Conditioned odor preference and <i>Arc</i> expression in amygdala and insular cortex.

<p>(A) Schematic of the procedure used for behavioral and catFISH studies. (B) Consumption of odorized water (grey bar) or plain water (open bar) per 30 min during a two-bottle choice test. (C) Representative image from the basolateral amygdala showing Arc localization following stimulus presentation in a Paired animal. a) Neuron responding only to the first stimulation (odor) shows Arc staining (in red) in the cytoplasm surrounding the nucleus (counterstained green). b) Neuron responding only to the second stimulation (taste) shows dense Arc foci within the nucleus. c) Neuron responding to both odor and taste shows cytoplasmic and nuclear staining. Scale bar, 10 µm. **, *: intra-group difference (p<0.01; p<0.05).</p

LIM-homeobox gene Lhx5 is required for normal development of Cajal-Retzius cells

Cajal-Retzius (C-R) cells play important roles in the lamination of the mammalian cortex via reelin secretion. The genetic mechanisms underlying the development of these neurons have just begun to be unraveled. Here, we show that two closely related LIM-homeobox genes Lhx1 and Lhx5 are expressed in reelin+ cells in various regions in the mouse telencephalon at or adjacent to sites where the C-R cells are generated, including the cortical hem, the mantle region of the septal/retrobulbar area, and the ventral pallium. Whereas Lhx5 is expressed in all of these reelin-expressing domains, Lhx1 is preferentially expressed in the septal area and in a continuous domain spanning from lateral olfactory region to caudomedial territories. Genetic ablation of Lhx5 results in decreased reelin+ and p73+ cells in the neocortical anlage, in the cortical hem, and in the septal, olfactory, and caudomedial telencephalic regions. The overall reduction in number of C-R cells in Lhx5 mutants is accompanied by formation of ectopic reelin+ cell clusters at the caudal telencephalon. Based on differential expression of molecular markers and by fluorescent cell tracing in cultured embryos, we located the origin of reelin+ ectopic cell clusters at the caudomedial telencephalic region. We also confirmed the existence of a normal migration stream of reelin+ cells from the caudomedial area to telencephalic olfactory territories in wild-type embryos. These results reveal a complex role for Lhx5 in regulating the development and normal distribution of C-R cells in the developing forebrain. Copyright © 2010 the authors.Peer Reviewe

Slit-Robo signals regulate pioneer axon pathfinding of the tract of the postoptic commissure in the mammalian forebrain

11 p., 5 figures and references.During early vertebrate forebrain development, pioneer axons establish a symmetrical scaffold descending longitudinally through the rostral forebrain, thus forming the tract of the postoptic commissure (TPOC). In mouse embryos, this tract begins to appear at embryonic day 9.5 (E9.5) as a bundle of axons tightly constrained at a specific dorsoventral level. We have characterized the participation of the Slit chemorepellants and their Robo receptors in the control of TPOC axon projection. In E9.5-E11.5 mouse embryos, Robo1 and Robo2 are expressed in the nucleus origin of the TPOC (nTPOC), and Slit expression domains flank the TPOC trajectory. These findings suggested that these proteins are important factors in the dorsoventral positioning of the TPOC axons. Consistently with this role, Slit2 inhibited TPOC axon growth in collagen gel cultures, and interfering with Robo function in cultured embryos induced projection errors in TPOC axons. Moreover, absence of both Slit1 and Slit2 or Robo1 and Robo2 in mutant mouse embryos revealed aberrant TPOC trajectories, resulting in abnormal spreading of the tract and misprojections into both ventral and dorsal tissues. These results reveal that Slit-Robo signaling regulates the dorsoventral position of this pioneer tract in the developing forebrain.Contract grant sponsor: The Wellcome Trust; Contract grant number: GR071174; Contract grant sponsor: CONACYT; Contract grant number: 101433 (to A.V.-E.); Contract grant sponsor: CONACYT (to I.R.-C. and C.M.G.-P.); Contract grant sponsor: Program Ramón y Cajal-2004, Spanish Ministry of Health, Instituto de Salud Carlos III-CIBERSAM; Contract grant sponsor: MEC; Contract grant number: SAF2008-01004; Contract grant sponsor: NIH; Contract grant number: P20 RR-016464; Contract grant sponsor: INBRE Program of the National Center for Research Resources; Contract grant number: HD38069; Contract grant number: NS054740; Contract grant sponsor: March of Dimes; Contract grant number: 1-FY06-387 (to G.S.M.); Contract grant sponsor: DGAPA-UNAM (to A.M.).Peer reviewe