival of injured cells following injury.
Isolation of intact capillaries and capillary plasma membranes from frozen human brain
Authors: Pardridge W. M. , Yang J. , Eisenberg J. , Tourtellotte W. W. 
Published: January 2005

AbstractThe development of methods for the isolation of brain capillaries and brain capillary plasma membranes makes possible biochemical studies of the blood‐brain barrier (BBB), which is made up of brain capillaries. Studies aimed at assessing the role of the BBB in the pathogenesis of specific neurologic diseases, e.g., Alzheimer's disease or multiple sclerosis, will necessitate the isolataion of capillaries from brain involved with specific pathology. Such tissue is most readily available from banks containing frozen human brain. The present studies show that intact capillaries and capillary plasma membranes can be isolated from frozen human brain, including as little as five g of multiple sclerosis plaque tissue. Capillaries from frozen human brain are enriched in gamma‐glutamyl transpeptidase, factor VIII antigen, and a 46K protein which has recently been shown to be a BBB‐specific protein. These studies provide the basis for future biochemical studies of human brain microvessels in neurologic disease.
Effect of phenytoin on cytoskeletal protein phosphorylation and neuronal structure in the rat sensory cortex
Authors: Ruiz G. , Flores O. G. , González‐Plaza R. , Inestrosa N. C. 
Published: January 2005

AbstractPhenytoin (PH) is commonly used as an anticonvulsant drug, and it causes several collateral effects including morphological changes in brain cortex neurons and teratogenic lesions in infants of epileptic mothers. Several lines of evidence indicate that PH may exert its action through the modification of phosphorylation patterns of neuronal polypeptides. We have studied the effects of PH on the phosphorylation of cytoskeletal proteins, because this could be relted to the structural modifications induced by PH administration. The dendritic pattern of deep layers of the somatosensory cortex is clearly modified by PH but not the cell number, indicating that the drug disturbs the architecture of the neurons examined. In fact, the pattern of phosphorylation in cytoskeletal extracts of brains of 30‐day‐old rats is changed by PH. In vitro labeling experiments show decrease in the [32P] level of a 43‐kDa polypeptide, whereas 38‐ and 120‐kDa polypeptides show increases in their [32P] contents. The 43‐kDa polypeptide has been identified as actin by in vitro experiments using a novel approach to determine cytoskeletal poypeptide behvior. We conclude that PH affects the posttranslational phosphorylation of actin and other related cytoskeletal proteins and in this manner may alter the normal morphological layout of dendritic patterns in the somatosensory cortex.
Sodium‐dependent high‐affinity uptake of taurine in cultured cerebellar granule cells and astrocytes
Authors: Holopainen I. , Malminen O. , Kontro P. 
Published: January 2005

AbstractTaurine uptake in cultured cerebellar granule cells and astrocytes consisted of a saturable high‐affinity component and nonsaturable diffusion. The transport constant (Km) was significantly lower and the maximal velocity (V) higher in granule cells than in astrocytes. The uptakes were strictly sodium dependent and also moderately decreased in potassium‐free medium. The specificity profile of taurine uptake was similar in both cell types, hypotaurine β‐alanine, and guanidinoethanesulphonic acid being the most potent inhibitors, followed by GABA and homotaurine. Glutamate inhibited taurine uptake more in astrocytes than in granule cells. In principle, the uptake systems were similar in granule cells and astrocytes, exhibiting features characteristic of uptake of a neurotransmitter or ‐modulator.
Nerve growth factor protein level increases in the adult rat hippocampus aftera specific cholinergic lesion
Authors: Lärkfors L. , Strömberg I. , Ebendal T. , Olson L. 
Published: January 2005

AbstractNerve growth factor (NGF) is the best‐characterized neurotrophic substance and has recently been shown to influence cholinergic neurons in the basal forebrain. Hippocampus and neocortex, the primary targets for these central neurons, have further been found to contain high levels of NGF. Using enzyme immunoassay and acetylcholine esterase (AChE) histochemistry we have now studied the levels of NGF and AChE after a specific cholinergic lesion, transection of the fimbria fornix comprising the major cholinergic input to hippocampus. Fimbriectomy in adult rats led to a marked decrease in AChE‐positive nerve terminals in both hippocampus and neocortex 10 days later, and to an increase (40%) of NGF protein concentration in hippocampus. Thirty days after surgery, NGF had returned to control levels and remained there after 90 days. Removal of superior cervical ganglion did not after the results. The density of cholinergic terminals in both hippocampus and neocortex increased with time (90 days) after fimbrial transection. The results support the idea that cholinergic neurons in the basal forebrain take up and retrogradely transport NGF from their target areas and suggest that transection of the pathway interrupts the transport thereby increasing NGF distal to the lesion. The return of NGF to control levels probably reflects reestablished cholinergic contacts in the hippocampus.
Effect of injury on nerve growth factor uptake by sensory ganglia
Authors: Khan T. , Green B. , Perez‐Polo R. J. 
Published: January 2005

AbstractThe level of the nerve growth factor protein, NGF, in vivo has a profound influence on axonal sprouting by sensory neurons of vertebrate dorsal root ganglia. There is evidence also that NGF may play similar roles in cholinergic central structures in brain. In both instances, retrograde transport of NGF has been demonstrated. Here we examined uptake of NGF by DRG neurons in response to contusion injury of the spinal cord. Under these conditions there was uptake and tranport of NGF into large DRG neurons via central processes but no uptake by non‐DRG central neurons. Thus, any effects of NGF on spinal neurons or their processes would be secondary to the direct effects of NGF on DRG Neurons.
Perinatal, not adult, hypothyroidism suppresses dopaminergic axon sprouting in the deafferented olfactory tubercle of adult rat
Authors: Gottesfeld Z. , Garcia C. J. , Chronister R. B. 
Published: January 2005

AbstractWe reported recently that chronic thyroid deficiency in rat, beginning in utero and terminating after maturity, suppresses lesion‐induced central catecholaminergic axon sprouting in the adult brain [Gottesfeld et al, 1985]. The present work was undertaken to define the critical period of hypothroidism on subsequent neuronal sprouting.Thyroid hormones deficiency was induced in rats by methimazole during (a) gestational days 8–21 (20 mg/kg/day in the drinking water); (b)postnatal days 1–15 (0.2 or 0.4 mg/pup/day; i.p.), or (c) in the mature animal for 4 weeks (20 mg/kg/day in the drinking water). The olfactory tubercles (ITs) were used as a model to study sprouting of dopaminergic (DA) nerve terminals, elicited by olfactory bulbectomy. Animals in each group received lesions or sham operations as adults, and sacrificed 3 weeks after the operation. Thus, for each of the above treatments four subgroups were formed: (c) hypothyroid/sham‐operation, and (d)hypothyroid/lesion.Sprouting of DA axon ternminals in the OTs was identified by biochemical assays and quantitative immunofluorescent microscopy, using throxine levels served as an index of the thyroid status.The results demonstrate that lesion‐induced sprouting of DA axon terminals in OTs of adult rats is suppressed by hypothyroidism induced prenatally of during the early postnatal period, but not after maturity. Thus, there is a perinatal critical period during which altered thyroid funciton exerts long‐term effects on neuronal plasticity.
Visual acuity loss ion rhesus monkey infants fed a taurine‐free human infant formula
Authors: Neuringer M. , Sturman J. 
Published: January 2005

AbstractThis study examinedthe effects of dietary taurine deprivation on visual development in rhesus monkeys. From birth to 3 months of age, rhesus monkeys were fed a taurine‐free, soy protein‐based infant formula, or the same formula supplemented with taurine. The early postnatal development of visual function was assessed with behavioral measurements of visual acuity.Plasma taurine levels in the taurine‐deprived group fell to 35–50% of control values, as in human infants fed similar formulas. The visual acuity of the taurine‐deprived infants was significantly impaired: acuity thresholds differed from control values by nearly a factor of 2 at 4, 8, and 12 weeks of age. The loss of acuity is associated with morphological changes in photoreceptors, particularly cones in the foveal region.These results provide direct evidence that taurine is essential for normal visual development in primates, and they support the nutritional importance of taurine for human infants.