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Tracing Study (tracing + study)
Selected AbstractsReciprocal connections between olfactory structures and the cortex of the rostral superior temporal sulcus in the Macaca fascicularis monkeyEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2005A. Mohedano-Moriano Abstract Convergence of sensory modalities in the nonhuman primate cerebral cortex is still poorly understood. We present an anatomical tracing study in which polysensory association cortex located at the fundus and upper bank of the rostral superior temporal sulcus presents reciprocal connections with primary olfactory structures. At the same time, projections from this polysensory area reach multiple primary olfactory centres. Retrograde (Fast Blue) and anterograde (biotinylated dextran,amine and 3H-amino acids) tracers were injected into primary olfactory structures and rostral superior temporal sulcus. Retrograde tracers restricted to the anterior olfactory nucleus resulted in labelled neurons in the rostral portion of the upper bank and fundus of superior temporal sulcus. Injections of biotinylated dextran,amine at the fundus and upper bank of the superior temporal sulcus confirmed this projection by labelling axons in the dorsal and lateral portions of the anterior olfactory nucleus, as well as piriform, periamygdaloid and entorhinal cortices. Retrograde tracer injections at the rostral superior temporal sulcus resulted in neuronal labelling in the anterior olfactory nucleus, piriform, periamygdaloid and entorhinal cortices, thus providing confirmation of the reciprocity between primary olfactory structures and the cortex at the rostral superior temporal sulcus. The reciprocal connections between the rostral part of superior temporal sulcus and primary olfactory structures represent a convergence for olfactory and other sensory modalities at the cortex of the rostral temporal lobe. [source] Somatic and visceral afferents to the ,vasodepressor region' of the caudal midline medulla in the ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2003Jason R. Potas Abstract Previous research has found that the integrity of a restricted region of the caudal midline medulla (including caudal portions of nucleus raphé obscurus and nucleus raphé pallidus) was critical for vasodepression (hypotension, bradycardia, decreased cardiac contractility) evoked either by haemorrhage or deep pain. In this anatomical tracing study we found that the vasodepressor part of the caudal midline medulla (CMM) receives inputs arising from spinal cord, spinal trigeminal nucleus (SpV) and nucleus of the solitary tract (NTS). Specifically: (i) a spinal,CMM projection arises from neurons of the deep dorsal horn, medial ventral horn and lamina X at all spinal segmental levels, with approximately 60% of the projection originating from the upper cervical spinal cord (C1,C4); (ii) a SpV,CMM projection arises primarily from neurons at the transition between subnucleus caudalis and subnucleus interpolaris; (iii) a NTS,CMM projection arises primarily from neurons in ventrolateral and medial subnuclei. In combination, the specific spinal, SpV and NTS regions which project to the CMM receive the complete range of somatic and visceral afferents known to trigger vasodepression. The role(s) of each specific projection is discussed. [source] The immunosuppressant mycophenolate mofetil improves preservation of the perforant path in organotypic hippocampal slice cultures: A retrograde tracing studyHIPPOCAMPUS, Issue 5 2006Tilman M. Oest Abstract Previous studies with excitotoxically lesioned organotypic hippocampal slice cultures (OHSC) have revealed that the immunosuppressant mycophenolate mofetil (MMF) inhibits microglial activation and suppresses neuronal injury in the dentate gyrus. We here investigate whether MMF also has beneficial effects on axon survival in a long-range projection, the perforant path. Complex OHSC including the entorhinal cortex were obtained from Wistar rats (p8); the plane of section ensuring that perforant path integrity was preserved. These preparations were cultured for 9 days in vitro with or without MMF (100 ,g/ml). After fixation, the perforant path was retrogradely labeled by application of the fluorescent dye DiI (1,1,-dioctadecyl-3,3,3,,3,-tetramethylindo-carbocyanine) in the hilus of the dentate gyrus, and neuronal perikarya were immunohistochemically stained by the neuron-specific marker NeuN. Analysis of DiI-labeled and NeuN-stained OHSC by confocal laser scanning microscopy revealed double-labeled neurons in the entorhinal cortex, which projected to the dentate gyrus via the perforant path. Quantitative analysis showed that the number of these double-labeled neurons was 19-fold higher in OHSC treated with MMF than in control cultures (P < 0.05). Our findings indicate that MMF treatment improves preservation of the perforant path and encourage further studies on development and regeneration of long-range projections under the influence of immunosuppressants. © 2006 Wiley-Liss, Inc. [source] Genetic fate mapping of Olig2 progenitors in the injured adult cerebral cortex reveals preferential differentiation into astrocytesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 16 2008Kouko Tatsumi Abstract Olig2 is a basic helix-loop-helix (bHLH) transcription factor essential for development of motoneurons and oligodendrocytes. It is known that Olig2+ cells persist in the central nervous system (CNS) from embryonic to adult stages and that the number of Olig2+ progenitors increases in the injured adult CNS. Recent studies have demonstrated an inhibitory action of Olig2 on neurogenesis in adult CNS, but the fate of Olig2+ cells in the injured state remains largely unknown. To trace directly the fate of Olig2 cells in the adult cerebral cortex after injury, we employed the CreER/loxP system to target the olig2 locus. In this genetic tracing study, green fluorescent protein (GFP) reporter-positive cells labeled after cryoinjury coexpressed glial fibrillary acidic protein (GFAP), an astrocytic marker. Electron microscopy also showed that GFP+ cells have the ultrastructural characteristics of astrocytes. Furthermore, GFP+ cells labeled before injury, most of which had been NG2 cells, also produced bushy astrocytes. Here we show direct evidence that Olig2+ cells preferentially differentiate into astrocytes, which strongly express GFAP, in response to injury in the adult cerebral cortex. These results suggest that reactive astrocytes, known to be the main contributors to glial scars, originate, at least in part, from Olig2+ cells. © 2008 Wiley-Liss, Inc. [source] | ||||||||||