bluuebunny/crossref_metadata_2025_split huggingface dataset:
Postnatal development of different classes of cat retinal ganglion cells
Authors: Ault Steven J. , Leventhal Audie G. 
Published: January 2005

AbstractPrevious investigators have documented the postnatal development of alpha and beta type ganglion cells in cat retinae (Ramoa et al. [1987] Science 237:522–525; Ramoa et al. [1988] J. Neurosci. 8:4239–4261; Dann et al. [1987] Neurosci. Lett. 80:21–26; Dann et al. [1988] J. Neurosci. 8(5):1485–1499). The development of the remaining cells (about 50%), which constitute a heterogeneous group and are referred to here collectively as gamma cells (Boycott and Wässle, '74), has not been studied in detail. The purpose of this study was to compare the postnatal development of alpha, beta, and gamma cells in kitten and adult retinae using horseradish peroxidase histochemistry and the fluorescent dye Dil. In the kitten, alpha, beta, and gamma cells are recognizable. We find, as have others, that kitten alpha and beta cell bodies and dendritic fields are significantly smaller than in the adult. However, kitten gamma cells are nearly adult sized. In fact, at birth the cell bodies of beta cells throughout the retina are significantly smaller than those of gamma cells. During the first 12 weeks of life, alpha and beta cell bodies increase in size from 90% to 680% depending upon eccentricity. Gamma cells hardly increase in size at all. Also, the normal adult center‐to‐peripheral cell size gradient for alpha and beta cells is not seen in the neonate. Gamma cells show no such gradient in the neonate or adult. Our results suggest that the morphological development of alpha and beta cells occurs later than that of gamma cells and may explain some of the differences in the effects of visual deprivation and surgical manipulation upon the parallel Y‐, X‐, and W‐cell pathways. © 1994 Wiley‐Liss, Inc.
Postembryonic development of γ‐aminobutyric acid‐like Immunoreactivity in the brain of the sphinx moth Manduca sexta
Authors: Homberg Uwe , Hildebrand John G. 
Published: January 2005

AbstractWe have investigated the distribution of immunocytochemical staining for the neurotransmitter γ‐aminobutyric acid (GABA) in the brain of the sphinx moth Manduca sexta during larval, pupal, and adult development. In the larval brain, about 300 neurons are GABA‐immunoreactive. All neuropil areas except the mushroom bodies and central complex show intense immunostaining. Only minor changes in the pattern of immunoreactivity occur during larval development. During metamorphosis, changes in immunostaining occur in two phases. Beginning in wandering fifth‐instar larvae (stage W2), immunoreactivity appears in numerous neurons of the central body and optic lobe and becomes more intense during early pupal stages. At the same time, GABA‐like immunoreactivity disappears in most neuropil areas of the brain and becomes faint in many immunoreactive somata. Neurons with arborizations in the ventrolateral protocerebrum, however, continue to exhibit intense immunostaining during this period, and strongly immunolabeled fibers connect these areas with the ventral nerve cord. The second phase of transformation begins around pupal stage P5/P6, when faint immunostaining appears in many previously nonimmunoreactive somata and most neuropil areas of the brain. In subsequent stages (P8–P10), this immunoreactivity disappears again in most somata, but in certain cell groups, it becomes more intense and gradually develops to the adult pattern. Most larval GABA‐immunoreactive neurons appear to survive through metamorphosis into the adult. Neurons in the midbrain that acquire GABA‐like immunoreactivity during metamorphosis usually lie adjacent to larval immunostained neurons, suggesting common lineages. The onsets of the two developmental phases of GABA‐like immunoreactivity correlate with sharp rises in hemolymph titers of ecdysteroid hormones, suggesting a role for ecdysteroids in the regulation of GABA synthesis. We hypothesize that the disappearance of GABA in many areas of the brain starting 2 days prior to pupation dramatically alters its functional circuitry and thus may account for profound changes in the behavior of the animal. © 1994 Wiley‐Liss, Inc.
Synaptic interrelationships between the optic tectum and the ipsilateral nucleus isthmi in Rana pipiens
Authors: Gruberg Edward R. , Hughes Thomas E. , Karten Harvey J. 
Published: January 2005

AbstractThe nucleus isthmi is reciprocally connected to the ipsilateral optic tectum. Ablation of the nucleus isthmi compromises visually guided behavior that is mediated by the tectum. In this paper, horseradish peroxidase (HRP) histochemistry and electron microscopy were used to explore the synaptic interrelationships between the optic tectum and the ipsilateral nucleus isthmi. After localized injections of HRP into the optic tectum, there are retrogradely labeled isthmotectal neurons and orthogradely labeled fibers and terminals in the ipsilateral nucleus isthmi. These terminals contain round. Clear vesicles of medium diameter (40–52 nm). These terminals make synaptic contact with dendrites of nucleus isthmi cells. Almost half of these postsynaptic dendrites are retrogradely labeled, indicating that there are monosynaptic tectoisthmotectal connections.Localized HRP injection into the nucleus isthmi labels terminals primarily in tectal layers B, E, F, and 8. The terminals contain medium‐sized clear vesicles and they form synaptic contacts with tectal dendrites. There are no instances of labeled isthmotectal terminals contacting labeled dendrites. Retrogradely labeled tectoisthmal neurons are contacted by unlabeled terminals containing medium‐sized and small clear vesicles. Fifty‐four percent of the labeled fibers connecting the nucleus isthmi and ipsilateral tectum are myelinated fibers (average diameter approximately 0.6 μm). The remainder are unmyelinated fibers (average diameter approximately 0.4 μm). © 1994 Wiley‐Liss, Inc.
Auditory nerve terminals in the cochlear nucleus magnocellularis: Differences between low and high frequencies
Authors: Köppl Christine 
Published: January 2005

AbstractPrimary auditory nerve fibers were labelled in the barn owl by localized horseradish peroxidase (HRP) injections into the cochlear nucleus angularis. They were followed to their terminal sites in the hearing organ (basilar papilla), confirming that they were auditory, and to the cochlear nucleus magnocellularis. The terminal sites of low‐frequency fibers within nucleus magnocellularis always included an area previously described as the lagenar part, i.e., an area receiving primary input which is probably only vestibular. Furthermore, a number of differences were recognized between these low‐frequency (up to 0.64 kHz) and the high‐frequency (1.8 kHz and above) auditory nerve projections to nucleus magnocellularis. Most importantly, the collaterals given off by low‐frequency fibers into the nucleus typically showed multiple terminal branching, with both en passant and terminal bouton‐like swellings. High‐frequency fiber collaterals, in contrast, terminated unbranched in a single endbulb of Held. Nucleus magnocellularis is the first station in a brainstem auditory pathway processing stimulus timing information, coded through neuronal phase locking. The prominent difference in terminal shape found between its low‐ and high‐frequency input fibers is interpreted as reflecting different requirements of the absolute temporal precision for significant phase locking. Terminals in the shape of endbulbs of Held are probably a specialization to improve the temporal precision of synaptic transmission, allowing phase locking to higher frequencies. © 1994 Wiley‐Liss, Inc.
Age‐related increase in the total number of corticotropin‐releasing hormone neurons in the human paraventricular nucleus in controls and alzheimer's disease: Comparison of the disector with an unfolding method
Authors: Raadsheer F. C. , Oorschot D. E. , Verwer R. W. H. , Tilders F. J. H. , Swaab D. F. 
Published: January 2005

AbstractIt has been hypothesized that the corticotropin‐releasing hormone (CRH) neurons of the hypothalamic paraventricular nucleus (PVN) become hyperactive with age, and even more so in Alzheimer's disease. This hyperactivity could be due to an increased production of CRH per neuron, or an increased number of PVN neurons producing CRH, or both. As a first step in elucidating which of these biological mechanisms might be operative, we have estimated the absolute number of CRH immunoreactive neurons in the PVN of 10 human control subjects between 36 and 91 years of age and 10 Alzheimer patients between 40 and 97 years of age. CRH neurons were immunocytochemically detected in 6 μm paraffin sections with the aid of a highly specific monoclonal antibody to CRH. The antibody signal was amplified by the biotinstreptavidin and alkaline phosphatase methods. The absolute number of CRH neurons in the PVN was obtained by multiplying the number of CRH neurons in a unit volume (Nv) by the total volume of the PVN. Two different methods were used to estimate the Nv: an unfolding method and a disector method (about three times more time‐consuming). Compared to the disector, the unfolding method consistently yielded a lower cell number for all patients by 38% (± 2.8%; mean ± SEM). However, both methods yielded an increase in the absolute number of CRH neurons in control and Alzheimer patients with age. No statistically significant difference in the absolute number of CRH neurons was found between control and Alzheinler patients with both methods. The age‐dependent increase in the absolute number of CRH neurons within the PVN of both control and Alzheimer patients is interpreted as a sign of activation of the CRH neurons with age. © 1994 Wiley‐Liss, Inc.
Tenascin in the injured rat optic nerve and in non‐neuronal cells in vitro: Potential role in neural repair
Authors: Ajemian A. , Ness R. , David S. 
Published: January 2005

AbstractThe distribution of tenascin was examined in the lesioned adult rat optic nerve and central nervous system (CNS) non‐neuronal cells in vitro, by means of a double immunofluorescence technique. Tenascin‐like immunoreactivity is localized to the leptomeninges and astrocytes that border the site of optic nerve transection. Anti‐tenascin labeling was observed as early as 24 hours after transection, when it appeared as a fine interface between leptomeninges and neural tissue. The anti‐tenascin labeling increased in the cells at this border zone during the next 2 weeks, and disappeared 18–21 days after transection. In vitro studies further confirmed that both astrocytes and leptomeningeal cells express tenascin as detected by immunofluorescence labeling with anti‐tenascin antibodies. However, the pattern of immunolabeling associated with the two cell types differed. Astrocytes showed exclusively punctate labeling of the cell surface, while leptomeningeal cells showed mainly coarse, fibrillary, matrix‐like deposits. Astrocytes and leptomeningeal cells remained segregated when cocultured. In these cultures, an increased amount of the fibrillary, matrix‐like deposits of tenascin was also observed in the region of the interface between astrocytes and leptomeningeal cells when these two cell types contact each other. Given the antiadhesive and antispreading properties of tenascin, these in vivo and in vitro results suggest that tenascin might playa role in the initial segregation of leptomeningeal cells from neural tissue at the site of CNS trauma during the first 2 weeks after injury, i.e., prior to the formation of a fully differentiated glia limitans. Therefore, tenascin may influence the early stages in the formation of the glia limitans, and thus prevent the indiscriminate migration of leptomeningeal cells into CNS tissue after injury. © Wiley‐Liss, Inc.
Enkephalin‐positive and acetylcholinesterase‐positive patch systems in the superior colliculus have matching distributions but distinct developmental histories
Authors: Graybiel A. M. , Illing R.‐B. 
Published: January 2005

AbstractHistochemical stains for acetylcholinesterase activity and enkephalin‐like immunoreactivity both demonstrate a high degree of patterning in the superior colliculus, particularly in the intermediate and deep layers. Both markers occur predominantly in the neuropil of these layers, and both are principally distributed in distinct macroscopic compartments. We report here that patches of heightened acetylcholinesterase activity correspond to patches of high enkephalin‐like immunoreactivity. The two markers thus delineate largely the same domain in the intermediate and deep layers. The most prominent zones of staining for enkephalin‐like peptide and for acetylcholinesterase also coincided in the dorsolateral periaqueductal gray matter. These findings suggest a close interlocking of one or more acetylcholinesterasecontaining systems with one or more pathways related to endogenous opioids in the superior colliculus. As the acetylcholinesterase expression in the patches is known to match in detail choline acetyltransferase expression, our results also suggest the possibility of local cholinergicopiatergic interactions.In some sections, blood vessels associated with enkephalin‐rich and acetylcholinesteraserich patches extended beyond the colliculus into the periaqueductal gray matter, where they again became surrounded by dense fibrous labeling. This pattern suggests that neurohumoral signal exchange might occur through blood vessels even in a sensory‐motor structure such as the colliculus.In a postnatal developmental series of kitten brains we found that enkephalin‐like immunoreactivity was already distinctly compartmental in the intermediate layers at birth and continued to show this distribution throughout postnatal development. By contrast, acetylcholinesterase staining was nearly homogeneous at birth and became compartmental gradually during the first postnatal weeks. Thus, despite the eventual near coincidence of the enkephalinrich and acetylcholinesterase‐rich compartments of the superior colliculus, they mark systems that follow distinct programs of neurochemical development. © Wiley‐Liss, Inc.
Effects of estrogen on the number of neurons expressing β‐endorphin in the medial basal hypothalamus of the female guinea pig
Authors: Thornton Janice E. , Loose Michael D. , Kelly Martin J. , Rönnekleiv Oline K. 
Published: January 2005

AbstractThe distribution pattern of immunoreactive β‐endorphin neurons was studied in female guinea pigs that were ovariectomized, and one week later were injected with 25 μg estradiol benzoate or oil. The animals (5 from each group) were perfused after 24 hours with 4% paraformaldehyde. The locations of β‐endorphin cells and fibers were determined using avidin‐biotin immunohistochemistry on free‐floating vibratome sections. β‐endorphin‐immunoreactive fibers were distributed widely throughout specific regions of the rostral forebrain, similar to what has been described in other species. β‐endorphin cell bodies were found in the arcuate nucleus and in adjacent ventrolateral areas throughout the rostrocaudal extent of the basal hypothalamus. Cells immunoreactive to β‐endorphin were also present in the caudal part of the ventromedial nucleus of the hypothalamus. The number of β‐endorphin neurons was quantified in anatomically matched sections through the rostral, medial and caudal basal hypothalamus of estradiol benzoate‐ and oil‐treated guinea pigs. Analysis of variance revealed that the number of immunoreactive β‐endorphin cells was significantly increased in all regions of the basal hypothalamus of estrogen‐treated guinea pigs as compared to vehicle‐treated animals (P < 0.01). These data indicate that in the guinea pig, the number of neurons expressing β‐endorphin is increased in the arcuate nucleus 24 hours after estrogen treatment.
Local circuit neurons immunoreactive for calretinin, calbindin D‐28k or parvalbumin in monkey prefronatal cortex: Distribution and morphology
Authors: Condé Françoise , Lund Jennifer S. , Jacobowitz David M. , Baimbridge Kenneth G. , Lewis David A. 
Published: January 2005

AbstractIn the cerebral cortex, local circuit neurons provide critical inhibitory control over the activity of pyramidal neurons, the major class of excitatory efferent cortical cells. The calciumbinding proteins, calretinin, calbindin, and parvalbumin, are expressed in a variety of cortical local circuit neurons. However, in the primate prefrontal cortex, relatively little is known, especially with regard to calretinin, about the specific classes or distribution of local circuit neurons that contain these calcium‐binding proteins. In this study, we used immunohistochemical techniques to characterize and compare the morphological features and distribution in macaque monkey prefrontal cortex of local circuit neurons that contain each of these calcium‐binding proteins.On the basis of the axonal features of the labeled neurons, and correlations with previous Golgi studies, calretinin appeared to be present in double‐bouquet neurons, calbindin in neurogliaform neurons and Martinotti cells, and parvalbumin in chandelier and wide arbor (basket) neurons. Calretinin was also found in other cell populations, such as a distinctive group of large neurons in the infragranular layers, but it was not possible to assign these neurons to a known cell class. In addition, although the animals studied were adults, immunoreactivity for both calretinin and calbindin was found in Cajal‐Retzius neurons of layer I. Dual labeling studies confirmed that with the exception of the Cajal‐Retzius neurons, each calcium‐binding protein was expressed in separate populations of prefrontal cortical neurons.Comparisons of the laminar distributions of the labeled neurons also indicated that these calcium‐binding proteins were segregated into discrete neuronal populations. Calretinin‐positive neurons were present in greatest density in deep layer I and layer II, calbindin‐immuno‐reactive cells were most dense in layers II‐superficial III, and parvalbumin‐containing neurons were present in greatest density in the middle cortical layers. In addition, the relative density of calretinin‐labeled neurons was approximately twice that of the calbindin‐ and parvalbumin‐positive neurons. However, within each group of labeled neurons, their laminar distribution and relative density did not differ substantially across regions of the prefrontal cortex.These findings demonstrate that calretinin, calbindin, and parvalbumin are markers of separate populations of local circuit neurons in monkey prefrontal cortex, and that they may be useful tools in unraveling the intrinsic inhibitory circuitry of the primate prefrontal cortex in both normal and disease states.
Intra‐amygdaloid projections of the lateral nucleus in the cat: PHA‐L anterograde labeling combined with postembedding GABA and glutamate immunocytochemistry
Authors: Smith Y. , Paré D. 
Published: January 2005

AbstractResearch on the implication of the amygdala in classical fear conditioning suggests that the central amygdaloid nucleus is the output station of the amygdala for conditioned fear responses, while the lateral nucleus acts as the input nucleus, at least for auditory conditioned stimuli. However, the nature and locus of the plastic changes taking place between these two nuclei are unknown partly because the neurotransmitter(s) used by intra‐amygdaloid projections of the lateral nucleus has not been identified. To address this issue in cats, anterograde tracing with Phaseolus vulgaris‐leucoagglutinin (PHA‐L) was combined with postembedding immunocytochemistry for gamma‐aminobutyric acid (GABA) and glutamate.Two sectors can be recognized in the lateral nucleus of the cat: a shell located laterally along the external capsule, and a core. Iontophoretic injections of PHA‐L in these two sectors revealed that they have nonoverlapping intra‐amygdaloid targets with the exception of a common projection to the central lateral nucleus. The core projects mainly to itself and to the basomedial nucleus, whereas the shell contributes a massive projection to the basolateral nucleus. No projection of the lateral nucleus to the central medial nucleus was found. Electron microscopically, PHA‐L‐labeled axon terminals in the lateral, basomedial, basolateral, and central lateral nuclei as well as in the perirhinal and insular cortices formed asymmetric synapses (100%; n = 289) with dendritic spines (77–100%). Moreover, postembedding immunocytochemistry revealed that PHA‐L‐labeled axon terminals are immunoreactive for glutamate but not GABA.Since most amygdaloid projections to the brainstem originate in the central medial nucleus, these results suggest that intra‐amygdaloid targets of the lateral nucleus are involved in the transmission of auditory conditioned stimuli to the central medial nucleus. Moreover, these findings imply that intra‐amygdaloid projections of the lateral nucleus use glutamate but not GABA as a neurotransmitter. © 1994 Wiley‐Liss, Inc.
Peripheral innervation patterns of vestibular nerve afferents in the bullfrog utriculus
Authors: Baird R. A. , Schuff N. R. 
Published: January 2005

AbstractVestibular nerve afferents innervating the bullfrog utriculus differ in their response dynamics and sensitivity to natural stimulation. They also supply hair cells that differ markedly in hair bundle morphology. To examine the peripheral innervation patterns of individual utricular afferents more closely, afferent fibers were labeled by the extracellular injection of horseradish peroxidase (HRP) into the vestibular nerve after sectioning the vestibular nerve medial to Scarpa's ganglion to allow the degeneration of sympathetic and efferent fibers. The peripheral arborizations of individual afferents were then correlated with the diameters of their parent axons, the regions of the macula they innervate, and the number and type of hair cells they supply.The utriculus is divided by the striola, a narrow zone of distinctive morphology, into medial and lateral parts. Utricular afferents were classified as striolar or extrastriolar according to the epithelial entrance of their parent axons and the location of their terminal fields. In general, striolar afferents had thicker parent axons, fewer subepithelial bifurcations, larger terminal fields, and more synaptic endings than afferents in extrastriolar regions. Afferents in a juxtastriolar zone, immediately adjacent to the medial striola, had innervation patterns transitional between those in the striola and more peripheral parts of the medial extrastriola. Most afferents innervated only a single macular zone. The terminal fields of striolar afferents, with the notable exception of a few afferents with thin parent axons, were generally confined to one side of the striola.Hair cells in the bullfrog utriculus have previously been classified into four types based on hair bundle morphology (Lewis and Li: Brain Res. 83:35–50, 1975). Afferents in the extrastriolar and juxtastriolar zones largely or exclusively innervated Type B hair cells, the predominant hair cell type in the utricular macula. Striolar afferents supplied a mixture of four hair cell types, but largely contacted Type B and Type C hair cells, particularly on the outer rows of the medial striola. Afferents supplying more central striolar regions innervated fewer Type B and larger numbers of Type E and Type F hair cells. Striolar afferents with thin parent axons largely supplied Type E hair cells with bulbed kinocilia in the innermost striolar rows. © 1994 Wiley‐Liss, Inc.