bluuebunny/crossref_metadata_2025_split huggingface dataset:
Embryonic development of the chick primary trigeminal sensory‐motor complex
Authors: Covell David A. , Noden Drew M. 
Published: January 2005

AbstractThe objective of this study is to define the development of all components in the chick embryonic trigeminal primary sensory‐motor complex, from their first appearance through the formation of central and peripheral axonal projections up to stage 34 (8 days of incubation). This was accomplished by two labeling procedures: application of the monoclonal antibody HNK‐1, which binds to the precursors of all these components except the placode‐derived neurons, and application of HRP to axons cut immediately distal to the trigeminal ganglion.Single immunopositive motor neuron precursors are present at stage 12. These accumulate in the transient medial motor column, whose neurons initiate axon outgrowth by stage 13–14, concomitant with the onset of translocation of their somata to form the definitive trigeminal lateral motor column (LMC). Intiially these translocating somata accumulate on the medial margin of the LMC. Beginning on incubation day 5, axons growing from newly formed motor neurons pass beside the lateral margin of the LMC, and the nuclei of these cells subsequently follow this pathway. These events follow a rostral‐to‐caudal sequence, and this phase of motor nucleus formation is complete by day 8. The lateral translocation of some caudally located nuclei is arrested beginning on day 5. This cessation, which proceeds rostrally, demarcates neurons that form the dorsal motor nucleus of the trigeminal complex.Sensory neurite formation is intiated in ophthalmic placode‐derived cells at stage 14.5, one stage later by maxillomandibular neurons, and from mesencephalic V cells at stage 15. Neural crest cells do not initiate axon formation until at least day 4 to 5. Following application of HRP distal to the condensing ganglion at stage 16, labeled ophthalmic nerve projections appear in contact with the wall of the hindbrain centrally and overlying the optic vesicle peripherally. Fibers forming the descending tract elongate rapidly, reaching the level of the VIIth nerve root (200 m̈m caudal to the trigeminal root) by stage 18 and the cervical cord by stage 22. Labeled terminal arborizations of descending trigeminal afferents are first visible at stage 22 and are evident along the entire descending and proximal ascending tracts by stage 27. Later‐developing descending axons grow in close association with existing trigeminal fibers, though a few growth cones are consistently evident superficial to the other fibers. No projections different from those reported in adult birds are seen, nor are there any contralateral afferent projections.Peripheral axons from neurons in the mesencephalic trigeminal nucleus emerge from the trigeminal ganglion beginning at stage 21. These cells are labeled only when tracer is applied to the mandibular nerve.
Effect of fetal infraorbital nerve transection upon trigeminal primary afferent projections in the rat
Authors: Rhoades Robert W. , Chiaia Nicolas L. , MacDonald Gordon J. , Jacquin Mark F. 
Published: January 2005

AbstractTransganglionic tracing with a combination of horseradish peroxidase (HRP) and wheat germ agglutinin–conjugated HRP (WGA‐HRP) was employed to compare the trigeminal (V) innervation of the brainstem in adult rats that sustained transection of the infraorbital nerve (ION) on either the day of birth or just prior to the beginning of the 17th embryonic day (E‐17). The same methods were also employed to assess the effects of such lesions upon the innervation of the brainstem by the lingual, inferior alveolar, mylohyoid, and auriculotemporal V branches. Previous experiments (Chiaia et al.: Dev. Brain Res. 36:75–88, '87) showed that application of HRPand WGA‐HRP to the ION in normal adult rats (N = 3) labelled 12,553 ± 1,455 (mean ± s.d.) V ganglion cells while application of these tracers to the regenerated ION after neonatal transection (N –9) labelled 5,001 ± 1,287 ganglion cells. Application of HRP and WGA‐HRP to the regenerated ION in adulthood (N = 6) after fetal transection labelled 5,476 ± 3,056 ganglion cells. Thus, the numbers of ganglion cells giving rise to the regenerated ION after fetal and neonatal transection were equivalent (P >.05).The central projections of the ION after fetal transection were qualitatively different from those observed after neonatal injury. After neonatal transection, the central terminal field of regenerated ION fibers in adulthood is almost completely restricted to layers I and II of subnucleus caudalis (SpC; Jacquin and Rhoades: Brain Res. 269:137–144, '83; Chiaia et al.: Dev. Brain Res. 36:75–88, '87). After fetal transection, regenerated ION axons terminate heavily in all portions of the V brainstem complex.After neonatal ION transection, we (Jacquin and Rhoades: J. Comp. Neurol. 235:129–143, '85) have been unable to detect central sprouting of undamaged V mandibular axons by means of transganglionic tracing with HRP and WGA‐HRP. Such sprouting was evident in both V subnucleus interpolaris (SpI) and SpC after fetal ION transection.We carried out one additional experiment to determine whether ION ganglion cells that survived fetal axotomy were more resistant to axonal damage than the population of neurons that normally contribute to this nerve on theday of birth. Rats (N = 9) sustained transection of the ION on E‐17 and again on the day of birth. The regenerated ION was then labelled with HRP and WGA‐HRP when the animals reached adulthood. Anaverage of 1,798 ± 1,050 ganglion cells were labelled in these rats and the transganglionic labelling was restricted to layers I and II of SpC. Thus, V ganglion cells that sustain axotomy on E‐17 respond to damage on the day of birth in the same manneras primary afferent neurons that have not been subjected to previous injury.
Anatomical study of the connections of the primary auditory area in the rat
Authors: Roger Michel , Arnault Patricia 
Published: January 2005

AbstractThe aim of the present study was to identify in the rat the overall input‐output pattern of connections of the primary auditory field, with special attention to the topographical organization of the geniculocortical auditory projection. By using cytoarchitectural criteria, three temporal cortical fields were distinguished in the rat: Te1, Te2, and Te3. The primary auditory field Te1 is characterized by a relatively specific differentiation of its layers when compared with other temporal fields. The afferent and efferent connections of Te1 were identified by using the retrograde and anterograde transport of wheat germ agglutinin conjugated with horseradish peroxidase (WGA‐HRP).The results indicate that Te1 is connected by a dense and reciprocal system of fibers with the auditory thalamus. Based on the nomenclature of Morest ('64) in the cat, five cytoarchitectural subdivisions of the medial geniculate complex (MG) were identified in the rat: ventral (MGv), dorsal (MGd), medial (MGm), suprageniculate (Sg), and peripeduncular (PPA). The major rostrocaudal extent of the MGv is connected to Te1. The surrounding cortical fields Te2 and Te3 do not receive a projection from the MGv, except from its most caudal pole. The MGv projection is topographically organized. When the deposit area of the tracer is shifted from dorsal to ventral upon Te1, the corresponding labeled zone within the MGv moves from rostral to caudal, whereas a cortical displacement of the deposit area of the tracer from rostrodorsal to caudoventral leads to a medial to lateral shift of the labeled zone in the MGv. In addition, more dorsal parts of the MGv project on more dorsal sectors of Te1.Te1 receives a sparser, topographically organized projection from the deep dorsal subdivision of the MGd. The MGm and the lateral part of the posterior group of thalamic nuclei (Pol) also distribute fibers to the primary auditory field.Te1 is reciprocally connected by a system of callosal fibers with the contralateral homotypic cortex. Finally, Te1 sends fibers to the dorsal and, to a lesser extent, external cortices of the inferior colliculus, caudomedial caudateputamen complex, and caudoventral thalamic reticular nucleus.
Localization of immunoreactive alpha‐bag‐cell peptide in the central nervous system of Aplysia
Authors: Painter Sherry D. , Kalman Vivian K. , Nagle Gregg T. , Blankenship James E. 
Published: January 2005

AbstractThe bag cells of the marine mollusc Aplysia are well‐characterized neuroendocrine cells that initiate egg laying, but the natural stimulus triggering bag‐cell activity has not been determined. As a first step toward identifying central neurons that might provide synaptic or neurohormonal input onto the bag‐cell network, antibodies specific for alpha‐bag‐cell peptide (α‐BCP) were generated. This peptide belongs to a small family of structurally related peptides that can elicit bag‐cell activity in vitro. Antibody specificity was established by immunodot assay and preabsorption studies: immunocytochemical labeling was abolished in each ganglion when the antibodies were preincubated with either α‐BCP‐thyroglobulin conjugate or α‐BCP‐(1–8) but was not affected by preincubation with thyroglobulin or thyroglobulin‐thyroglobulin conjugate. The antibodies specifically labeled the bag cells in the abdominal ganglion and ectopic bag cells in both the abdominal and right pleural ganglia. The ectopic bag cells were similar to conventional bag cells in size and morphology, but varied in number and location among preparations. In the cerebral ganglion, the antibodies labeled a bilaterally symmetrical pair of cell clusters, containing approximately ten cells each, on the dorsal surface of the ganglion. The cerebral cells were smaller than bag cells, were constant in location, and sent their processes into the neuropil rather than the connective tissue sheath. Immunoreactive processes were observed in the neuropils of the cerebral, pleural, and pedal ganglia and among the axons of the cerebropedal, cerebropleural, and pleurovisceral connectives. No immunoreactive cell bodies were observed in the buccal or pedal ganglia. Identical patterns of labeling were observed in Aplysia californica, A. Brasiliana, and A. Dactylomela. The distribution of immunoreactive cell bodies within the circumesophageal ganglia of all three species thus parallels the distribution of receptive sites for the in vitro induction of bag‐cell activity by atrial gland peptide B, a peptide structurally related to α‐BCP. These observations suggest that the immunoreactive cells identified in these studies, or a subset of them, may be involved in the physiological induction of bag‐cell activity. Since low doses of α‐BCP have additional inhibitory actions on the bag cells, however, it is possible that the identified cells could play a more complex role in the regulation of bag‐cell activity.
Ontogeny of cholinergic neurons in the mouse forebrain
Authors: Schambra U. B. , Sulik K. K. , Petrusz P. , Lauder J. M. 
Published: January 2005

AbstractThe development of cholinergic neurons in the mouse forebrain was studied by immunocytochemistry with a monoclonal antibody to choline acetyl‐transferase (ChAT), the rate‐limiting enzyme for acetylcholine synthesis. Since this antibody stained dividing cells in ventricular germinal zones as well as differentiating neurons, likely routes of migration could be inferred on the basis of the location of immunoreactive (IR) cells at different gestational ages. Germinal zones for cholinergic cells were observed in all ventricular zones of the forebrain with the ventral zones generating the earliest cells by gestational day 13.5 (GD13.5). On GD14, ChAT IR cells were visible in the germinal zones of the eye, olfactory ventricle, anterior horn, and dorsolateral aspect of the lateral ventricle, lateral ganglionic eminence, ventro‐ and dorsolateral third ventricle, and in the pineal anlage (epiphysis). ChAT IR neurons continued to develop in these and additional germinal zones on GD15, including the medial, dorsal, and dorsomedial walls of the lateral ventricle, and the medial and dorsal ganglionic eminence. On GD16, ChAT IR neurons were located in the prelimbic, pyriform, and parietal cortices and the lamina terminalis, and a cluster of IR cells was observed in the ventricular zone of the caudatopallial angle. On GD17–18, neurons in the anterior olfactory nucleus, olfactory tubercle, horizontal and vertical nucleus of the diagonal band, and medial septal nucleus stained more darkly and were multipolar, whereas immature bipolar neurons appeared to continue their migration into the hippocampus and along major fiber tracts, such as the corpus callosum, external capsule, fornix and anterior commissure.This study provides a comprehensive view of the zones of origin, probable routes of migration, and final destination of cholinergic neurons in the mouse forebrain.
Prodynorphin peptide distribution in the forebrain of the syrian hamster and rat: A comparative study with antisera against dynorphin A, dynorphin B, and the C‐terminus of the prodynorphin precursor molecule
Authors: Neal Charles Richard , Newman Sarah Winans 
Published: January 2005

AbstractThe neuroanatomical distribution of the prodynorphin precursor molecule in the forebrain of the male Syrian hamster (Mesocricetus auratus) has been studied with a novel antiserum directed against the C‐terminus of the leumorphin [dynorphin B (1–29)] peptide product. C‐peptide staining in sections from colchicine‐treated hamsters is compared to staining in sections from untreated animals. In addition, the pattern of C‐peptide immunostaining in hamster brain is compared to that in the rat brain. Finally, the C‐peptide immunolabeling patterns in hamsters and rats are compared to those obtained with antisera to dynorphin A (1–17) and dynorphin B (1–13).Areas of heaviest prodynorphin immunoreactivity in the hamster include the hippocampal formation, lateral septum, bed nucleus of the stria terminalis, medial preoptic area, medial and central amygdaloid nuclei, ventral pallidum, substantia nigra, and numerous hypothalamic nuclei. Although this C‐peptide staining pattern is similar to dynorphin staining reported previously in the rat, several species differences are apparent. Whereas moderate dentate gyrus granule cell staining and no CA4 cell staining have been reported in the rat hippocampal formation, intense immunostaining in the dentate gyrus and CA4 cell labeling are observed in the hamster. In addition, the medial preoptic area, bed nucleus of the stria terminalis, and medial nucleus of the amygdala stain lightly for prodynorphin‐containing fibers and cells in the rat, compared to heavy cell and fiber staining in the hamster in all three of these regions.In the rat there is no differential staining between tissues processed with the C‐peptide, dynorphin A, and dynorphin B antisera, but numerous areas of the hamster brain show striking differences. In most hamster brain areas containing prodynorphin peptides, the C‐peptide antiserum immunolabels more cells and fibers than the dynorphin B antiserum, which in turn labels more cells and fibers than dynorphin A antiserum. However, exceptions to this hierarchy of staining intensity are found in the lateral hypothalamus, substantia nigra, arcuate nucleus, and habenula. The differences in staining patterns between rat and hamster are greatest when C‐peptide antiserum is used; apparent species differences are present, though less pronounced, in dynorphin B– and dynorphin A–immunostained material.
Reorganization of visual pathways following posthatching removal of one retina in pigeons
Authors: Bagnoli P. , Casini G. , Fontanesi G. , Sebastiani L. 
Published: January 2005

AbstractOrganization of visual pathways was studied in 2‐month‐old pigeons that underwent unilateral retinal removal on either the day of hatching (ERA, i.e., early retinal ablated) or the 9th day after hatching (LRA, i.e., late retinal ablated).A general size reduction of visual areas contralateral to the removed retina was found in ERA pigeons, which additionally showed an altered differentiation of thalamic visual targets as well as a different cytoarchitectonic arrangement of the superficial layers of the optic tectum. No comparable modification were found in LRA pigeons.The retinal projections of the remaining eye were studied following intraocular injections of 3H‐proline. Both in ERA and LRA pigeons, the distribution of retinofugal afferents to primary visual regions contralateral to the injected eye was similar to that of control pigeons. Anomalous ipsilateral projections from the remaining retina to primary retinorecipient regions were found in ERA pigeons only.Effects of early ablation of one retina on second‐order visual connections were also studied. Following injections of wheat germ agglutinin‐conjugated horseradish peroxidase (WGA‐HRP) into the visual Wulst contralateral to the operated eye, a smaller number of ipsilateral projecting thalamo‐Wulst neurons was found as compared with control pigeons. In contrast, the contralateral thalamo‐Wulst projections were increased. No changes in thalamo‐Wulst projections were found following tracer injections into the opposite Wulst, i.e., ipsilateral to the operated eye.The present study demonstrates a substantial anatomical reorganization of both primary and secondary visual pathways following unilateral retinal removal immediately after hatching, when maturation of the visual system is not yet completed.
Evidence for the stability of positional markers in the goldfish tectum
Authors: Busse Ursula , Stuermer Claudia A. O. 
Published: January 2005

AbstractPositional markers in the tectum, which are thought to guide growing axons to their target sites, have been proposed to be induced by axons, to be only transiently associated with the tectal cells, and then lost after long‐term denervation periods (Schmidt: J. Comp. Neurol. 177: 279–300, '78). To further investigate this concept, retinal axons were induced to regenerate into ipsilateral tecta which had been deprived of their retinal afferents for shorter (0–4 months) and longer periods (4–8 months). The paths of HRP‐labeled regenerating axons of known retinal origin were traced and used as an operational test to decide whether the axons might navigate under the influence of positional markers. Two different kinds of experiments were performed:

The axons from a subpopulation of all ganglion cells in the retina were labeled by applying a small crystal of HRP at defined retinal regions. Independent of the denervation period of the tectum, the labeled regenerating axons traveled in abnormal but nonrandom routes. In early regeneration stages, axons exhibited signs of exploratory growth. They extended branches equipped with growth cones and filopodia into various regions of the tectum. In late regeneration stages, the axons lost these branches, exhibited U‐turns and bends, and ended in terminal arbors in the retinotopic target region. These findings suggest that the axons travel under the influence of tectal positional markers and that these markers are not transient.

Axons from a surgically created temporal hemiretina were labeled by application of HRP to the optic nerve to test whether the temporal axons might expand into the caudal tectum in long‐term‐denervated tecta. The HRP‐labeled axons coursed over rostral and midtectal regions. Instead of invading the caudal tectum they bent and terminated in the rostral tectal half. These results add further support for the conclusion that the path of regenerating retinal axons is governed by long‐lasting positional markers.
Localization of L‐glutamic acid decarboxylase mRNA in monkey and human retina by in situ hybridization
Authors: Sarthy P. Vijay , Fu Marlene 
Published: January 2005

AbstractImmunocytochemical studies with γ‐aminobutyric acid (GABA) antibodies and glutamic acid decarboxylase antibodies have shown that the primate retina contains GABAergic amacrine, interplexiform, and displaced amacrine cells. In addition, subpopulations of photoreceptors and horizontal cells have also been suggested to be GABAergic in this retina. In the present study, we have used in situ hybridization to localize GABAergic neurons in human and monkey retinas. In situ hybridizations were carried out with 35S‐labeled DNA and RNA probes derived from human and cat glutamic acid decarboxylase cDNA clones. In the monkey retina, labeled cells were present in the inner nuclear and ganglion cells layers. The outer nuclear layer or the inner segment layer had only background levels of labeling. In the inner nuclear layer, all labeled somata were located in the vitread‐half bordering the inner nuclear layer/inner plexiform layer boundary. These cells constituted ∼83% of all labeled cells. Labeled cells were also seen in the ganglion cell layer.In the human retina, labeled somata were observed only in the inner nuclear and the ganglion cell layers. In the inner nuclear layer, the majority of labeled cells were located close to the inner nuclear layer/inner plexiform layer boundary although a minor population of labeled somata (∼20%) were found deeper in the inner nuclear layer. The distribution of glutamic acid decarboxylase mRNA–containing cells we observed is in good agreement with the known location of GABAergic neurons. We, however, did not find glutamic acid decarboxylase mRNA in either horizontal cells or photoreceptors in monkey and human retina.
Cell death in the inner and outer nuclear layers of the developing retina in the wallaby setonix brachyurus (quokka)
Authors: Harman A. M. , Snell L. L. , Beazley L. D. 
Published: January 2005

AbstractWe have examined the number and distribution of dying cells in the developing inner (INL) and outer (ONL) nuclear layers of sectioned quokka retinae (N = 31) from embryonic day (E)24 to postnatal day (P)192.Before birth, dying cells were seen in the optic fissure. Thereafter two major phases of cell death took place in the INL. The first phase was more pronounced within the vitread part with peak numbers of dying cells at P50. By contrast, during the second phase, cell death was more extensive in the sclerad portion; peak numbers of dying cells were recorded at P85 and P100 for the vitread and sclerad parts respectively. At these stages, photoreceptors were seen in the INL suggesting that these ectopic cells contribute to the pool of dying cells. The pattern of cell death broadly followed a central to peripheral sequence in the first phase but, in the second, was seen initially in midtemporal retina and then became panretinal. Dying cells were seen in the ONL but in smaller numbers than in the INL. There was a peak of cell death at P26 which may represent death of mitotic cells at the ventricular surface.In the quokka, retinal cell genesis takes place in two phases (Harman and Beazley: Neuroscience 28:219–232, ′89). The two major phases of cell death described here peak approximately 40 days after episodes of maximal cell genesis. These findings, together with data for the mouse, suggest that a biphasic pattern of cell genesis and cell death may be a feature of eutherian as well as marsupial retinal development.