Lei Zhang

Tongji Medical University, Shanghai, Shanghai Shi, China

Are you Lei Zhang?

Claim your profile

Publications (7)31.15 Total impact

  • Article: [Achievements of moxibustion therapy in Wushier Bingfang (prescriptions for fifty-two diseases) of Mawangdui silk manuscript].
    Lei Zhang, Rong-Lin Cai, Ling Hu
    [show abstract] [hide abstract]
    ABSTRACT: Wushier Bingfang (Prescriptions for Fifty-two Diseases), the unearthed Mawangdui silk manuscript from the Han Dynasty (206 B. C.-220 A. D. ) is studied in this article. It is held that the book preserved the earliest prescription of moxibustion. It recorded intensive indications of moxibustion, abundant materials as well as manipulations of moxibustioin. The value and achievements of the book is further revealed.
    Zhongguo zhen jiu = Chinese acupuncture & moxibustion 03/2013; 33(3):279-80.
  • Source
    Article: Adult raphe-specific deletion of Lmx1b leads to central serotonin deficiency.
    [show abstract] [hide abstract]
    ABSTRACT: The transcription factor Lmx1b is essential for the differentiation and survival of central serotonergic (5-HTergic) neurons during embryonic development. However, the role of Lmx1b in adult 5-HTergic neurons is unknown. We used an inducible Cre-LoxP system to selectively inactivate Lmx1b expression in the raphe nuclei of adult mice. Pet1-CreER(T2) mice were generated and crossed with Lmx1b(flox/flox) mice to obtain Pet1-CreER(T2); Lmx1b(flox/flox) mice (which termed as Lmx1b iCKO). After administration of tamoxifen, the level of 5-HT in the brain of Lmx1b iCKO mice was reduced to 60% of that in control mice, and the expression of tryptophan hydroxylase 2 (Tph2), serotonin transporter (Sert) and vesicular monoamine transporter 2 (Vmat2) was greatly down-regulated. On the other hand, the expression of dopamine and norepinephrine as well as aromatic L-amino acid decarboxylase (Aadc) and Pet1 was unchanged. Our results reveal that Lmx1b is required for the biosynthesis of 5-HT in adult mouse brain, and it may be involved in maintaining normal functions of central 5-HTergic neurons by regulating the expression of Tph2, Sert and Vmat2.
    PLoS ONE 02/2013; 6(1):e15998. · 4.09 Impact Factor
  • Article: Expression of Transcription Factor Satb2 in Adult Mouse Brain.
    [show abstract] [hide abstract]
    ABSTRACT: Previous investigations on the expression and function of special AT-rich sequence binding protein 2 (Satb2) are largely limited to the cerebral cortex. Here, we explore the expression of Satb2 thoroughly by immunohistochemistry in the adult mouse central nervous system (CNS). Besides the cerebral cortex, we found that Satb2 is specifically expressed in the bed nucleus of the stria terminalis, horizontal limb of the diagonal band, lateral hypothalamic area, arcuate nucleus, hypothalamic paraventricular nucleus, ventral tegmental nucleus, laterodorsal tegmental nucleus, dorsal raphe nucleus, rostral periolivary region, and parabrachial nucleus. Double immunostaining showed that Satb2 is exclusively expressed in the excitatory neurons of neocortex. In addition, Satb2 is specifically expressed in A12 group of hypothalamic dopaminergic neurons and in serotonergic neurons in the dorsal part of the dorsal raphe nucleus. Our results present a comprehensive overview of Satb2 expression in the adult brain and provide insights for studying the role of Satb2 in the mature CNS. Anat Rec, 2013. © 2013 Wiley Periodicals, Inc.
    The Anatomical Record Advances in Integrative Anatomy and Evolutionary Biology 02/2013; · 1.47 Impact Factor
  • Source
    Article: Satb2 is required for dendritic arborization and soma spacing in mouse cerebral cortex.
    [show abstract] [hide abstract]
    ABSTRACT: Self-avoidance is a mechanism by which dendrites from the same neuron repel one another in order to establish uniform coverage of the dendritic field. The importance of self-avoidance for the development of complex arborization patterns has been highlighted by studies of Drosophila sensory and mouse retinal neurons. However, it is unclear whether branch patterning in the mammalian central nervous system is also governed by this strategy. We reduced Satb2 expression in a population of layer II/III pyramidal neurons in vivo by RNA interference and found that the somas of Satb2-deficient neurons clumped together, and their dendrites failed to expand laterally but instead formed fascicles. Furthermore, experiments showed that reducing Satb2 caused the adhesion of not only neighboring Satb2-deficient neurons but also neighboring wild-type neurons. Our results indicate a cell autonomous and non-cell autonomous role for Satb2 in regulating the adhesive and/or repulsive properties of cerebral pyramidal neurons.
    Cerebral Cortex 09/2011; 22(7):1510-9. · 6.54 Impact Factor
  • Source
    Article: Distribution of Satb1 in the central nervous system of adult mice.
    [show abstract] [hide abstract]
    ABSTRACT: This study consists of a thorough immunohistochemical examination of the expression profile of the transcription factor Satb1 (special AT-rich sequence binding protein 1) in the adult mouse central nervous system (CNS). Satb1-positive neurons were abundant in the deep layers of the neocortex, subiculum, anterior olfactory nucleus, nucleus of diagonal band, anterior part of the basolateral amygdaloid nucleus, compact part of substantia nigra, ventral tegmental area, ventral and dorsal tegmental nuclei, laterodorsal tegmental nucleus, and medullary and spinal dorsal horns. Relatively smaller populations of Satb1-positive neurons were observed in the piriform cortex, hippocampus, other subnuclei of the amygdala, centrolateral thalamic nucleus, parafascicular thalamic nucleus, posterior hypothalamic area, ventral part of the premammillary nucleus, supramammillary nucleus, deep layers of the superior colliculus, dorsal raphe nucleus, nucleus of trapezoid body, superior periolivary nucleus and nucleus of lateral lemniscus, and parabrachial region. Double immunostaining showed that Satb1 was expressed in midbrain dopaminergic neurons, but not in cholinergic or serotonergic neurons. Satb1 expression was never observed in glial cells. This study presents a comprehensive overview of Satb1 expression in the CNS, and provides insights for investigating the role of Satb1 in the mature CNS.
    Neuroscience Research 06/2011; 71(1):12-21. · 2.25 Impact Factor
  • Source
    Article: Zbtb20 is essential for the specification of CA1 field identity in the developing hippocampus.
    [show abstract] [hide abstract]
    ABSTRACT: The development of hippocampal circuitry depends on the proper assembly of correctly specified and fully differentiated hippocampal neurons. Little is known about factors that control the hippocampal specification. Here, we show that zinc finger protein Zbtb20 is essential for the specification of hippocampal CA1 field identity. We found that Zbtb20 expression was initially activated in the hippocampal anlage at the onset of corticogenesis, and persisted in immature hippocampal neurons. Targeted deletion of Zbtb20 in mice did not compromise the progenitor proliferation in the hippocampal and adjacent transitional ventricular zone, but led to the transformation of the hippocampal CA1 field into a transitional neocortex-like structure, as evidenced by cytoarchitectural, neuronal migration, and gene expression phenotypes. Correspondingly, the subiculum was ectopically located adjacent to the CA3 in mutant. Although the field identities of the mutant CA3 and dentate gyrus (DG) were largely maintained, their projections were severely impaired. The hippocampus of Zbtb20 null mice was reduced in size, and exhibited increased apoptotic cell death during postnatal development. Our data establish an essential role of Zbtb20 in the specification of CA1 field identity by repressing adjacent transitional neocortex-specific fate determination.
    Proceedings of the National Academy of Sciences 03/2010; 107(14):6510-5. · 9.68 Impact Factor
  • Source
    Article: Activity-dependent development of callosal projections in the somatosensory cortex.
    [show abstract] [hide abstract]
    ABSTRACT: The corpus callosum is the largest commissural system in the mammalian brain, but the mechanisms underlying its development are not well understood. Here we report that neuronal activity is necessary for the normal development and maintenance of callosal projections in the mouse somatosensory cortex. We labeled a subpopulation of layer II/III callosal neurons via in utero electroporation and traced their axons in the contralateral cortex at different postnatal stages. Callosal axons displayed region- and layer-specific projection patterns within the first 2 weeks postnatally. Prenatal suppression of neuronal excitation was achieved via electroporation-induced overexpression of the inward rectifying potassium channel Kir2.1 in layer II/III cortical neurons. This resulted in abnormal callosal projections with many axons extending beyond layers II-III to terminate in layer I. Others failed to terminate at the border between the primary and secondary somatosensory cortices. Blocking synaptic transmission via expression of the tetanus toxin light chain (TeNT-LC) in these axons produced a more pronounced reduction in the projections to the border region, and the eventual disappearance of callosal projections over the entire somatosensory cortex. When Kir2.1 and TeNT-LC were coexpressed, callosal axon targeting exhibited a more severe phenotype that appeared to represent the addition of the effects produced by individual expression of Kir2.1 and TeNT-LC. These results underscore the importance of activity in regulating the developing neural connections and suggest that neuronal and synaptic activities are involved in regulating different aspects of the development of callosal projection.
    Journal of Neuroscience 11/2007; 27(42):11334-42. · 7.11 Impact Factor