bluuebunny/crossref_metadata_2025_split huggingface dataset:
Descending brain‐spinal cord projections in a primitive vertebrate, the lamprey: Cerebrospinal fluid‐contacting and dopaminergic neurons
Authors: Barreiro‐Iglesias Antón , Villar‐Cerviño Verona , Anadón Ramón , Rodicio María Celina 
Published: October 2008

AbstractWe used Neurobiotin as a retrograde tract tracer in both larval and adult sea lampreys and observed a number of neuronal brainstem populations (mainly reticular and octaval populations and some diencephalic nuclei) that project to the spinal cord, in agreement with the results of previous tracer studies. We also observed small labeled neurons in the ventral hypothalamus, the mammillary region, and the paratubercular nucleus, nuclei that were not reported as spinal projecting. Notably, most of the labeled cells of the mammillary region and some of the ventral hypothalamus were cerebrospinal fluid‐contacting (CSF‐c) neurons. Combined tract tracing and immunocytochemistry showed that some of the labeled neurons of the mammillary and paratubercular nuclei were dopamine immunoreactive. In addition, some CSF‐c cells were labeled in the caudal rhombencephalon and rostral spinal cord, and many were also dopamine immunoreactive. Results with other tracers (biotinylated dextran amines, horseradish peroxidase, and the carbocyanine dye DiI) also demonstrated that the molecular weight or the molecular nature of the tracer was determinant in revealing diencephalic cells with very thin axons. The results show that descending systems afferent to the spinal cord in lampreys are more varied than previously reported, and reveal a descending projection from CSF‐c cells, which is unknown in vertebrates. The present results also reveal the existence of large differences between agnathans and gnathostomes in the organization of the dopaminergic cells that project to the spinal cord. J. Comp. Neurol. 511:711–723, 2008. © 2008 Wiley‐Liss, Inc.
Increased AMPA receptor GluR1 subunit incorporation in rat hippocampal CA1 synapses during benzodiazepine withdrawal
Authors: Das Paromita , Lilly Scott M. , Zerda Ricardo , Gunning William T. , Alvarez Francisco J. , Tietz Elizabeth I. 
Published: October 2008

AbstractProlonged benzodiazepine treatment leads to tolerance and increases the risk of dependence. Flurazepam (FZP) withdrawal is associated with increased anxiety correlated with increased alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid‐type glutamate receptor (AMPAR)‐mediated synaptic function and AMPAR binding in CA1 pyramidal neurons. Enhanced AMPAR synaptic strength is also associated with a shift toward inward rectification of synaptic currents and increased expression of GluR1, but not GluR2, subunits, suggesting augmented membrane incorporation of GluR1‐containing, GluR2‐lacking AMPARs. To test this hypothesis, the postsynaptic incorporation of GluR1 and GluR2 subunits in CA1 neurons after FZP withdrawal was examined by postembedding immunogold quantitative electron microscopy. The percentage of GluR1 positively labeled stratum radiatum (SR) synapses was significantly increased in FZP‐withdrawn rats (88.2% ± 2.2%) compared with controls (74.4% ± 1.9%). In addition, GluR1 immunogold density was significantly increased by 30% in SR synapses in CA1 neurons from FZP‐withdrawn rats compared with control rats (FZP: 14.1 ± 0.3 gold particles/μm; CON: 10.8 ± 0.4 gold particles/μm). In contrast, GluR2 immunogold density was not significantly different between groups. Taken together with recent functional data from our laboratory, the current study suggests that the enhanced glutamatergic strength at CA1 neuron synapses during benzodiazepine withdrawal is mediated by increased incorporation of GluR1‐containing AMPARs. Mechanisms underlying synaptic plasticity in this model of drug dependence are therefore fundamentally similar to those that operate during activity‐dependent plasticity. J. Comp. Neurol. 511:832–846, 2008. © 2008 Wiley‐Liss, Inc.
Tau isoform regulation is region‐ and cell‐specific in mouse brain
Authors: McMillan Pamela , Korvatska Elena , Poorkaj Parvoneh , Evstafjeva Zana , Robinson Linda , Greenup Lynne , Leverenz James , Schellenberg Gerard D. , D'Souza Ian 
Published: October 2008

AbstractTau is a microtubule‐associated protein implicated in neurodegenerative tauopathies. Alternative splicing of the tau gene (MAPT) generates six tau isoforms, distinguishable by the exclusion or inclusion of a repeat region of exon 10, which are referred to as 3‐repeat (3R) and 4‐repeat (4R) tau, respectively. We developed transgenic mouse models that express the entire human MAPT gene in the presence and absence of the mouse Mapt gene and compared the expression and regulation of mouse and human tau isoforms during development and in the young adult. We found differences between mouse and human tau in the regulation of exon 10 inclusion. Despite these differences, the isoform splicing pattern seen in normal human brain is replicated in our mouse models. In addition, we found that all tau, both in the neonate and young adult, is phosphorylated. We also examined the normal anatomic distribution of mouse and human tau isoforms in mouse brain. We observed developmental and species‐specific variations in the expression of 3R‐ and 4R‐tau within the frontal cortex and hippocampus. In addition, there were differences in the cellular distribution of the isoforms. Mice transgenic for the human MAPT gene exhibited higher levels of neuronal cell body expression of tau compared to wildtype mice. This neuronal cell body expression of tau was limited to the 3R isoform, whereas expression of 4R‐tau was more “synaptic like,” with granular staining of neuropil rather than in neuronal cell bodies. These developmental and species‐specific differences in the regulation and distribution of tau isoforms may be important to the understanding of normal and pathologic tau isoform expression. J. Comp. Neurol. 511:788–803, 2008. © 2008 Wiley‐Liss, Inc.
Inputs to the ventrolateral bed nucleus of the stria terminalis
Authors: Shin Jung‐Won , Geerling Joel C. , Loewy Arthur D. 
Published: October 2008

AbstractThe ventrolateral bed nucleus of the stria terminalis (BSTvl) receives direct input from two specific subpopulations of neurons in the nucleus tractus solitarius (NTS). It is heavily innervated by aldosterone‐sensitive NTS neurons, which are selectively activated by sodium depletion, and by the A2 noradrenergic neurons, which are activated by visceral and immune‐ and stress‐related stimuli. Here, we used a retrograde neuronal tracer to identify other brain sites that innervate the BSTvl. Five general brain regions contained retrogradely labeled neurons:cerebral cortex(infralimbic and insular regions),rostral forebrain structures(subfornical organ, organum vasculosum of the lamina terminalis, taenia tecta, nucleus accumbens, lateral septum, endopiriform nucleus, dorsal BST, substantia innominata, and, most prominently the amygdala—primarily its basomedial and central subnuclei),thalamus(central medial, intermediodorsal, reuniens, and, most prominently the paraventricular thalamic nucleus),hypothalamus(medial preoptic area, perifornical, arcuate, dorsomedial, parasubthalamic, and posterior hypothalamic nuclei), andbrainstem(periaqueductal gray matter, dorsal and central superior raphe nuclei, parabrachial nucleus, pre‐locus coeruleus region, NTS, and A1 noradrenergic neurons in the caudal ventrolateral medulla). In the arcuate hypothalamic nucleus, some retrogradely labeled neurons contained either agouti‐related peptide or cocaine/amphetamine‐regulated transcript. Of the numerous retrogradely labeled neurons in the perifornical hypothalamic area, few contained melanin‐concentrating hormone or orexin. In the brainstem, many retrogradely labeled neurons were either serotoninergic or catecholaminergic. In summary, the BSTvl receives inputs from a variety of brain sites implicated in hunger, salt and water intake, stress, arousal, and reward. J. Comp. Neurol. 511:628–657, 2008. © 2008 Wiley‐Liss, Inc.
Differential expression of canonical (classical) transient receptor potential channels in guinea pig enteric nervous system
Authors: Liu Sumei , Qu Mei‐Hua , Ren Wei , Hu Hong‐Zhen , Gao Na , Wang Guo‐Du , Wang Xi‐Yu , Fei Guijun , Zuo Fei , Xia Yun , Wood Jackie D. 
Published: October 2008

AbstractThe canonical transient receptor potential (TRPC) family of ion channels is implicated in many neuronal processes including calcium homeostasis, membrane excitability, synaptic transmission, and axon guidance. TRPC channels are postulated to be important in the functional neurobiology of the enteric nervous system (ENS); nevertheless, details for expression in the ENS are lacking. Reverse transcriptase‐polymerase chain reaction, Western blotting, and immunohistochemistry were used to study the expression and localization of TRPC channels. We found mRNA transcripts, protein on Western blots, and immunoreactivity (IR) for TRPC1/3/4/6 expressed in the small intestinal ENS of adult guinea pigs. TRPC1/3/4/6‐IR was localized to distinct subpopulations of enteric neurons and was differentially distributed between the myenteric and submucosal divisions of the ENS. TRPC1‐IR was widely distributed and localized to neurons with cholinergic, calretinin, and nitrergic neuronal immunochemical codes in the myenteric plexus. It was localized to both cholinergic and noncholinergic secretomotor neurons in the submucosal plexus. TRPC3‐IR was found only in the submucosal plexus and was expressed exclusively by neuropeptide Y‐IR neurons. TRPC4/6‐IR was expressed in only a small population of myenteric neurons, but was abundantly expressed in the submucosal plexus. TRPC4/6‐IR was coexpressed with both cholinergic and nitrergic neurochemical codes in the myenteric plexus. In the submucosal plexus, TRPC4/6‐IR was expressed exclusively in noncholinergic secretomotor neurons. No TRPC1/3/4/6‐IR was found in calbindin‐IR neurons. TRPC3/4/6‐IR was widely expressed along varicose nerve fibers and colocalized with synaptophysin‐IR at putative neurotransmitter release sites. Our results suggest important roles for TRPC channels in ENS physiology and neuronal regulation of gut function. J. Comp. Neurol. 511:847–862, 2008. © 2008 Wiley‐Liss, Inc.
Conservation and diversity of Foxp2 expression in muroid rodents: Functional implications
Authors: Campbell Polly , Reep Roger L. , Stoll Margaret L. , Ophir Alexander G. , Phelps Steven M. 
Published: October 2008

AbstractFOXP2, the first gene causally linked to a human language disorder, is implicated in song acquisition, production, and perception in oscine songbirds, the evolution of speech and language in hominids, and the evolution of echolocation in bats. Despite the evident relevance of Foxp2 to vertebrate acoustic communication, a comprehensive description of neural expression patterns is currently lacking in mammals. Here we use immunocytochemistry to systematically describe the neural distribution of Foxp2 protein in four species of muroid rodents: Scotinomys teguina and S. xerampelinus (“singing mice”), the deer mouse, Peromyscus maniculatus, and the lab mouse, Mus musculus. While expression patterns were generally highly conserved across brain regions, we identified subtle but consistent interspecific differences in Foxp2 distribution, most notably in the medial amygdala and nucleus accumbens, and in layer V cortex throughout the brain. Throughout the brain, Foxp2 was highly enriched in areas involved in modulation of fine motor output (striatum, mesolimbic dopamine circuit, olivocerebellar system) and in multimodal sensory processing and sensorimotor integration (thalamus, cortex). We propose a generalized model for Foxp2‐modulated pathways in the adult brain including, but not limited to, fine motor production and auditory perception. J. Comp. Neurol. 512:84–100, 2009. © 2008 Wiley‐Liss, Inc.
Cochlear implant use following neonatal deafness influences the cochleotopic organization of the primary auditory cortex in cats
Authors: Fallon James B. , Irvine Dexter R.F. , Shepherd Robert K. 
Published: October 2008

AbstractElectrical stimulation of spiral ganglion neurons in a deafened cochlea, via a cochlear implant, provides a means of investigating the effects of the removal and subsequent restoration of afferent input on the functional organization of the primary auditory cortex (AI). We neonatally deafened 17 cats before the onset of hearing, thereby abolishing virtually all afferent input from the auditory periphery. In seven animals the auditory pathway was chronically reactivated with environmentally derived electrical stimuli presented via a multichannel intracochlear electrode array implanted at 8 weeks of age. Electrical stimulation was provided by a clinical cochlear implant that was used continuously for periods of up to 7 months. In 10 long‐term deafened cats and three age‐matched normal‐hearing controls, an intracochlear electrode array was implanted immediately prior to cortical recording. We recorded from a total of 812 single unit and multiunit clusters in AI of all cats as adults using a combination of single tungsten and multichannel silicon electrode arrays. The absence of afferent activity in the long‐term deafened animals had little effect on the basic response properties of AI neurons but resulted in complete loss of the normal cochleotopic organization of AI. This effect was almost completely reversed by chronic reactivation of the auditory pathway via the cochlear implant. We hypothesize that maintenance or reestablishment of a cochleotopically organized AI by activation of a restricted sector of the cochlea, as demonstrated in the present study, contributes to the remarkable clinical performance observed among human patients implanted at a young age. J. Comp. Neurol. 512:101–114, 2009. © 2008 Wiley‐Liss, Inc.
Selective reduction in synaptic proteins involved in vesicle docking and signalling at synapses in the ataxic mutant mouse stargazer
Authors: Leitch Beulah , Shevtsova Olga , Kerr John Richard 
Published: October 2008

AbstractThe spontaneous recessive mutant mouse stargazer has a specific and pronounced deficit in brain‐derived neurotrophic factor (BDNF) mRNA expression in the cerebellum. Cerebellar granule cells, in particular, show a selective and near‐total loss of BDNF. The mutation involves a defect in the calcium channel subunit Cacng2. This severely reduces expression of stargazin. A stargazin‐induced failure in BDNF expression is thought to underlie the cerebellar ataxia with which the mutant presents. BDNF is known to regulate plasticity at cerebellar synapses. However, relatively little is known about the mechanism involved. We previously demonstrated that the stargazer mutation affects the phenotype of cerebellar glutamatergic neurons. Stargazer neurons have less glutamate and proportionally fewer docked vesicles at presynaptic sites than controls. In the current study, we investigate the mechanism underlying BDNF‐induced synaptic changes by analyzing alterations in synaptic signalling proteins in the stargazer cerebellum. Expression levels of synaptic proteins were evaluated by measuring relative density of immunogold label over granule cell terminals in ultrathin sections from ataxic stargazer mutants compared with matched nonataxic littermates. We show that there is a selective and marked depletion in the levels of vesicle‐associated proteins (synaptobrevin, synaptophysin, synaptotagmin, and Rab3a) but not of plasma membrane‐associated protein (SNAP‐25) in the terminals of the BDNF‐deficient granule cells. Changes are restricted to the cerebellum; levels in the hippocampus are unaltered. These data suggest that the BDNF deficits in the cerebellum of stargazer affect synaptic vesicle docking by selectively altering synaptic‐protein distribution and abundance. J. Comp. Neurol. 512:52–73, 2009. © 2008 Wiley‐Liss, Inc.
Genetic tracing of subpopulation neurons in the prethalamus of mice (Mus musculus)
Authors: Delaunay Delphine , Heydon Katharina , Miguez Andres , Schwab Markus , Nave Klaus‐Armin , Thomas Jean Leon , Spassky Nathalie , Martinez Salvador , Zalc Bernard 
Published: October 2008

AbstractGenetic labeling based on the Cre/lox reporter system has allowed the creation of fate maps for progenitor cells and their offspring. In the diencephalon, pools of progenitors express the plp transcripts in the zona limitans intrathalamica (ZLI), the basal plate of the diencephalon (bpD), and the posterior part of the hypothalamus. We used plp‐Cre transgenics crossed with either Rosa26‐lox‐lacZ (R26R) or actin‐lox gfp (Z/EG) reporter mice to investigate the progeny of plp‐expressing ventricular cells in the diencephalon. We describe the subpopulations of prethalamic neurons derived from plp‐activated progenitors, their possible migratory routes as development proceeds, and their final positional identity. Neurons derived from plp‐expressing progenitors issued from the ZLI contribute to GABAergic cells in the zona incerta, the subgeniculate nucleus, the ventral lateral geniculate, and the intergeniculate leaflet. Plp+ progenitors in the bpD and posterior hypothalamus appear to generate glutamatergic neurons in the subthalamic nucleus and GABAergic neurons in the mammillary and retromammillary tegmentum derivatives. In all these nuclei the contribution of plp+ progenitors is only partial, illustrating the heterogeneity of origin of neurons in prethalamic and caudal hypothalamic nuclei. J. Comp. Neurol. 512:74–83, 2009. © 2008 Wiley‐Liss, Inc.
Postmortem changes in the neuroanatomical characteristics of the primate brain: Hippocampal formation
Authors: Lavenex Pierre , Lavenex Pamela Banta , Bennett Jeffrey L. , Amaral David G. 
Published: October 2008

AbstractComparative studies of the structural organization of the brain are fundamental to our understanding of human brain function. However, whereas brains of experimental animals are fixed by perfusion of a fixative through the vasculature, human or ape brains are fixed by immersion after varying postmortem intervals. Although differential treatments might affect the fundamental characteristics of the tissue, this question has not been evaluated empirically in primate brains. Monkey brains were either perfused or acquired after varying postmortem intervals before immersion‐fixation in 4% paraformaldehyde. We found that the fixation method affected the neuroanatomical characteristics of the monkey hippocampal formation. Soma size was smaller in Nissl‐stained, immersion‐fixed tissue, although overall brain volume was larger as compared to perfusion‐fixed tissue. Nonphosphorylated high‐molecular‐weight neurofilament immunoreactivity was lower in CA3 pyramidal neurons, dentate mossy cells, and the entorhinal cortex, whereas it was higher in the mossy fiber pathway in immersion‐fixed tissue. Serotonin‐immunoreactive fibers were well stained in perfused tissue but were undetectable in immersion‐fixed tissue. Although regional immunoreactivity patterns for calcium‐binding proteins were not affected, intracellular staining degraded with increasing postmortem intervals. Somatostatin‐immunoreactive clusters of large axonal varicosities, previously reported only in humans, were observed in immersion‐fixed monkey tissue. In addition, calretinin‐immunoreactive multipolar neurons, previously observed only in rodents, were found in the rostral dentate gyrus in both perfused and immersion‐fixed brains. In conclusion, comparative studies of the brain must evaluate the effects of fixation on the staining pattern of each marker in every structure of interest before drawing conclusions about species differences. J. Comp. Neurol. 512:27–51, 2009. © 2008 Wiley‐Liss, Inc.
Usefulness of repeat cytology at the time of first colposcopy
Authors: Alves Rosane Ribeiro Figueiredo , Rabelo‐Santos Silvia Helena , Ribeiro Andrea Alves , Carneiro Megmar Aparecida dos Santos , Ximenes Yara , Tavares Suelene Brito do Nascimento , Saddi Vera , Zeferino Luiz Carlos 
Published: October 2008

AbstractThe value of repeat cytology in the detection of high‐grade preinvasive or invasive disease was analyzed at the time of colposcopy in cases of patients with abnormal referral cytology. A series of 136 patients with squamous abnormalities in their referral cytology, who had undergone repeat cytology and for whom outcome had been established, were included in the study. Final diagnosis consisted of 27 negative results (20%), 37 cases of CIN1 (27%), 31 CIN2 (23%), 39 CIN3 (29%), and 2 (1%) cases of squamous cell carcinoma (SCC). Referral and repeat cytology suggestive of atypical squamous cells cannot exclude high‐grade squamous intraepithelial lesion (ASC‐H), high‐grade squamous intraepithelial lesion (HSIL) were findings significantly associated with a final diagnosis of CIN2 or worse. Sensitivity and positive predictive value of repeat cytology for the histological diagnosis of significant histological neoplasia (CIN2 or worse) were 81.9% and 77.6%, respectively. In women with referral cytology findings of atypical squamous cells of undetermined significance or low‐grade squamous intraepithelial lesion (ASC‐US/LSIL), repeat cytology was suggestive of HSIL in 20% of cases (11/54), and in 4% (2/54) biopsy was negative or CIN1, and the final diagnosis established by LLETZ was CIN3. Eight cases (10%) of HSIL in referral and repeat cytology in which biopsies were negative or insufficient were diagnosed as CIN3 or worse in the final diagnosis. Repeat cytology would have changed therapeutic management in 4 and 10%, respectively, of patients included as ASC‐US/LSIL and ASC‐H/HSIL in referral cytology. Diagn. Cytopathol. 2009. © 2008 Wiley‐Liss, Inc.
Using developmental cognitive neuroscience to study behavioral and attentional control
Authors: Astle Duncan E. , Scerif Gaia 
Published: October 2008

AbstractAdult cognitive neuroscience employs a wide variety of techniques to investigate a broad range of behavioral and cognitive functions. One prominent area of study is that of executive control, complemented by a smaller but growing literature exploring thedevelopmentalcognitive neuroscience of executive control. To date this approach has often compared children with specific developmental disorders, such as ADHD and ASD, with typically developing controls. Whilst these comparisons have done much to advance our understanding of the neural markers that underpin behavioral difficulties at specific time‐points in development, we contend that they should leave developmental cognitive neuroscientists wanting. Studying the neural correlates of typical changes in executive control in their own right can reveal how different neural mechanisms characteristic of the adult end‐state emerge, and it can therefore inform the adult cognitive neuroscience of executive control itself. The current review addresses the extent to which developmentalists and adult cognitive neuroscientists have tapped this common ground. Some very elegant investigations illustrate how seemingly common processes in adulthood present as separable in childhood, on the basis of their distinctive developmental trajectories. These demonstrations have implications not only for an understanding of changing behavior from infancy through childhood and adolescence into adulthood, but, moreover, for our grasp of the adult end‐state per se. We contend that, if used appropriately, developmental cognitive neuroscience could enable us to construct a moremechanisticaccount of executive control. © 2008 Wiley Periodicals, Inc. Dev Psychobiol 51: 107–118, 2009