bluuebunny/crossref_metadata_2025_split huggingface dataset:
Emx and Otx homeobox genes in the developing mouse brain
Authors: Boncinelli Edoardo , Gulisano Massimo , Broccoli Vania 
Published: January 2005

AbstractWe have analyzed the expression of four mouse homeobox genes related to two Drosophila genes expressed in the developing head of the fly. Two of these genes, Emx1 and Emx2, are related to empty spiracles, and two genes, termed Otx1 and Otx2, are related to orthodenticle. These genes are all expressed in the developing rostral brain of E10 mouse embryos and their expression domains can be compared. Otx2 is expressed in all dorsal and most ventral regions of telencephalon, diencephalon, and mesencephalon. The Otx1 expression domain is similar to that of Otx2, but smaller and contained within it. The Emx2 expression domain is comprised of dorsal telencephalon and small diencephalic regions, both dorsally and ventrally. Finally, Emx1 expression is exclusively confined to the dorsal telencephalon. At the time when regional specification of major brain regions takes place, the expression domains of the four genes appear to be continuous regions contained within each other in the sequence Emx1 <Emx2 < Otx1 < Otx2. The first appearance of transcripts of the four genes is also sequential: Otx2 is expressed first (E5.5), followed by Otx1 and Emx2 (E8–8.5), and finally by Emx1 (E9.5). It is tempting to speculate about a possible role of the four genes in establishing and/or signalling the limits of the various embryonic brain regions in a discrete progressive process with its center in the dorsal telencephalon. © 1993 John Wiley & Sons, Inc.
Synapse elimination from the mouse neuromuscular junction in vitro: A non‐hebbian activity‐dependent process
Authors: Nelson Phillip G. , Fields R. Douglas , Yu Chang , Liu Yuan 
Published: January 2005

AbstractThe effect of action potentials on elimination of mouse neuromuscular junctions (NMJ) was studied in a three compartment cell culture preparation. Axons from superior cervical ganglion or ventral spinal cord neurons in two lateral compartments formed multiple neuromuscular junctions with muscle cells in a central compartment. The loss of synapses over a 2–7‐day period was determined by serial electrophysiological recording and a functional assay. Electrical stimulation of axons from one side compartment during this period, using 30‐Hz bursts of 2‐s duration, repeated at 10‐s intervals, caused a significant increase in synapse elimination compared to unstimulated cultures (p< 0.001). The extent of homosynaptic and heterosynaptic elimination was comparable, i. e., of the 226 functional synapses of each type studied, 111 (49%) of the synapses that had been stimulated were eliminated, and 87 (39%) of unstimulated synapses on the same muscle cells were eliminated. Also, simultaneous bilateral stimulation caused significantly greater elimination of synapses than unilateral stimulation (p< 0.005). These observations are contrary to the Hebbian hypothesis of synaptic plasticity. A spatial effect of stimulus‐induced synapse elimination was also evident following simultaneous bilateral stimulation. Prior to stimulation, most muscle cells were innervated by axons from both side compartments, but after bilateral stimulation, muscle cells were predominantly unilaterally innervated by axons from the closer compartment. These experiments suggest that synapse elimination at the NMJ is an activity‐dependent process, but it does not follow Hebbian or anti‐Hebbian rules of synaptic plasticity. Rather, elimination is a consequence of postsynaptic activation and a function of location of the muscle cell relative to the neuron. An interaction between spatial and activity‐dependent effects on synapse elimination could help produce optimal refinement of synaptic connections during postnatal development. © 1993 John Wiley & Sons, Inc.
Calcium‐dependent postsynaptic exocytosis: A possible mechanism for activity‐dependent synaptic modulation
Authors: Dan Yang , Poo Mu‐ming 
Published: January 2005

AbstractElevation of cytosolic Ca2+ level in the postsynaptic cell is critical for the induction of many forms of activity‐dependent synaptic modulation. Based on our recent evidence that in muscle cells and fibroblasts constitutive exocytosis is increased by elevating cytosolic Ca2+ levels, we hypothesize that Ca2+ ‐dependent exocytosis at the postsynaptic site may provide a mechanism for a localized, activitt‐dependent synaptic modulation. 1994 John Wiley & Sons, Inc.
Regeneration and molting effects on a proprioceptor organ in the dungeness crab, Cancer magister
Authors: Hartman H. Bernard , Cooper Robin L. 
Published: January 2005

AbstractDecapoda Crustacea molt in order to grow; some species, such as the Dungeness crab Cancer magister, achieve a very large size. Does sendory neuron hyperplasia in internal proprioceptors accompany this growth? To determine this, neurons in propodite‐dactylopodite (PD) chordotonal organs were counted in first walking legs of juvenile (5th through 9th instar) and adult (10th through 13th instar) C. magister. We found that the PD organs of J5 crabs have about 56 neurons; the number increases to about 61 neurons in J6 crabs. Significant hyperplasia now occurs because an average of 79 neurons are found in the PD organs of J7 crabs. Little to no hyperplasia accompanies the several succeeding juvenile and adult molts (ca. 82–86 neurons are present). Because autotomized limbs are regenerated upon molting, we also examined how the number of PD organ neurons in regenerated legs compare with those of pristine legs. Newly regenerated legs (termed 1st stage regenerates) have fewer sensory neurons than do their contralateral pristine partners (65 vs 81); larger regenerated legs which have attained nearly normal size as a result of additional molts (2nd stage regenerates) still have fewer neurons than their pristine partners (69 vs 81). Additionally, in contrast to those of pristine walking legs, the elastic strand of PD organs from 1st stage regenerates is a misshapen sheet containing a cluster of small neurons with no obvious functional organization. Nonetheless, neurophysiological recordings indicate that all the receptor types typical for pristine legs (movement and position cells) are represented. The PD organs of 2nd stage regenerates differentiate to the shape and neuronal organization of pristine legs. © 1994 John Wiley & Sons, Inc.
Thyroxine treatment and the recovery of pyramidal cells of the cerebral cortex from changes induced by juvenile‐onset hypothyroidism
Authors: Ruiz‐Marcos Antonio , Cartagena‐Abella Pedro , Martinez‐Galan Juan Ramón , Calvo Rosa , de Escobar Gabriela Morreale , del Rey Francisco Escobar 
Published: January 2005

AbstractIn contrast to the permanent alterations resulting from neonatal hypothyroidism, the effects of juvenile‐onset hypothyroidism on the number and distribution of spines along the apical shaft by pyramidal neurons of the visual cortex appeared to be potentially reversible with adequate thyroxine (T4) therapy (Ruiz‐Marcos et al., 1980, Brain Res. 185:91–102 and 1982, Brain Res. 239:559–574). Treatment with 0.20 or 1.50 μg T4/100 g body weight per day had, however, only partially reversed the changes induced by juvenile‐onset hypothyroidism. We here study whether or not a higher dose of T4 would totally reverse these effects. A group of rats were thryoid‐ectomized at 40 days of age, and injected once daily with placebo or T4 (1.75 μg/100 g BW per day) from 70 to 90 days of age, a group on 1.50 μg being included to compare with previous results. Spine number and distribution‐were measured, as well as the concentrations of T4 and triidothyronine (T3) in plasma, liver and brain. The activities of two hepatic enzymes were measured as thyroid hormone‐sensitive biological end points. The 1.75‐μg dose restored spine number to 88% of normal values and was markedly more effective than the 1.50‐μg dose, which increased it to 68%. The degree of restoration appeared related to the concentration of T3. It is concluded that the changes caused by juvenile‐onset hypothyroidism in the number and distribution of dendritic spines along the apical shafts of pyramidal neurons are reversible, although complete restoration might require a higher dose of T4, a continuous mode of administration, or longer period of treatment. 1994 John Wiley & Sons, Inc.
Sexual differentiation of brain and behavior in the zebra finch: Critical periods for effects of early estrogen treatment
Authors: Adkins‐Regan E. , Mansukhani V. , Seiwert C. , Thompson R. 
Published: January 2005

AbstractIn order to determine the critical period(s) during which estrogen alters sexually dimorphic behavior and neuroanatomy in zebra finches (Poephila guttata), nestlings were injected daily 20 μg estradiol benzoate (EB) during posthatching week 1, week 2, week 3, or weeks 1, 2, and 3. At 7 months of age, birds were implanted with testosterone propionate and tested with female partners for singing, dancing, and copulatory mounting. Brains were subsequently processed for morphometry, and the volumes of the song system nuclei HVC, area X, and RA and the soma sizes and densities of neurons in RA were determined. Males given EB during week 1 failed to mount. Females given EB during week 1 were fully masculinized with respect to dancing and RA neuron soma size and density, and were partially masculinized with respect to song nuclei volumes and singing. Treatment beginning after week 1 was ineffective or less effective for all measures. Only for RA neuron measures was treatment for all three weeks more effective than week 1 treatment. Thus the first post‐hatching week is the most influential period of those tested for effects of exogenous estrogen on sexual differentiation in this species, and is a period during which both masculinization of females and demasculinization of males is possible. 1994 John Wiley & Sons, Inc.
Differential neural regulation of a neuromuscular junction‐associated antigen in muscle fibers and Schwann cells
Authors: Astrow Stephanie H. , Son Young‐Jin , Thompson Wesley J. 
Published: January 2005

AbstractMonoclonal antibodies 3G2 and 4E2 recognize a postsynaptic component of rat neuromuscular junctions. In contrast to many other postsynaptic junctional antigens, expression of this antigen is nerve‐dependent: immunoreactivity disappears form junctions following denervation and returns upon reinnervation (Astrow et al., 1992 J. Neurosci. 12:1602–1615). Here we show that the epitope is also expressed by Schwann cells and that this expression is also neurally regulated. Weak mAb 3G2/4E2 immunoreactivity was found in myelinating Schwann cells but was not detected in either nonmyelinating Schwann cells or in terminal Schwann cells at the neuromuscular junction. Following axotomy, immunoreactivity increased in myelinating Schwann cells, and nonmyelinating and terminal Schwann cells became immmunopositive. Moreover, the immunoreactivity in terminal Schwann cells revealed their extensive sprouting in response to denervation (Reynolds and Woolf, 1992, J. Neurocytol. 21:50–66). After nerve regeneration, mAb 3G2/4E2 immunoreactivity in all Schwann cells returned towards normal: it disappeared from temrinal Schwann cells, returned to low levels in myelinating Schwann cells, and decreased in nonmyelinating Schwann cells. Immunoblots of axotomized nerve and cultured muscle fibers revealed the same set of immunoreactive bands. Therefore, Schwann cells and muscle fibers share the expression of an epitope that is under neural control, but is regulated differently at each site. In Schwann cells, the presence of the nerve suppresses expression of the epitope, whereas in muscle fibers, the nerve terminal promotes this expression. The differential regulation of mAb 3G2/4E2 immunoreactivity in terminal Schwann cells and muscle fibers suggests that the epitope may be involved in interactions between nerve terminals and these cells. 1994 John Wiley & Sons, Inc.
Cell surface contact mediates neuronal recognition and synapse formation between two identified leech neurons
Authors: Merz David C. , Drapeau Pierre 
Published: January 2005

AbstractAn early event in the formation of the serotonergic synapse by the Retzius (R) onto the pressure‐sensitive (P) neurons of the leech is the elimination of an extrasynaptic response to transmitter from sites of contact on the postsynaptic cell. This event during synapse formation is cell‐specific in that it is elicited in vitro by contact with the presynaptic R cell but not with other neurons. In the study reported here, we investigated the nature of this interaction between R and P neurons. The loss of the extrasynaptic response of the P cell was elicited by contact with R cells fixed in a mild paraformaldehyde solution, but not by R cells treated with the proteolytic enzyme trypsin prior to fixation. As well, a variety of lectins were assayed for their ability to interfere with synapse formation. The transmitter responses of P cells plated on lectin‐coated substrates were unaffected. However, exposure of the R cell to the lectin wheat germ agglutinin (WGA), but not to other lectins, prior to pairing prevented the loss of the extrasynaptic response in contacted P cells and blocked the formation of the RP synapse in culture. We conclude that recognition by the P cell of the R cell during synapse formation may be mediated by an R cell‐specific surface protein which binds wheat germ agglutinin. 1994 John Wiley & Sons, Inc.
Identification of CDK‐ and cyclin‐like proteins in the eye of Bulla gouldiana
Authors: Krucher Nancy A. , Roberts Michael H. 
Published: January 2005

AbstractThe ocular circadian rhythm in the eye of Bulla gouldiana is generated by a rhythm in membrane potential of retinal neurons that is driven by alterations in potassium conductance. Since potassium conductance may be modulated by the phosphorylation of potassium channels, the circadian rhythm may reflect rhythmic changes in protein kinase activity. Furthermore, the circadian rhythm recorded from the Bulla eye can be phase shifted by agents that affect protein synthesis and protein phosphorylation on tyrosine residues. Interestingly, the eukaryotic cell division residues. Interestingly, the eukaryotic cell division cycle is generated by similar processes. Rhythmic cell division is regulated by periodic synthesis and degradation of a protein, cyclin, and periodic tyrosine phosphorylation of a cyclin‐dependent kinase (cdk), p34cdc2. The interaction between these two proteins results in rhythmic kinase activity of p34cdc2. Both cyclin and p34cdc2 are pat of two diverse gene families, some of whose members have been localized to postmitotic cell types with no function yet determined. In the current work, we identify proteins similar to the cdks and cyclin in the eye of Bulla. Neither of these ocular proteins are found in mitotic cells in Bulla, and the cdk‐like protein (p40) is specific to the eye. Furthermore, the concentration of the cyclin‐like protein (p66) is affected by treatments that phase shift the circadain rhythm. The identification of cdk and cyclin‐like proteins in the Bulla eye is consistent with the hypothesis that the biochemical mechanism responsible for generating the ocular circadian rhythm in Bulla is related to the biochemical mechnism that regulates the eukaryotic cell division cycle. 1994 John Wiley & Sons, Inc.
Activity‐dependent and hormonal regulation of neurotrophin mRNA levels in brain–implications for neuronal plasticity
Authors: Lindholm Dan , Castrén Eero , Berzaghi Maria , Blöchl Andrea , Thoenen Hans 
Published: January 2005

AbstractThe neurotrophins exhibit neurotrophic effects on specific, partially overlapping populations of neurons both in the peripheral and the central nervous system (CNS). In the periphery, they are synthesized by a variety of nonneuronal cells, and their synthesis seems to be independent of the neuronal input. In contrast, in the CNS all neurotrophins are expressed under physiological conditions primarily by neurons. The production of NGF and BDNF is controlled by neuronal activity: up‐regulation by glutamate and acetylcholine, down‐regulation by gamma‐aminobutyric acid. In contrast, NT‐3 regulation is independent of neuronal activity, but it is up‐regulated by thyroid hormones and BDNF. The latter observation suggests that NT‐3 might be controlled indirectly by neuronal activity via BDNF. In peripheral nonneuronal tissues, glucocorticoid hormones down‐regulate NGF mRNA levels both in vitro and in vivo. In contrast, in the CNS, neuronal production of NGF is enhanced by glucocorticoids. The rapid regulation of NGF and BDNF by subtle physiological stimuli together with the recent demonstration that the neurotrophin release neurotransmitters such as acetylcholine opens up interesting perspectives for the function of neurotrophins as mediators of neuronal plasticity. 1994 John Wiley & Sons, Inc.
Dorsoventral patterning of the avian mesencephalon/metencephalon: Role of the notochord and floor plate in suppressing Engrailed‐2
Authors: Darnell Diana K. , Schoenwolf Gary C. 
Published: January 2005

AbstractTranscription factors that are spatially and temporally restricted within the embryo may be used for dorsoventral and rostrocaudal positional information during development. The Engrailed‐2 (En‐2) gene is expressed across the mesencephalon/metencephalon (mes/met) boundary in the cerebellar primordium with strong dorsolateral expression and limited expression in the floor plate. In a previous experiment we demonstrated that, after removal of Hensen's node, embryos lacked a notochord in the head and the pattern of En‐2 expression was normal rostrocaudally, but it was expanded into the ventral midline of the neural tube. This suggested that the notochord suppresses En‐2 in the ventral neural tube during normal development. To test further the ability of the notochord (and floor plate) to suppress En‐2, we transplanted ventral midline tissues from HH 5–9 quail embryos beneath the rostral neural plate of HH 4–6 chick embryos. After 24 hours in culture, 90% of the embryos with quail notochord or floor plate near the mes/met of the host lacked En‐2 expression adjacent to the graft, and suppression was distance dependent. Enzymatically isolated notochords also suppressed En‐2 (71%), but the results from isolated floor plates were inconclusive. Other grafts served as controls and included tissues from the trunk ventral midline, mes/met level dorsolateral neural plate, and trunk dorsolateral neural plate/somite. Collectively, the results suggest that during normal development the notochord and possibly the floor plate are important regulators of normal En‐2 expression. © 1995 John Wiley & Sons, Inc.
Development of wing sensory axons in the central nervous system of Drosophila during metamorphosis
Authors: Whitlock Kathleen E. , Palka John 
Published: January 2005

AbstractThe development of new, adult‐specific axonal pathways in the central nervous system (CNS) of insects during metamorphosis is still largely uncharacterized. Here we used axonal labeling with DiI to describe the timing and pattern of growth of sensory axons originating in the wing of Drosophila as they establish their adult projection pattern in the CNS during pupal life. The wing of Drosophila carries a small number of readily identifiable sensory organs (sensilla) whose neurons are located in the periphery and whose axons travel along specific routes within the adult CNS. The neurons are born and undergo axonogenesis in a characteristic order. The order of axon arrival in the CNS appears to be the same as that of their development in the periphery. Within the CNS, the formation of four prominent axon bundles leading to distant termination sites is followed by the formation of a compact axon termination site near the point of wing nerve entry into the CNS. This sensillum‐specific pattern persists into adulthood without discernible modification. We also find a small number of axons filled with DiI prior to the formation of the four permanent bundles. We have only been able to fill them for a few hours in early pupal life and therefore consider them to be transient. The bundles of wing sensory axons travel within tracts that contain other axons as well. Using immunocytochemistry, the tracts start to be histologically identifiable at around 12 h after pupariation (AP), and grow substantially as metamorphosis proceeds. Wing sensory neurons are found in the tracts by 18–20 h AP and the full adult pattern is established by 48 h AP. When sensory axons first enter the CNS, they fan out in the region where their appropriate tracts are located, but they do not wander extensively. They quickly form bundles that become increasingly compact over time. Calculations show that the rate of axon extension within the CNS varies from bundle to bundle and is equal to or greater than that of the same axons growing through wing tissue. © 1995 John Wiley & Sons, Inc.
Postnatal maturation of gamma‐aminobutyric acidA and B‐mediated inhibition in the CA3 hippocampal region of the rat
Authors: Gaiarsa Jean‐Luc , McLean Heather , Congar Patrice , Leinekugel Xavier , Khazipov Rustem , Tseeb Vadim , Ben‐Ari Yehezkel 
Published: January 2005

AbstractIn the adult central nervous system, GABAergic synaptic inhibition is known to play a crucial role in preventing the spread of excitatory glutamatergic activity. This inhibition is achieved by a membrane hyperpolarization through the activation of postsynaptic γ‐aminobutyric acidA (GABAA) and GABAB receptors. In addition, GABA also depress transmitter release acting through presynaptic GABAB receptors. Despite the wealth of data regarding the role of GABA in regulating the degree of synchronous activity in the adult, little is known about GABA transmission during early stages of development. In the following we report that GABA mediates most of the excitatory drive at early stages of development in the hippocampal CA3 region. Activation of GABAA receptors induces a depolarization and excitation of immature CA3 pyramidal neurons and increases intracellular Ca2+ ([Ca2+]i) during the first postnatal week of life. During the same developmental period, the postsynaptic GABAB‐mediated inhibition is poorly developed. In contrast, the presynaptic GABAB‐mediated inhibition is well developed at birth and plays a crucial role in modulating the postsynaptic activity by depressing transmitter release at early postnatal stages. We have also shown that GABA plays a trophic role in the neuritic outgrowth of cultured hippocampal neurons. © 1995 John Wiley & Sons, Inc.
Retrograde but not anterograde bead movement in intact axons requires dynein
Authors: Wang Chang , Asai David J. , Robinson Kenneth R. 
Published: January 2005

AbstractDynein and kinesin have been implicated as the molecular motors that are responsible for the fast transport of axonal membranous organelles and vesicles. Experiments performed in vitro with partially reconstituted preparations have led to the hypothesis that kinesin moves organelles in the anterograde direction and dynein moves them in the retrograde direction. However, the molecular basis of transport directionality remains unclear. In the experiments described here, carboxylated fluorescent beads were injected into living Mauthner axons of lamprey and the beads were observed to move in both the anterograde and retrograde directions. The bead movement in both directions required intact microtubules, occurred at velocities approaching organelle fast transport in vivo, and was inhibited by vanadate at concentrations that inhibit organelle fast transport. When living axons were injected with micromolar concentrations of vanadate and irradiated at 365 nm prior to bead injections, a treatment that results in the V1 photolysis of dynein, the retrograde movement of the beads was specifically abolished. Neither the ultraviolet irradiation alone nor the vanadate alone produced the retrograde‐specific inhibition. These results support the hypothesis that dynein is required for retrograde, but not anterograde, transport in vivo. © 1995 John Wiley & Sons, Inc.