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Hippocampal Fields (hippocampal + field)

Distribution by Scientific Domains

Life Sciences	100%

Selected Abstracts

Nicotinic acetylcholine receptor expression in the hippocampus of 27 mouse strains reveals novel inhibitory circuitry

HIPPOCAMPUS, Issue 8 2008
Lorise C. Gahring
Abstract Mouse strains are well-characterized to exhibit differences in their physiological and behavioral responses to nicotine. This report examines the expression of the high-affinity nicotine binding receptor subunit, neuronal nicotinic receptor subunit alpha4 (nAChR,4), in the dorsal hippocampus of 27 inbred mouse strains. Multiple differences among mouse strains in the cellular expression of nAChR,4 between subregions of the hippocampal field are evident. Differences that we describe in the expression of nAChR,4 suggest mouse strains of diverse genetic origin could exhibit significant variation in how this receptor contributes to modulating intrahippocampal circuitry. These findings define a genetic frame-work in which the strain-specific responses to nicotine include underlying contributions by the varied anatomical context in which nAChRs are expressed. © 2008 Wiley-Liss, Inc. [source]

Effect of canonical Wnt inhibition in the neurogenic cortex, hippocampus, and premigratory dentate gyrus progenitor pool

DEVELOPMENTAL DYNAMICS, Issue 7 2008
Nina Solberg
Abstract Canonical Wnt signaling is crucial for the correct development of both cortical and hippocampal structures in the dorsal telencephalon. In this study, we examined the role of the canonical Wnt signaling in the dorsal telencephalon of mouse embryos at defined time periods by inhibition of the pathway with ectopic expression of Dkk1. Transgenic mice with the D6-driven Dkk1 gene exhibited reduced canonical Wnt signaling in the cortex and hippocampus. As a result, all hippocampal fields were reduced in size. Neurogenesis in the dentate gyrus was severely reduced both in the premigratory and migratory progenitor pool. The lower number of progenitors in the dentate gyrus was not rescued after migration to the subgranular zone and thus the dentate gyrus lacked the entire internal blade and a part of the external blade from postnatal to adult stages. Developmental Dynamics 237:1799,1811, 2008. © 2008 Wiley-Liss, Inc. [source]

Organization of connections of the basal and accessory basal nuclei in the monkey amygdala

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2000
Eva Bonda
Abstract PLEASE NOTE: Expression of Concern (EJN, 12:11, p4153) The present study investigated the intrinsic connections of the basal and accessory basal nuclei of the Macaca fascicularis monkey by means of the anterograde tracers Phaseolus vulgaris-leucoagglutinin (PHA-L) and biotinylated dextran amine (BDA). Analysis of the intranuclear connections of the basal nucleus indicates that there are five modules: dorsal, intermediate, ventral lateral, ventral medial and periamygdaloid sulcal cortex. The dorsal division projects to the intermediate division. Laterally, the intermediate division projects to the ventral lateral division and dorsal parts of the ventral medial division. Ventrally, the ventral lateral division projects to the ventral medial division and periamygdaloid sulcal cortex, which appears to constitute a medial extension of the basal nucleus onto the cortical surface of the amygdala. Medially, the ventral medial division projects to the intermediate and dorsal divisions. Thus, the connections between these modules form functional microcolumns within the nucleus with distinct patterns of information flow that are dorsal to ventral laterally, lateral to medial ventrally, and ventral to dorsal medially. Observations on the intranuclear connections of the accessory basal nucleus suggest that they are organized into two relatively distinct domains: the dorsal division projects to the ventral division and the ventral division projects primarily to the ventromedial division. Projections to other amygdaloid areas originate in select divisions of the basal and accessory basal nuclei, and are topographically distributed. The organization of intrinsic connections of the basal nuclei correlates with specific amygdalo-cortical connections and suggests that extensive convergence of information takes place within the amygdala, which potentially influences activity at both the temporal and parietal pathways and hippocampal fields. [source]

Characterization of neuropeptide Y2 receptor protein expression in the mouse brain.

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 3 2006

Abstract Neuropeptide Y (NPY), a 36-amino-acid peptide, mediates biological effects by activating Y1, Y2, Y5, and y6 receptors. NPY neurons innervate many brain regions, including the hypothalamus, where NPY is involved in regulation of a broad range of homeostatic functions. We examined, by immunohistochemistry with tyramide signal amplification, the expression of the NPY Y2 receptor (Y2R) in the mouse brain with a newly developed rabbit polyclonal antibody. Y2R immunoreactivity was specific with its absence in Y2R knockout (KO) mice and in adjacent sections following preadsorption with the immunogenic peptide (10,5 M). Y2R-positive processes were located in many brain regions, including the olfactory bulb, some cortical areas, septum, basal forebrain, nucleus accumbens, amygdala, hippocampus, hypothalamus, substantia nigra compacta, locus coeruleus, and solitary tract nucleus. However, colchicine treatment was needed to detect Y2R-like immunoreactivity in cell bodies in many, but not all, areas. The densest distributions of cell bodies were located in the septum basal forebrain, including the bed nucleus, and amygdala, with lower density in the anterior olfactory nucleus, nucleus accumbens, caudal striatum, CA1, CA2, and CA3 hippocampal fields, preoptic nuclei lateral hypothalamus, and A13 DA cells. The widespread distribution of Y2R-positive cell bodies and fibers suggests that NPY signaling through the Y2R is common in the mouse brain. Localization of the Y2R suggests that it is mostly presynaptic, a view supported by its frequent absence in cell bodies in the normal mouse and its dramatic increase in cell bodies of colchicine-treated mice. J. Comp. Neurol. 499:357,390, 2006. © 2006 Wiley-Liss, Inc. [source]