bluuebunny/crossref_metadata_2025_split huggingface dataset:
Astroglial plasticity in hemizygous and heterozygous jimpy mice
Authors: Best Todd T. , Skoff Robert P. , Bartlett William P. 
Published: April 2003

AbstractGliosis is a common phenomenon which occurs in many human diseases and in experimentally altered nervous tissue. The factors activating astrocytes to respond are still unclear but recent evidence suggests that diverse substances can provoke a gliotic response. This paper describes the nature of the gliosis in the myelin deficient jimpy and relates these findings to other recent studies of experimentally induced demyelination in which gliosis is a prominent feature of the disorder.In jimpy males, an astroglial hypertrophy which consists of an increase in the number of cell processes can be demonstrated by both electron microscopy and immunocytochemistry using antibodies to glial fibrillary acidic protein. Increased glial fibrillary acidic protein staining in the white matter of jimpy males correlates with the normal time of myelination in different tracts. The immunostaining is not, however, restricted to white matter. Increased staining can be demonstrated in spinal cord grey matter when hardly any myelinated fibers are present, it is especially prominent around blood vessels of both white and grey matter, and is found in the corpus callosum and in the underlying subventricular zone shortly before or at the time myelination begins in this tract. These observations suggest that the hypertrophy is not simply a response by the astrocyte to the absence of myelin sheaths.While an astroglial hypertrophy is dramatic in jimpy males, quantitative counts of astrocytes and electron microscopic autoradiograms do not reveal an increase in the total number of this cell type. These findings suggest that hyperplasia and hypertrophy of astrocytes may be under separate regulatory control with different factors involved in each phenomenon.In the female carriers of the jimpy gene, myelination is temporarily delayed during postnatal development but after several months, the amount of myelin, whether measured morphometrically or biochemically, reaches normal levels. In the white matter of the young female carrier, staining for glial fibrillary acidic protein is increased in terms of the number of processes and the total volume of neuropil but a normal pattern of staining is observed within a year. These and other observations suggest that the glial hypertrophy in the young mosaic is temporary and that regression and reorganization of glial processes takes place as myelination proceeds.
Neuron‐specific enolase during the development of the organ of corti
Authors: Whitlon Donna S. , Sobkowicz Hanna M. 
Published: April 2003

AbstractNSE immunoreactivity has been studied in the organ of Corti of the developing mouse from birth to 21 days. NSE immunohistochemical stain is observed in spiral ganglion cells, in nerve fibers and in nerve endings of inner and outer hair cells, and in both populations of sensory cells. Spiral ganglion cells in lower and central parts of the ganglion stain for NSE at birth, but all nerve cells are stained by day 4. Radial and spiral fibers and the endings on inner hair cells stain at birth, but the nerve endings on outer hair cells develop NSE between days 3 and 6. The inner and outer hair cells are NSE‐positive at day 2 but the NSE immunoreactivity in the outer hair cells decreases at the end of the second week until the cells become negative. The NSE stain in the neuronal pathways of the inner and outer hair cell regions increases for about 19 days, showing a predominant accumulation in neuronal endings. The data suggest that the development of NSE expression in the organ of Corti reflects the nascence and maturation of the synaptic contacts.Spiral neurons, their fibers and endings as well as inner and outer hair cells express NSE in the isolated organ of Corti in culture. Variability of stain among the different cell populations indicates a role of local factors in the regulation of NSE expression.
Ontogenetic and pharmacological dissociation of various components of locomotor activity and habituation in the rat
Authors: Laviola Giovanni , Renna Giuseppe , Bignami Giorgio , Cuomo Vincenzo 
Published: April 2003

AbstractSprague‐Dawley‐derived male rats were used to investigate locomotor activity and habituation in an open field as a joint function of developmental age (2–6 weeks), pattern of test exposure (single 30‐min test vs three 5‐min tests at 24‐hr intervals), and treatment conditions (i.p. saline, d‐amphetamine sulfate 1mg/kg, or scopolamine hydrocloride 0.5 mg/kg). No‐drug animals showed low activity levels in both tests at the end of the second week, intermediate response rates at the end of the third week, and a typical adult‐like pattern at later ages (high initial activity followed by marked withinsession or between‐session habituation). Amphetamine effects varied considerably depending jointly on age and type of test. At the end of the second week, the drug hyperactivity was much more marked in successive brief tests than in the single extended test. One week later, the response increase was rather uniform in both tests. At the end of the fourth week, the sensitivity profile was reversed, consisting of a large drug effect in the extended test but not in successive brief tests. Scopolamine was still without effects at this age, while a typical hyperactivity was produced by the drug in 6‐week‐old animals. These data show that, at least in the rat strain used, the functional maturation of muscarinic regulatory systems is not a necessary condition either for the appearance of an adult‐like response pattern, or for the occurrence of the age‐ and test‐related changes of the amphetamine profile. Overall, the data point (i) to the existence of some mechanism serving the suppression of locomotion during the initial phase of exposure to a novel environment at 2 weeks and (ii) to separate mechanisms for within‐session and between‐session habituation developing at later stages.
Isolated hippocampal neurons in cryopreserved long‐term cultures: Development of neuroarchitecture and sensitivity to NMDA
Authors: Mattson Mark P. , Kater S. B. 
Published: April 2003

AbstractIsolated neurons in long‐term culture provide a unique opportunity to address important problems in neuronal development. In the present study we established conditions for cryopreservation and long‐term primary culture of isolated embryonic hippocampal neurons. This culture system was then used for initial characterizations of the development of neuroarchitecture and neurotransmitter response systems. Cryoprotection with 8% dimethylsulfoxide, slow freezing, and rapid thawing provided high‐yield cultures which appeared normal in terms of cell types, mitotic ability, axonal and dendritic outgrowth, and sensitivity to glutamate neurotoxicity. A reduced medium volume and moderate elevation in extracellular K+ to 20 mM promoted survival of isolated neurons through 3 weeks of culture. The outgrowth of axons and dendrites in pyramidal‐like neurons was found to differ over a 3‐week culture period such that axons continued to grow at a relatively constant rate while dendritic outgrowth slowed during the second week and ceased by the end of week 3. Developmental changes were also observed in the sensitivity of pyramidal neurons to glutamate neurotoxicity; functional kainate/ quisqualate receptors were present during the first week of culture, while responses to N‐methyl‐d‐aspartic acid (NMDA) did not appear until the second week. The technologies for cryopreservation and long‐term culture of isolated hippocampal neurons reported here provide a useful system in which to address a variety of problems in developmental neuroscience.
Expression of the three opioid receptor subtypes μ, δ and κ in guinea pig and rat brain cell cultures andin vivo
Authors: Barg Jacob , Levy Rivka , Simantov Rabi 
Published: April 2003

AbstractExpression of the three opioid receptor subtypes mu, delta and kappa in aggregating cell cultures prepared from embryonic guinea pig or rat brains was compared with thein vivo expression of the receptors in the brain of developing and adult animals of the same species. At the day of culturing, one third of the receptors in the brain of guinea pig embryos were of the kappa type. In culture, however, the aggregating brain cells acquired within 14 days a high percentage (75%) of kappa receptors. As only 28% of the receptors in the adult guinea pig brain are of this subtype, an attempt was made to further analyse the specificity of this developmental process.In guinea pig, the 2‐fold increase in kappa receptors in culture was accompanied with a decline in both the percentage and the density (per protein) of mu and delta subtypes. In contrast, a marked increase in delta receptors was observed in rat whole brain, forebrain or hindbrain cultures. Thus, the developmental pattern of the three receptor subtypes in rat brain cultures, but not in guinea pig, was similar to thatin vivo. These and additional experiments suggest that at the developmental stage taken to prepare the cultures, neurons expressing opioid receptors were already programmed in the rat but not in guinea pig brain.
Proliferation‐related responses in rat astrocytes to epidermal growth factor
Authors: Huff Kenneth R. , Schreier Wayne , Ibric Luminita 
Published: April 2003

AbstractThe signals which regulate the proliferation of astrocytes have relevance to both normal developmental processes and abnormal states of gliosis or glial tumor formation. We have extended studies of astrocyte proliferation and related responses in primary cultures of rat telencephalic cortical astrocytes as a result of treatment with epidermal growth factor. Epidermal growth factor stimulates the rate of DNA synthesis five fold and maintains the rate of protein synthesis. The stimulation occurs at a dose of 2 ng/ml and is greater in higher density cultures than in lower density cultures, perhaps representing a relative starvation for the growth factor. The astrocyte response is still present even after being cultured 31/2 weeks in serum‐free and non‐growth factor or hormone‐supplemented media. Combined immunofluorescence and thymidine autoradiography disclose that glial fibrillary acidic protein containing cells are the cells synthesizing DNA in response to the growth factor, and combined rhodamine and fluorescein‐linked stains disclose that epidermal growth factor is in the glial fibrillary acidic protein containing cells. Proliferation‐related 2‐deoxyglucose uptake is stimulated at approximately the same dose as DNA synthesis is stimulated, but the time course is relatively slow, maximizing at 48 hr. Ornithine decarboxylase is stimulated in 6 hr indicating more rapid nuclear stimulation by the signal. In conclusion, epidermal growth factor has a clear direct interaction with glial fibrillary acidic protein‐containing cells which is greater in higher density cultures, is still present in long‐quiescent cells, and includes DNA synthesis, cell cycle progression, hexose uptake, and polyamine synthesis.
Postnatal development of two nicotinic cholinergic receptors in seven mouse brain regions
Authors: Fiedler Eric P. , Marks Michael J. , Collins Allan C. 
Published: April 2003

AbstractThe developmental profiles for binding of α‐[125I]bungarotoxin and l‐[3H]nicotine to putative nicotinic cholinergic receptors were determined in seven mouse brain regions. The overall pattern of development of α‐bungarotoxin binding was similar in all of the regions. Neonatal binding values tended to be greater than those observed in adult brain regions. Maximal binding occurred within 10 days of birth and adult binding values were reached by 20 days of age. The patterns of development of nicotine binding in each of the seven brain regions differed according to region. Gross similarities in developmental profiles for nicotine binding were found among the more caudal and among the more rostral regions. In hindbrain and cerebellum, maximal nicotine binding was found at birth (5 days of age in cerebellum); binding declined approximately 4‐fold by 20 days and remained relatively constant thereafter. In midbrain and hypothalamus, a less extensive decrease in nicotine binding occurred from birth to adulthood (midbrain, 25%; hypothalamus, 50%). Nicotine binding in hippocampus and cortex remained unchanged between birth and adulthood. The developmental pattern for nicotine binding in striatum differed from that found in the other brain regions. At 5 days of age, binding was about 65% of adult binding, which was reached at 30 days of age. In most of the brain regions the developmental profile for α‐bungarotoxin binding was different from that of nicotine. This difference was especially notable in striatum, where adult nicotine binding was higher than neonatal nicotine binding, whereas adult α‐bungarotoxin binding was lower than neonatal α‐bungarotoxin binding.
Synapse formation on trochlear motor neurons under conditions of increased and decreased cell death during development
Authors: Sohal G.S. , Kumaresan K. , Hirano S. , Ali M.M. 
Published: April 2003

AbstractThere is a normally occurring death of about half of the trochlear motor neurons during development. Early removal of the target muscle results in death of almost all neurons whereas neuromuscular blockade prevents neuron death. The present investigation was undertaken to determine whether the number of central afferent synapses on motor neurons is altered under conditions which either accentuate cell loss or rescue neurons. The sole peripheral target of innervation of the trochlear motor neurons, the superior oblique muscle, was extirpated in duck embryos before the motor axon out‐growth begins. The neuromuscular blockade was achieved by application of paralyzing dosages of alpha bungarotoxin on to the vascularized chorioallantoic membrane. This treatment began prior to the onset of cell death and embryos were treated daily throughout the period of cell death. Brains were processed for electron microscopy and quantitative observations were made on synapses at the onset, during the period of, and at the end of cell death. It was found that there was no significant difference in the number of synapses on neurons following target removal, following neuromuscular blockade, and those developing normally. This observation indicates that the number of central afferent synapses on cell soma is not altered under conditions which either decrease or increase neuron survival. These results suggest that the synapse number per se may not be directly involved in the process of naturally occurring cell death. The results also suggest that the number of synapses on trochlear motor neurons is independent of interactions with the target.
Individual C6 glioma cells migrate in adult rat brain after neural homografting
Authors: Goldberg William J. , Laws Edward R. , Bernstein Jerald J. 
Published: April 2003

AbstractCultured C6 glioma cells were prelabeled with the plant lectin Phaseolus vulgaris leucoagglutinin (PHAL) and grafted as a cell suspension (106 cells in 5.0 μl) into freshly made cortical implantation pockets in adult host rats. Animals were killed 1–21 days post‐implantation (DPI). The brains were removed, dehydrated, embedded in paraffin and sectioned at 8 μm. Paraffin sections were processed for light level immunofluorescent double labeling for PHAL, a marker for graft derived cells, and glial fibrillary acidic protein (GFAP), a specific marker for C6 glioma cells and astrocytes. Cells positive for both PHAL and GFAP were graft‐derived C6 cells. By 7 DPI a large mass developed which extended above the surface of the brain and invaded (displacement of host tissue by a cell mass) the host parenchyma. This mass increased in size over the next 14 days. The invading tumor mass contained double labeled cells at all time periods examined. In addition to the invasion process, grafted C6 cells spread through the host parenchyma by migration (movement of single cells). Individual graft‐derived C6 (GFAP/PHAL positive) cells migrated into host cortex surrounding the implantation pocket, corpus callosum ventral to the implantation pocket, ipsilateral internal capsule and bilaterally in the habenula.
Recovery of vestibular function in young guinea pigs after streptomycin treatment. Glutamate decarboxylase activity and nystagmus response assessment
Authors: Meza Graciela , Solano‐Flores Luis P. , Poblano Adrián 
Published: April 2003

AbstractFifty‐day streptomycin (STP) treatment in guinea pigs causes specific vestibular hair cell (VHC) types I and II (HCI; HCII) degeneration, depletion of glutamate decarboxylase (GAD) and a gradual disappearance of postrotatory nystagmus response (PRNR), which is a sign of vestibular function alteration. In order to look for a possible spontaneous reversibility and its time course guinea pigs receiving 300 mg/kg STP daily were monitored for PRNR and vestibular GAD loss. Once PRNR was lost, STP was interrupted and the animal was allowed to recover; at the time that PRNR was completely reestablished, vestibular GAD was measured.PRNR was lost within 22–25 days of STP treatment. Vestibular GAD showed a loss that, with time of treatment, gave two slopes: a fast decrement (45% in 20 days) and a slow one (40% in the remaining 30). Stopping of the STP treatment after 22–25 days and animal recovery resulted in the return of both PRNR and GAD activity 22 days after STP stoppage.These results suggest two STP‐susceptible GAD‐containing VHC populations, one more sensitive than the other, possibly HCI followed by hair cell II (HCII). As hypothetic HCI loss and PRNR disappearance is simultaneous, the important role of the former for vestibular function could be inferred. Interruption of STP treatment after PRNR loss results in a long range restoration of both GAD activity and vestibular function, and thus recovery of HCI, the first evidence of its occurrence in a mammalian vestibule, could be suggested. The intimate mechanism of this recovery remains to be seen.
Age‐related changes in NMDA‐induced [3H]acetylcholine release from brain slices of senescene‐accelerated mouse
Authors: Zhao Xue‐Hui , Kitamura Yoshihisa , Nomura Yasuyuki 
Published: April 2003

AbstractFrom the brain slices of normal mice (ddY strain, subcloned from dd strain in National Institute of Health in Japan), N‐methyl‐d‐aspartic acid (NMDA) at 0.01~1 mM evoked [3H]acetylcholine (ACh) release in a concentration dependent manner. [3H]ACh release evoked by 1 mM NMDA was significantly inhibited by 2‐amino‐5‐phosphonovaleric acid (APV), phencyclidine (PCP) and 5‐methyl‐10,11‐dihydroxy‐5H‐dibenzo[a,d]cyclo‐hepten‐5,10‐imine maleate (MK‐801). The effects of NMDA were not seen in the Ca2+ free medium and were inhibited by physiological concentration (0.83 mM) of Mg2+. NMDA seems to cause ACh release from nerve terminals through the receptorion channel mediated mechanism in the mouse brain. Based upon these results, we determined the activity of a high K+‐ or NMDA‐evoked [3H] ACh release using prone/8 strain of senescence‐accelerated mouse (SAM‐P/8) (a murine model of accelerated aging and memory dysfunction) and SAM‐resistance/1 strain (SAM‐R/1) (normal aging mice as the control) and these release activities were compared between both strains and during aging. [3H]ACh release evoked by 30 mM KCl was significantly lower than that of age‐matched SAM‐R/1 at 9 and 12 months. NMDA evoked the [3H]ACh release at 2, 6, 10 and 14 months in R/1 mice. In SAM‐P/8 mice the activity of NMDA‐evoked release was seen at 2 months, but markedly decreased afterwards. Nonsignificant difference was observed on the uptake of [3H]choline and on the spontaneous release of [3H]ACh between SAM‐P/8 and SAM‐R/1 strains, and during aging. These results suggest: (1) NMDA receptor‐ion channels are involved in the ACh release from nerve terminals in the CNS; (2) the NMDA‐evoked ACh release is decreased after 6 months in SAM‐P/8 mice but not in SAM‐R/1 mice; and (3) the high K+‐evoked ACh release is decreased at an earlier age in SAM‐P/8 than it is in SAM‐R/1. These results suggest that the NMDA‐ and cholinergic‐system in the CNS seems to be deficient in SAM‐P/8 and that this deterioration may be a possible cause for their dysfunction of learning and memory.
Morphological correlates of physiological responses in partially denervated mouse muscle during aging
Authors: Fahim Mohamed A. 
Published: April 2003

AbstractTo evaluate the effect of partial denervation on age changes, morphological and physiological parameters were studied in young versus old extensor digitorum longus (EDL) muscles. The aims of this study were to elucidate synaptic maintenance in general and specifically to assess the adaptability of motor neurons from young and old animals to an enlarged field of innervation. Partial denervation was carried out in two groups of 30–40 g mice, aged within 6 or 24 months, by sectioning of the nerve supplying EDL muscle under methoxyfluorane anaesthesia. Sham operations were carried out on additional animals which served as controls. Five weeks' post‐surgery, the safety factor of synaptic transmission was estimated by dividing the nerve‐evoked twitch tension generated in 1 mM Ca2+ Krebs by that generated in 2.5 mM Ca2+ Krebs. Low Ca2+ Krebs caused a more pronounced decline in twitch tension in young control EDL muscles than old control. After partial denervation, young EDL twitch tensions were not significantly different while old were 20% of those in normal Krebs. Zinc Iodide Osmium (ZIO) stained nerve terminal parameters were significantly increased with aging. After partial denervation, nerve terminal areas were 46 and 39% larger in young and old mice, respectively, compared to their corresponding controls. Present data suggest that motor neurons of old mice are unable to develop and maintain an enlarged field of innervation.
Peripheral nerve regeneration: Role of growth factors and their receptors
Authors: Raivich Gennadij , Kreutzberg Georg W. 
Published: April 2003

AbstractGrowth factors play a central role in the regulation of normal and injury‐induced regenerative cell growth. The purpose of this article is to summarize the available data on the expression of different growth factors and their receptors in the injured peripheral nervous system and to discuss their possible role in promoting peripheral nerve regeneration.
Environmental regulation of brain trophic interactions
Authors: Black Ira B. 
Published: April 2003

AbstractEmerging evidence indicates that trophic interactions that influence brain development are critical throughout life, mediating processes as diverse as learning, memory and regrowth after injury. This review summarizes recent work suggesting that impulse activity regulates trophic interactions in the brain, allowing the conversion of millisecond‐to‐millisecond signalling into long‐term changes in neural circuit function. For example, depolarizing stimuli regulate trophic factor gene expression, an effect mediated by excitatory transmitters. Responsiveness to trophic factors is also regulated by activity, since depolarization increases the expression of trophic receptor genes. Moreover, different excitatory transmitter receptor subtypes mediate trophic or regressive effects, allowing a neural system to precisely memorialize excitatory or inhibitory experiences. A number of open questions are articulated to define potential future directions.