Differentiation of cerebellar mossy fiber synapses in the rat: A quantitative electron microscope study

Hámori, J.; Somogyi, J.

doi:10.1002/cne.902200402

Cited by 176 publications

(134 citation statements)

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“…This MT regulation might control the MF growth cone enlargement and axon spreading that occurs when they contact GCs in vivo [11]. Crucial in vivo evidence demonstrated that Wnt-7a −/− mice had decreased complexity and synapsin-I levels at glomerular rosettes, consistent with the observation that WNT-7a could induce synapsin-I clustering in cultured MFs [10].…”

Section: Vertebrate Wnts As Retrograde Signals During Synapse Developsupporting

confidence: 62%

“…MFs from pontine explants grown in GC-conditioned medium displayed increased axonal area and growth cone size, in addition to complexity, features typically observed after MFs enter the cerebellar cortex and contact GCs [11]. These changes were mimicked by the addition of soluble WNT-7a or the GSK-3β inhibitor lithium chloride (LiCl), and blocked by the Wnt antagonist secreted Frizzled-related protein (sFRP) [10].…”

Section: Vertebrate Wnts As Retrograde Signals During Synapse Developmentioning

confidence: 99%

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Wnts: up-and-coming at the synapse

Speese

Budnik

2007

Trends in Neurosciences

119

105

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Synaptic development, function and plasticity are highly regulated processes requiring a precise coordination of pre-and postsynaptic events. Recent studies have begun to highlight Wingless-Int (Wnt) signaling as a key player in synapse differentiation and function. Emerging roles of Wnts include the differentiation of synaptic specializations, microtubule dynamics, architecture of synaptic protein organization, modulation of synaptic efficacy and regulation of gene expression. Wnt transduction pathways: a brief précisExciting roles for embryonic morphogens of the Wingless-Int family (Wnt) beyond those in early pattern formation are beginning to emerge. These include roles in axon guidance, dendrite morphology, synapse formation and plasticity [1,2]. These studies make a clear case for Wnt function in post-mitotic neurons, and highlight the multitude of mechanisms activated by Wnts within the nervous system. The Wnt pathway has pivotal roles in defining positional information in the embryo. Misregulation of this pathway is linked to cancer, and the pathogenesis of Alzheimer's and Huntington disease [3,4]. The best studied Wnt transduction cascade is the canonical pathway, in which Wnt binds to its receptor Frizzled (Fz) in the receiving cell (Figure 1a,b). This binding activates the postsynaptic density-95/Discs-Large (DLG)/zona occludens-1 (PDZ) protein dishevelled (DVL), which disrupts a so-called 'destruction complex' containing glycogen synthase kinase-3β (GSK-3β), Axin and adenomatous polyposis coli (APC). In the absence of Wnt signaling, this complex constitutively phosphorylates β-catenin, leading to its proteasomal degradation. The binding of Wnt to Fz disrupts the destruction complex, resulting in cytoplasmic stabilization of β-catenin and its import into the nucleus [5]. In the nucleus, β-catenin associates with lymphoid enhancer factor (also known as T-cell factor) (LEF/TCF) transcription factors to regulate transcription. Additionally, β-catenin can bind to cadherins [6,7], but this function is not discussed here.Two non-canonical Wnt pathways have a role in development: (i) the planar cell polarity (PCP) pathway, in which Fz acts through Jun N-terminal kinase (JNK) to regulate the cytoskeleton (Figure 1e), and (ii) the Wnt-Ca 2+ signaling pathway, in which Fz activation

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Section: Vertebrate Wnts As Retrograde Signals During Synapse Developsupporting

confidence: 62%

Section: Vertebrate Wnts As Retrograde Signals During Synapse Developmentioning

confidence: 99%

Wnts: up-and-coming at the synapse

Speese

Budnik

2007

Trends in Neurosciences

119

105

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“…Moreover, the majority of both α1 and α6 subunit proteins accumulated adjacent to the Golgi cell axon terminals. These results demonstrated that (1) GAD-positive growth cones and varicosities probably undergo a change to GABAergic terminals [26,48], (2) GABAergic synapses were massively formed during the second postnatal week [2,28,31,37], and (3) GABAergic innervation might initiate the expression of the GABA A receptor α1 and α6 subunit genes, as well as trafficking and clustering of proteins to the synaptic site [1,8,12,13,16,17,20,24,46,48,61].…”

Section: Formation and Maturation Of Gabaergic Synapses In The Cerebementioning

confidence: 99%

“…Several electron microscopic investigations demonstrated ontogeny of the GABAergic synapses [2,27,28,45]. Sequential to excitatory synapse assembly, inhibitory synapses appear at the end of the first postnatal week and the number of GABAergic synapses increases during the second and third postnatal week in the rat cerebellar granular layer [2,27,28].…”

Section: Introductionmentioning

confidence: 99%

“…Sequential to excitatory synapse assembly, inhibitory synapses appear at the end of the first postnatal week and the number of GABAergic synapses increases during the second and third postnatal week in the rat cerebellar granular layer [2,27,28]. During the same period, intracellular localization of glutamic acid decarboxylase (GAD), which is a synthetic enzyme of GABA [57,58,60], drastically changes [45].…”

Section: Introductionmentioning

confidence: 99%

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Morphological development and maturation of the GABAergic synapses in the mouse cerebellar granular layer

Takayama¹,

Inoue²

2004

Developmental Brain Research

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In the adult central nervous system (CNS), γ-amino butyric acid (GABA) is a predominant inhibitory neurotransmitter, which regulates glutamatergic activity. Recent studies have revealed that GABA serves as an excitatory transmitter in the immature CNS, and is involved in brain morphogenesis. To elucidate how GABA exerts its effect on immature neurons and how GABAergic synapses are formed, we examined both development of pre-and post-synaptic elements of the GABAergic synapses formed between granule and Golgi cells in the mouse cerebellar granular layer. Immunohistochemistry for glutamic acid decarboxylase (GAD) demonstrated that GABA was localized throughout the Golgi cells before postnatal day 7 (P7), and became confined to the axon terminals during the second postnatal week. Electron microscopic analysis demonstrated that GABAergic synapses were clearly detected at P10. In situ hybridization and immunohistochemistry for the GABA A receptor α1 and α6 subunits, which are mainly involved in inhibitory synaptic transmission, demonstrated that both subunits appeared at P7. Distribution of both subunits expanded in the granular layer with special reference to the development of GABAergic synapses.Furthermore, the majority of the subunits accumulated adjacent to the GABAergic terminals.These results suggested that in the granular layer, GABA might be non-synaptically secreted from Golgi cell axons and dendrites during the first postnatal week. From the second postnatal week, GABA is synaptically released and begins to mediate inhibitory transmission.Furthermore, it was suggested that GABAergic innervation could initiate expression and trafficking of the GABA A receptors containing the α1 and α6 subunits.

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Specificity of identified central synapses in the embryonic cockroach: Appropriate connections form before the onset of spontaneous afferent activity

1996

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The mechanisms by which neurons recognize the appropriate postsynaptic cells remain largely unknown. A useful approach to this problem is to use a system with a few identifiable neurons that form highly specific synaptic connections. We studied the development of synapses between two identified cercal sensory afferents and two giant interneurons (GIs) in the embryonic cockroach Periplaneta americana. By 46% of embryonic development, the axons of the filiform hair sensory neurons have entered the terminal ganglionic neuropil and grow alongside the GI primary dendrites, although they do not form synapses. From 50% of development, the GI dendrites grow outward from the center of the neuropil to contact the presynaptic axons and their branches. The sensory neurons begin to spike at 52% of development, and, from 55% of development, these action potentials evoked excitatory postsynaptic potentials in the GIs. Synaptic contacts were first seen at this time. The pattern of synaptic connections was highly specific from the outset. G12 had strong input from the medial (M) afferent and had almost negligible input from the lateral (L) afferent, whereas G13 had input from both. This specificity was present before bursts of spontaneous activity began in the sensory neurons at 59% of development. G12 filopodia selectively formed synaptic contacts with the M axon rather than the L axon. The few contacts made by G12 with the L axon had a normal morphology but fewer presynaptic densities. Filopodial insertions were not involved in selective synapse formation. In this system, highly specific synaptic recognition appears to be activity independent.

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Differentiation of cerebellar mossy fiber synapses in the rat: A quantitative electron microscope study

Cited by 176 publications

References 28 publications

Wnts: up-and-coming at the synapse

Wnts: up-and-coming at the synapse

Morphological development and maturation of the GABAergic synapses in the mouse cerebellar granular layer

Specificity of identified central synapses in the embryonic cockroach: Appropriate connections form before the onset of spontaneous afferent activity

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