Journal of Comparative Neurology
1096-9861
0021-9967
Mỹ
Cơ quản chủ quản: WILEY , Wiley-Liss Inc.
Lĩnh vực:
Neuroscience (miscellaneous)
Phân tích ảnh hưởng
Thông tin về tạp chí
Established in 1891, JCN is the oldest continually published basic neuroscience journal. Historically, as the name suggests, the journal focused on a comparison among species to uncover the intricacies of how the brain functions. In modern times, this research is called systems neuroscience where animal models are used to mimic core cognitive processes with the ultimate goal of understanding neural circuits and connections that give rise to behavioral patterns and different neural states. Research published in JCN covers all species from invertebrates to humans, and the reports inform the readers about the function and organization of nervous systems in species with an emphasis on the way that species adaptations inform about the function or organization of the nervous systems, rather than on their evolution per se. JCN publishes primary research articles and critical commentaries and review-type articles offering expert insight in to cutting edge research in the field of systems neuroscience; a complete list of contribution types is given in the Author Guidelines. For primary research contributions, only full-length investigative reports are desired; the journal does not accept short communications.
Các bài báo tiêu biểu
Characterization of <i>Drosophila fruitless‐gal4</i> transgenes reveals expression in male‐specific <i>fruitless</i> neurons and innervation of male reproductive structures Abstract The fruitless (fru ) gene acts in the central nervous system (CNS) of Drosophila melanogaster to establish male sexual behavior. Genetic dissection of the locus has shown that one of the fru gene's promoter, P1, controls the spatial and temporal expression of male‐specific FruM proteins critical to determining stereotypical male sexual behavior. By using the Gal4‐expression system, we show that a 16‐kb fragment of the fru P1 promoter's 5′ regulatory region drives the expression of Gal4 in a subset of FruM ‐expressing neurons within both the pupal and adult CNS. Colocalization of FruM and a Gal4‐responsive reporter shows that the fru (P1 )‐gal4 fusion construct generates expression in both previously characterized FruM ‐expressing neurons as well as within cells of both the CNS and the peripheral nervous system that have not been demonstrated as FruM ‐expressing. Gal4‐expressing neurons are shown to innervate abdominal organs directly relevant to fru function; specifically, the muscle of Lawrence (MOL) and the male internal reproductive organs. Innervations of the latter are shown to originate from identified FruM ‐serotonergic neurons. Furthermore, we show that the MOL neuromuscular junction is sexually dimorphic. Finally, we describe Gal4 expression in neurites innervating male reproductive structures that are hypothesized to be targets of fru function. Isolation of the regulatory sequences controlling the expression of fru in the CNS, therefore, provides a potent tool for the manipulation of FruM ‐expressing neurons and for understanding the cellular basis of Drosophila reproductive behavior. J. Comp. Neurol. 475:270–287, 2004. © 2004 Wiley‐Liss, Inc.
Tập 475 Số 2 - Trang 270-287 - 2004
On the chromaffin cells of the nerve ganglia of Hirudo medicinalis, Lin
Tập 76 Số 3 - Trang 367-401 - 1942
Distribution of hypophysiotropic thyrotropin‐releasing hormone (TRH)‐synthesizing neurons in the hypothalamic paraventricular nucleus of the mouse Abstract Hypophysiotropic thyrotropin‐releasing hormone (TRH) neurons, the central regulators of the hypothalamic‐pituitary‐thyroid axis, are located in the hypothalamic paraventricular nucleus (PVN) in a partly overlapping distribution with non‐hypophysiotropic TRH neurons. The distribution of hypophysiotropic TRH neurons in the rat PVN is well understood, but the localization of these neurons is unknown in mice. To determine the distribution and phenotype of hypophysiotropic TRH neurons in mice, double‐ and triple‐labeling experiments were performed on sections of intact mice, and mice treated intravenously and intraperitoneally with the retrograde tracer Fluoro‐Gold. TRH neurons were located in all parts of the PVN except the periventricular zone. Hypophysiotropic TRH neurons were observed only at the mid‐level of the PVN, primarily in the compact part. In this part of the PVN, TRH neurons were intermingled with oxytocin and vasopressin neurons, but based on their size, the TRH neurons were parvocellular and did not contain magnocellular neuropeptides. Co‐localization of TRH and cocaine‐ and amphetamine‐regulated transcript (CART) were observed only in areas where hypophysiotropic TRH neurons were located. In accordance with the morphological observations, hypothyroidism increased TRH mRNA content of neurons only at the mid‐level of the PVN. These data demonstrate that the distribution of hypophysiotropic TRH neurons in mice is vastly different from the pattern in rats, with a dominant occurrence of these neurosecretory cells in the compact part and adjacent regions at the mid‐level of the PVN. Furthermore, our data demonstrate that the organization of the PVN is markedly different in mice and rats. J. Comp. Neurol. 518:3948–3961, 2010. © 2010 Wiley‐Liss, Inc.
Tập 518 Số 19 - Trang 3948-3961 - 2010
The Edinger‐Westphal nucleus: A historical, structural, and functional perspective on a dichotomous terminology Abstract The eponymous term nucleus of Edinger‐Westphal (EW) has come to be used to describe two juxtaposed and somewhat intermingled cell groups of the midbrain that differ dramatically in their connectivity and neurochemistry. On one hand, the classically defined EW is the part of the oculomotor complex that is the source of the parasympathetic preganglionic motoneuron input to the ciliary ganglion (CG), through which it controls pupil constriction and lens accommodation. On the other hand, EW is applied to a population of centrally projecting neurons involved in sympathetic, consumptive, and stress‐related functions. This terminology problem arose because the name EW has historically been applied to the most prominent cell collection above or between the somatic oculomotor nuclei (III), an assumption based on the known location of the preganglionic motoneurons in monkeys. However, in many mammals, the nucleus designated as EW is not made up of cholinergic, preganglionic motoneurons supplying the CG and instead contains neurons using peptides, such as urocortin 1, with diverse central projections. As a result, the literature has become increasingly confusing. To resolve this problem, we suggest that the term EW be supplemented with terminology based on connectivity. Specifically, we recommend that 1) the cholinergic, preganglionic neurons supplying the CG be termed the Edinger‐Westphal preganglionic (EWpg) population and 2) the centrally projecting, peptidergic neurons be termed the Edinger‐Westphal centrally projecting (EWcp) population. The history of this nomenclature problem and the rationale for our solutions are discussed in this review. J. Comp. Neurol. 519:1413–1434, 2011. © 2010 Wiley‐Liss, Inc.
Tập 519 Số 8 - Trang 1413-1434 - 2011
Hypothalamic and brainstem sources of pituitary adenylate cyclase‐activating polypeptide nerve fibers innervating the hypothalamic paraventricular nucleus in the rat Abstract The hypothalamic paraventricular nucleus (PVN) coordinates major neuroendocrine and behavioral mechanisms, particularly responses to homeostatic challenges. Parvocellular and magnocellular PVN neurons are richly innervated by pituitary adenylate cyclase‐activating polypeptide (PACAP) axons. Our recent functional observations have also suggested that PACAP may be an excitatory neuropeptide at the level of the PVN. Nevertheless, the exact localization of PACAP‐producing neurons that project to the PVN is not understood. The present study examined the specific contribution of various brain areas sending PACAP innervation to the rat PVN by using iontophoretic microinjections of the retrograde neuroanatomical tracer cholera toxin B subunit (CTb). Retrograde transport was evaluated from hypothalamic and brainstem sections by using multiple labeling immunofluorescence for CTb and PACAP. PACAP‐containing cell groups were found to be retrogradely labeled from the PVN in the median preoptic nucleus; preoptic and lateral hypothalamic areas; arcuate, dorsomedial, ventromedial, and supramammillary nuclei; ventrolateral midbrain periaqueductal gray; rostral and midlevel ventrolateral medulla, including the C1 catecholamine cell group; nucleus of the solitary tract; and dorsal motor nucleus of vagus. Minor PACAP projections with scattered double‐labeled neurons originated from the parabrachial nucleus, pericoeruleus area, and caudal regions of the nucleus of the solitary tract and ventrolateral medulla. These observations indicate a multisite origin of PACAP innervation to the PVN and provide a strong chemical neuroanatomical foundation for interaction between PACAP and its potential target neurons in the PVN, such as parvocellular CRH neurons, controlling physiologic responses to stressful challenges and other neuroendocrine or preautonomic PVN neurons. J. Comp. Neurol. 500:761–776, 2007. © 2006 Wiley‐Liss, Inc.
Tập 500 Số 4 - Trang 761-776 - 2007
Functional implications of limited leptin receptor and ghrelin receptor coexpression in the brain Abstract The hormones leptin and ghrelin act in apposition to one another in the regulation of body weight homeostasis. Interestingly, both leptin receptor expression and ghrelin receptor expression have been observed within many of the same nuclei of the central nervous system (CNS), suggesting that these hormones may act on a common population of neurons to produce changes in food intake and energy expenditure. In the present study we explored the extent of this putative direct leptin and ghrelin interaction in the CNS and addressed the question of whether a loss of ghrelin signaling would affect sensitivity to leptin. Using histological mapping of leptin receptor and ghrelin receptor expression, we found that cells containing both leptin receptors and ghrelin receptors are mainly located in the medial part of the hypothalamic arcuate nucleus. In contrast, coexpression was much less extensive elsewhere in the brain. To assess the functional consequences of this observed receptor distribution, we explored the effect of ghrelin receptor deletion on leptin sensitivity. In particular, the responses of ad libitum‐fed, diet‐induced obese and fasted mice to the anorectic actions of leptin were examined. Surprisingly, we found that deletion of the ghrelin receptor did not affect the sensitivity to exogenously administrated leptin. Thus, we conclude that ghrelin and leptin act largely on distinct neuronal populations and that ghrelin receptor deficiency does not affect sensitivity to the anorexigenic and body weight‐lowering actions of leptin. J. Comp. Neurol. 520:281–294, 2012. © 2011 Wiley Periodicals, Inc.
Tập 520 Số 2 - Trang 281-294 - 2012
Neuroanatomical characterization of a growth hormone secretagogue receptor‐green fluorescent protein reporter mouse ABSTRACT Growth hormone secretagogue receptor (GHSR) 1a is the only molecularly identified receptor for ghrelin, mediating ghrelin‐related effects on eating, body weight, and blood glucose control, among others. The expression pattern of GHSR within the brain has been assessed previously by several neuroanatomical techniques. However, inherent limitations to these techniques and the lack of reliable anti‐GHSR antibodies and reporter rodent models that identify GHSR‐containing neurons have prevented a more comprehensive functional characterization of ghrelin‐responsive neurons. Here we have systematically characterized the brain expression of an enhanced green fluorescence protein (eGFP) transgene controlled by the Ghsr promoter in a recently reported GHSR reporter mouse. Expression of eGFP in coronal brain sections was compared with GHSR mRNA expression detected in the same sections by in situ hybridization histochemistry. eGFP immunoreactivity was detected in several areas, including the prefrontal cortex, insular cortex, olfactory bulb, amygdala, and hippocampus, which showed no or low GHSR mRNA expression. In contrast, eGFP expression was low in several midbrain regions and in several hypothalamic nuclei, particularly the arcuate nucleus, where robust GHSR mRNA expression has been well‐characterized. eGFP expression in several brainstem nuclei showed high to moderate degrees of colocalization with GHSR mRNA labeling. Further quantitative PCR and electrophysiological analyses of eGFP‐labeled hippocampal cells confirmed faithful expression of eGFP within GHSR‐containing, ghrelin‐responsive neurons. In summary, the GHSR‐eGFP reporter mouse model may be a useful tool for studying GHSR function, particularly within the brainstem and hippocampus; however, it underrepresents GHSR expression in nuclei within the hypothalamus and midbrain. J. Comp. Neurol. 522:3644–3666, 2014. © 2014 Wiley Periodicals, Inc.
Tập 522 Số 16 - Trang 3644-3666 - 2014
Expression of ghrelin receptor mRNA in the rat and the mouse brain
Tập 494 Số 3 - Trang 528-548 - 2006
Comparative localization of serotonin<sub>1A, 1C</sub>, and <sub>2</sub> receptor subtype mRNAs in rat brain Abstract Serotonin (5‐HT) mediates its effects on neurons in the central nervous system through a number of different receptor types. To gain better insight as to the localization of 5‐HT responsive cells, the distribution of cells expressing mRNAs encoding the three 5‐HT receptor subtypes 1A,1C, and 2 was examined in rat brain with in situ hybridization using cRNA probes. 5‐HT1A receptor mRNA labeling was most pronounced in the olfactory bulb, anterior hippocampal rudiment, septum, hippocampus (dentate gyrus and layers CAI‐3), entorhinal cortex, interpeduncular nucleus, and medullary raphe nuclei. 5‐HT 1C receptor mRNA labeling was the most abundant and widespread of the three 5‐HT receptor subtypes examined. Hybridization signal was denset in the choroid plexus, anterior olfactory nucleus, olfactory tubercle piriform cortex, septum, subiculum, entorhinal cortex, claustrum, accumbens nuclues, striatum, lateral amygdala, paratenial and paracentral thalamic nuclei, subthalamic nucleus, substantia nigra, and reticular cell groups. 5‐HT2 receptor mRNA was localized to the olfactory bulb, anteriorhippocampal rudiment, frontal cortex, piriform cortex, entorhinal cortex, claustrum, pontine nuclei, and cranial nerve motor nuclei including the oculomotor, trigeminal motor, facial, dorsal motor nucleus of the vagus, and hypoglossal nuclei. The distributions of mRNAs for the three different 5‐HT receptor subtypes overlap with regions that bind various 5‐HT receptor‐selective ligands and are present in nearly all areas known to receive serotonergic innervation. The results of this study demonstrate that nervous which express these 5‐HT receptor subtypes are very widespread in the central nervous system, yet possess unique distributions with in the rat brain. Moreover, previously unreported regions of 5‐HT receptor subtype expression were observed, particulary with the 5‐HT receptor riboprobe in the brainstem. Finally, several brain areas contain multiple 5‐HT receptor subtype mRNAs, which leads to the possibility that individual cells may express more than one 5‐HT receptor subtype. © 1995 Willy‐Liss, Inc.
Tập 351 Số 3 - Trang 357-373 - 1995
Blood‐eye barriers in the rat: Correlation of ultrastructure with function Abstract The function of different vascular beds in the rat eye and brain was evaluated by measuring the transfer of a vascular tracer, 14 C‐α‐amino‐isobutyric acid, from blood to tissue. The density of vascular pores was measured in electron micrographs of perfusion‐fixed, age‐matched tissue to determine whether the differences in tracer transfer were paralleled by differences in ultrastructure. Tracer transfer in retina was approximately four times that in brain of the same animal. The transfer constant was not changed by the inclusion of cold α‐amino‐isobutyric acid, showing that transport across retinal vessels is not saturable, and indicating that, as in brain, transport is due to passive diffusion. Ultrastructurally, retinal vessels have a higher density of interendothelial junctions and of endothelial vesicles, both of which suggest higher vascular permeability. However, pericytes, which contribute to a second line of defence in the blood‐brain barrier, are approximately four times as numerous in retina as in brain, and we suggest that in the retina, they act to compensate for a more permeable endothelial barrier. Ciliary body vessels had a high transfer of tracer, probably as a consequence of the fenestrations in their walls. Iridial vessels had a relatively low transfer of tracer, similar to that in retina even though a proportion of the interendothelial junctions in iridial vessels had expanded junctional clefts suggestive of open paracellular channels. However, both iris and ciliary body may lose tracer to the anterior chamber fluid, leading us to underestimate the vascular permeability in these sites. © Wiley‐Liss, Inc.
Tập 340 Số 4 - Trang 566-576 - 1994