bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development of the neuronal system containing neuropeptide Y in the rat hypothalamus
Authors: Kagotani Y. , Hashimoto T. , Tsuruo Y. , Kawano H. , Daikoku S. , Chihara K. 
Published: April 2003

AbstractIn the rat hypothalamus, neuropeptide Y‐containing neurons first appeared on day 14.5 of gestation in the arcuate nucleus and in the dorsolateral hypothalamic area. Until birth neuropeptide Y‐containing cell bodies increased in number in the arcuate, dorsomedial‐lateral and paraventricular nuclei, but disappeared thereafter, but some cells remaining in the arcuate nucleus. In animals treated neonatally with monosodium l‐glutamate to destroy the arcuate nucleus, neuropeptide Y‐immunoreactivity became evident in many cells scattered in the magnocellular paraventricular and dorsomediallateral hypothalamic nuclei on day 16 but not on days 60 and 120. These neuropeptide Y‐immunoreactive neurons which appeared in the paraventricular nucleus were also vasopressin‐positive. Neuropeptide Y fibers, on the contrary, remarkably diminished in number on day 16, particularly in the paraventricular and dorsomedial‐lateral nuclei, and the medial preoptic area, but made a considerable recovery on days 60 and 120. Hence it is probable that, in normal ontogenetic progress, the development of the neuropeptide Y fibers in these areas is inhibitorily affected by that of arcuate neuropeptide Y neurons.
Stimulation of choline acetyltransferase in spinal cord explants by limb mesenchyme
Authors: Muhlach William L. , Pollack Emanuel D. 
Published: April 2003

AbstractCholine acetyltransferase (ChAT) activity in developing spinal cord explants in vitro is shown to be dependent on the presence of co‐cultured immature limb tissue. Frog tadpole spinal cord explants grown on collagen or polylysine expressed stage‐appropriate levels of ChAT activity only when in the presence of the limb mesenchyme target. Neither skeletal muscle nor polylysine, both of which enhance neurite growth accompanied by increases in cord protein, were capable of maintaining the level of ChAT activity characteristic of these spinal cords in vivo. The results demonstrate that developmentally significant levels of ChAT can be maintained in vitro under appropriate conditions that may act in part through the maintenance of cholinergic motor neurons.
Cholinergic modulation of aged‐like retention deficits in young autoimmune mice
Authors: Forster Michael J. , Lal Harbans 
Published: April 2003

AbstractSeparate age groups of autoimmune NZB/BINJ and non‐autoimmune C57BL/BNNia mice were compared for habituation of locomotor activity and its retention over four separate testing sessions spaced at 24‐hr intervals. A decline in locomotion (distance in cm) or in the time spent in the center zone as a function of sessions was taken to indicate retention for habituation to stimuli within the test apparatus. The time spent in the center zone decreased as a function of sessions in young and mature C57BL/6NNia mice but failed to show reliable between‐session decreases in old (24–26‐months) C57BL/ 6NNia mice. When compared with the old C57BL/6NNia mice, young NZB/BINJ mice showed similar impairments. Habituation of locomotion was present in all age groups of C57BL/6NNia mice, but absent in NZB/BINJ mice regardless of age. The retention impairments of 2–4 month old NZB/BINJ mice were attenuated when i.p. injections of 0.04–0.16 mg physostigmine/kg were given just following each habituation session. The effectiveness of physostigmine was substantially reduced when injections were delayed by 20 min or longer following each habituation session. The time‐dependent reversal of the aged‐like retention deficits by the cholinesterase inhibitor, physostigmine, suggests that cholinergic modulation of memory storage processes may be impaired in NZB/BINJ mice.
Effects of NMDA antagonists on developmental plasticity in kitten visual cortex
Authors: Rauschecker Josef P. , Egert Ulrich , Kossel Albrecht 
Published: April 2003

AbstractThe existence of Hebb synapses in the visual cortex of young kittens has long been postulated. A mechanism for the correlation of activity in simultaneously active pre‐ and postsynaptic neurons could be provided by the properties of the N‐methyl‐d‐aspartate (NMDA) receptor and its associated Ca2+ channel, which opens in a transmitter‐ and voltage‐dependent manner. We have studied the effects on cortical plasticity of blocking NMDA receptors in different ways with competitive and non‐competitive NMDA antagonists.In our first approach, the non‐competitive NMDA antagonist ketamine, a short‐acting dissociative anaesthetic, was injected systemically after each of a series of brief monocular exposures. This procedure prevented the development of an ocular dominance shift towards the experienced eye in the visual cortex. Other short‐acting anaesthetics, such as xylazine or methohexital, while providing the same depth of anaesthesia, did not have the same effect on ocular dominance plasticity. We conclude, therefore, that ketamine quite specifically interferes with synaptic consolidation in the visual cortex.In order to establish a role of NMDA receptors for cortical plasticity directly in the visual cortex, we performed another series of experiments: 2‐amino‐5‐phosphono‐valerate (APV), a competitive NMDA antagonist, was infused intracortically by means of implanted osmotic minipumps in kittens, which were monocularly deprived for 1–2 weeks. Within a radius of 4–5 mm, the expected ocular dominance shift was prevented or reduced. In addition, however, physiologically determined cell density and responsiveness to visual stimuli were grossly abnormal around the infusion site, and histological cell density was also reduced. Similar effects were found when MK801 (a non‐competitive NMDA antagonist) was used in the same type of experiment.The outcome of both experimental approaches makes it very likely that NMDA antagonists somehow interfere with cortical plasticity. Their mode of action, however, remains ambiguous. Although it is quite possible that blocking of the NMDA channel prevents the Hebbian correlative process necessary for synaptic consolidation, more complex effects, such as an interference with a neurotrophic action normally exerted via the NMDA receptor, may have to be taken into account as well.
Treatment of mammalian spinal cord injury with antioxidants
Authors: Naftchi N. Eric 
Published: April 2003

AbstractAfter spinal cord injury, two groups of cats were treated with a combination of methylprednisolone sodium succinate (MP, 35 mg/kg) and epsilon‐aminocaproic acid (EACA, 350 mg/kg), and guanabenz acetate (0.65 mg/kg). Guanabenz acetate was administered twice daily for 8 weeks. In the first group, the treatment significantly increased blood flow in the abdominal aorta. All cats treated with guanabenz acetate 3 hr after spinal cord contusion had return of micturition and none suffered complete paraplegia. Four animals had partial and the other four had complete motor recovery. A superoxide (O2−) generating system, horseradish peroxidase, decreased [14C]gamma amino butyric acid uptake by mouse cortical slices by 33% but when superoxide dismutase was added to the medium, the uptake was reduced by only 9%. The nerve endings were also protected by superoxide dismutase from morphologic damage by (O2−) as observed by electron microscopy. The agents used in these studies produce their ameliorating effects by virtue of their anti‐inflammatory, antioxidant. and membrane stabilizing properties, and enhancing the regional microcirculation. In addition to having these properties, guanabenz acetate is also an alpha2 adrenoceptor agonist.
Iron‐induced lipid peroxidation and brain injury responses
Authors: Willmore L. James , Triggs William J. 
Published: April 2003

AbstractHead trauma with cerebral contusion causes extravasation of red blood cells, followed by hemolysis and deposition of iron‐containing blood products within the neuropil. Liberation of heme compounds is associated with deposition of hemosiderin, and with gliosis, neuronal loss and occasionally the development of seizures. In this experiment we injected components of red blood cell contents into rat amygdala, and then measured the rate of appearance of products of lipid peroxidation. Injection of microliter volumes of hemin and hemoglobin, with hematoprotoporphyrin and rodent plasma injection and contralateral uninjected tissue as controls, showed that the presence of the iron moiety within the protoporphyrin ring was required to initiate and propagate peroxidation. Free radical reactions initiated by iron or heme deposited within the neuropil may be a fundamental reaction associated with brain injury responses, and possibly with posttraumatic epileptogenesis.
Free radical scavenging systems in developing rat brain
Authors: Shivakumar Bangalore R. , Anandatheerthavarada Hindupur K. , Ravindranath Vijayalakshmi 
Published: April 2003

AbstractBecause the developing brain is subject to high oxygen tension and lacks a functional blood‐brain barrier, anti‐oxidant protection is important to development in the brain. The levels of superoxide dismutase, copper‐zinc superoxide dismutase. manganese superoxide dismutase. catalase, glutathione and related enzymes, namely, glutathione reductase and glutathione peroxidase were determined in rat brain at various stages of development. The levels of thiobarbituric acid reactive products, indicative of lipid peroxidation, were very low at birth and increased to adult levels by the 16th day after birth. Brain glutathione levels displayed significant variations during the first 2 weeks after birth but not thereafter. Catalase activity in developing brain slowly increased over 45 days. Total superoxide dismutase activity in 1‐day‐old rat brain, 80% of the adult rat brain level, subsequently decreased on day 6. Total superoxide dismutase activity, however, increased again in 10‐day‐old rats and remained constant thereafter. While the developmental pattern of manganese superoxide dismutase was similar to that of the total superoxide dismutase, the copper‐zinc superoxide dismutase levels were low at birth and reached adult levels on the 10th day after birth. There was no variation in glutathione reductase and peroxidase levels except for a decrease on day 16 of glutathione reductase and slow increase in adult levels by day 28. The present findings suggest that the overall levels of antioxidant enzymes in the developing brain are comparable to a large extent to those present in the adult brain. In contrast to the developing brain, hepatic levels of glutathione, total superoxide dismutase, manganese superoxide dismutase are significantly lower at birth and increase during development.
Transient appearance of beta‐endorphin immunoreactive cells within the germinal zone of neonatal rat forebrain
Authors: Loughlin Sandra E. , Kornblum Harley I. , Massamiri Tania , Leslie Frances M. 
Published: April 2003

AbstractRecent evidence implicates endogenous opioid systems in basic processes which underlie morphogenesis. The present report describes a population of cells within the germinal zone of the neonatal rat forebrain which are immunoreactive for the opioid peptide β‐endorphin and other peptides derived from the proopiomelanocortin precursor. These cells are present at the time of birth, but are no longer detectable by the sixth postnatal day. They have medially and laterally directed processes which extend to the ventricular wall and across the caudate putamen to its lateral border. Cells of similar morphology and distribution which are immunoreactive for two other proopiomelanocortin peptides, α‐melanocyte stimulating hormone and adrenocorticotrophic hormone, were also observed in similar distributions during the same developmental period. These data are consistent with the hypothesis that cells within the germinal zone transiently synthesize proopiomelanocortin, which is further processed to yield these three peptide products. This finding may be important in understanding the role of proopiomelanocortin‐derived peptides in neural development.
Growth factors attenuate the cholinotoxic effects of ethanol during early neuroembryogenesis in the chick embryo
Authors: Brodie Chaya , Kentroti Susan , Vernadakis Antonia 
Published: April 2003

AbstractThe interaction between growth factors and ethanol on cholinergic neuronal expression was studied in the chick embryo during early neuroembryogenesis using choline acetyltransferase activity as a cholinergic marker. As we have previously reported (Brodie & Vernadakis, Dev. Brain Res.56: 223–228, 1990; Kentroti and Vernadakis, Dev. Brain Res.56: 205–210, 1990), ethanol administration in ovo at embryonic days 1–3 produced a 30% decrease in choline acetyltransferase activity. Nerve growth factor and epidermal growth factor administration alone, at embryonic days 1–3, produced a slight increase in choline acetyltransferase activity of both brain and spinal cord when examined at embryonic day 8. Concomitant administration of either nerve growth factor or epidermal growth factor with ethanol eliminated the decrease in choline acetyltransferase activity produced by ethanol. Moreover, administration of either nerve growth factor or epidermal growth factor at embryonic days 4–7 to embryos pretreated with ethanol at days 1–3 raised choline acetyltransferase activity to a level similar to that observed in controls. Thus the growth factors reversed the ethanol‐induced cholinergic insult and restored the cholinergic population to normal.These findings provide evidence of a possible role of NGF and EGF in interfering with the neurotoxic effects of ethanol during embryogenesis.
Developmental changes in B‐50 (GAP‐43) in primary cultures of cerebral cortex: B‐50 immunolocalization, axonal elongation rate and growth cone morphology
Authors: Ramakers G.J.A. , Oestreicher A.B. , Wolters P.S. , van Leeuwen F.W. , De Graan P.N.E. , Gispen W.H. 
Published: April 2003

AbstractChanges in neurite outgrowth parameters and in the immunolocalization of the neuronal growth‐associated protein B‐50 (GAP‐43) were studied in cultured neocortex as a function of development. In addition, we studied the effects of chronic blockade of bioelectric activity (BEA) with tetrodotoxin (TTX) on these parameters.Axonal outgrowth rate in control cultures reached a maximum at 8 days in vitro (DIV) and declined to a low level at 21 DIV. B‐50 staining shifted from the perikaryon to the axons and growth cones during the first 3 DIV. In axons the intensity of B‐50 staining increased towards the growth cone. Within growth cones, the central/basal region and filopodia were intensely stained, whereas lamellipodia showed only marginal staining. Growth cone size gradually decreased after 3 DIV, due to the successive loss of lamellipodia and filopodia, and became club‐shaped during the second week, until by 21 DIV growth cones were completely lost, and axons started retracting and degenerated. In the central area of the cultures, growth cones also decreased in size with time, but became stabilized as presynaptic elements onto other neurons.Acute addition of TTX did not affect the outgrowth rate at 6 DIV. Chronic TTX treatment led to an earlier retraction and degeneration of axons than in control cultures and to a loss of B‐50‐stained cells and varicosities during the third week, but did not affect growth cone morphology or B‐50 staining. The regressive phenomena are probably due to an increased neuronal cell death shown to occur after chronic TTX treatment. The developmental changes in axonal elongation rate and growth cone morphology may be related to developmental changes in the content and/or phosphorylation of B‐50 (GAP‐43, which are studied in the same cultures in the following paper [Ramakers et al. (1991) Int. J. Devl Neurosci.9, 231–241].
Activity of hippocampal extract on development of [3H]5‐HT high‐affinity uptake in dissociated microcultures
Authors: Azmitia E.C. , Lama P. , Segal M. , Whitaker‐Azmitia P.M. , Murphy R.B. , Zhou F.C. 
Published: April 2003

AbstractSpecific and localized lesions of the 5‐HT fibers in the hippocampus induce homotypic collateral sprouting and enhance serotonergic fiber outgrowth from adult neurons and transplanted fetal tissue. In this study, hippocampal extracts were prepared and applied to primary cultures of fetal serotonergic neurons. The effects of plating density and serum additives were examined. The growth of the serotonergic neurons in the rostral brainstem dissociated cultures were estimated by measuring the specific uptake of [3H]5‐HT. The results indicate the presence of a trypsin‐sensitive factor which is active when prepared fresh at dilutions up to 1/10,000. The factor is higher in hippocampus than cerebellum. Young male tissue contained more activity than either female or aged hippocampus. Although both positive and negative effects are described, higher dilutions of factor (1/1,000) were generally stimulatory in high density cultures while lower dilutions (1/10) were inhibitory in low density cultures. Specific removal of 5‐HT hippocampal afferents with fornix‐fimbria microinjections of 5,7‐dihydroxytryptamine resulted in an initial loss of activity (2 days and 2 weeks) followed by an enhanced activity (2 months) compared to normal hippocampal extract. Several possibilities are discussed as to the identity of the serotonergic growth factor from hippocampal supernatant.
DIfferential effects of prenatal and postnatal acth or nicotine exposure on 5‐HT high affinity uptake in the neonatal rat brain
Authors: King Jean A. , Davila‐Garcia Martha , Azmitia Efrain C. , Strand Fleur L. 
Published: April 2003

AbstractThese studies were designed to examine the differential effects of prenatal or postnatal administration of ACTH 1‐39 and nicotine, on 5‐HT high affinity uptake in brainstem and hippocampal synaptosomes. ACTH was administered prenatally (to pregnant dams) and postnatally to the neonates. Postnatal administration of ACTH significantly increased high‐affinity 5‐HT uptake in the hippocampus and especially the brainstem at both 7 and 21 days after birth. Prenatal ACTH, on the other hand, transiently increased 5‐HT uptake in only the brainstem at 7 days, a change that was reversed at 21 days. While the effects of postnatal nicotine administration were essentially the same as those of postnatal ACTH treatment, prenatal nicotine, unlike ACTH, did not alter 5‐HT uptake in 7‐day‐old rats but did reduce uptake in both tissues at 21 days. The observation that postnatal nicotine mimics the effects of postnatal ACTH and that nicotine stimulates ACTH release, suggests that the postnatal effects of nicotine may be exerted through ACTH.
Fetal alcohol delays the developmental expression of myelin basic protein and transferrin in rat primary oligodendrocyte cultures
Authors: Chiappelli F. , Taylor A.N. , de los Monteros A. Espinosa , de Vellis J. 
Published: April 2003

AbstractThis study has examined the development of immunoreactive myelin basic protein and transferrin in primary glial cell cultures. Cultures were initiated from control and experimental Sprague‐Dawley rats 1–2 days postnatally. Experimental treatment involved exposure to 5% (w/v) ethanol in a liquid diet during the last two weeks of gestation. Prenatal alcohol administration delayed the expression of myelin basic protein and transferrin during the first three weeks postnatally. Other oligodendroglial and astroglial markers were little affected, if at all, by fetal alcohol exposure.
The structural and neurochemical development of the fetal guinea pig retina and optic nerve in experimental growth retardation
Authors: Rees Sandra , Bainbridge Andrew 
Published: April 2003

AbstractIn this study we have examined structural and neurochemical aspects of retinal and optic nerve development in experimentally growth‐retarded fetal guinea pigs following maternal unilateral artery ligation. Eye weight (n = 4) and total retinal area (n = 6) at 62 days gestation (term ∼66 days) were both relatively spared when expressed as a percentage of body weight but in absolute terms were significantly reduced by 18% (P<0.001) and 13% (P<0.05) respectively when compared with age‐matched controls.The numerical density of neurons in the ganglion cell layer was significantly higher at both 52 days (n = 4) and 62 days (n = 4) in growth‐retarded fetuses compared with controls. However, there was no difference between the groups in the total number of neurons in this retinal layer at either age, since retinal areas are reduced in growth retardation. The area of neuronal somata in the ganglion and inner nuclear layers was significantly reduced in growth‐retarded fetuses compared with controls. There was a concomitant reduction in the width of the cellular layers in the retina and also in the plexiform (synaptic) and photoreceptor layers. The growth of the outer segments of the photoreceptor layer was particularly affected in peripheral retina. The higher packing density of cells and the reduced growth of the plexiform layers suggests a reduction in the growth of the neuropile in growth‐retarded fetuses compared with controls. The radial bundling of ganglion cell axons coursing across the retina to enter the optic nerve head was poorly defined in growth retardation. In addition myelination was delayed in the optic nerve with the numerical density of myelinated axons being significantly reduced (P<0.005) in growth‐retarded fetuses compared with controls.There was a significant reduction (P < 0.01) in the number of amacrine cells in the inner plexiform layer expressing Substance P‐like immunoreactivity in growth‐retarded fetuses compared with controls. Glutamate‐like immunoreactivity was most intense in the five laminae of the inner plexiform layer and in the outer plexiform layer and less pronounced in photoreceptors, ganglion cells and their axons. There was no qualitative difference in glutamate immunoreactivity between control and growth‐retarded fetuses in any of these structures.Thus we have shown that intrauterine growth retardation has specific effects on the development of the fetal guinea pig retina, reducing the growth of several types of neurons and their processes and affecting the expression of the neuropeptide substance‐P in amacrine cells.
NMDA receptor levels in chronically depolarized long‐term neonatal rat neocortical explants
Authors: Baker R.E. , Vermeulen J.P. , Boer G.J. 
Published: April 2003

AbstractThe levels of the N‐methyl‐d‐aspartate subclass of glutamate receptor were determined in organotypic neocortical explants chronically exposed to a growth medium containing 25 mM potassium (K25). Explants exposed to 25 mM potassium for 2–3 weeks evinced significantly less binding of the non‐competitive N‐methyl‐d‐aspartate receptor‐associated channel antagonist 125I‐MK801 than did age‐matched controls. Surprisingly, cultures that were returned to control growth medium for a further 2 or 7 days showed even less binding of the ligand. The Kd values of binding were not affected and were similar to those of fresh postnatal cortex. The maximum number of binding sites did not vary between postnatal day 6 and 14 days in vitro control cultures, but were significantly less than those measured at postnatal day 20 (comparable age: 14 days in vitro).Several conclusions can be drawn from these findings: (i) the density of the N‐methyl‐d‐aspartate sub‐class glutamate receptor does not attain in vivo levels under the present culturing conditions, but remains at those levels associated with the stage of development at which the tissue was brought into culture, (ii) chronic depolarization results in a drastic reduction in N‐methyl‐d‐aspartate receptor density, which is not compensated for after the return to normal growth conditions, (iii) depolarization selectively inhibits cellular maturation of the neocortex (but not survival, as shown previously), including neurotransmitter receptor production and/or insertion into membranes or assembly.