Programmed and Induced Phenotype of the Hippocampal Granule Cells

Gómez-Lira, Gisela; Lamas, Marta; Romo-Parra, Héctor; Gutiérrez, Rafael

doi:10.1523/jneurosci.1674-05.2005

Cited by 81 publications

(62 citation statements)

References 51 publications

(64 reference statements)

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“…Similarly, in cerebellar mossy fiber terminals, VGAT was colocalized with VGLUT1 and VGLUT2, though here all mossy fiber terminals expressed the vesicular GABA transporter. In addition to singlecell PCR data demonstrating the presence of VGAT mRNA in hippocampal granule cells (Gó mez-Lira et al, 2005; this investigation), we show here the coexistence of VGAT and VGLUT in mossy fiber terminals at the electron microscopic level using a range of VGLUT and VGAT antibodies. Comparable to the auditory system (Gillespie et al, 2005), GABA and glutamate may be released simultaneously from developing hippocampal mossy fiber terminals (Walker et al, 2001;Gutiérrez et al, 2003;Kasyanov et al, 2004;Safiulina et al, 2006).…”

Section: Vgat In Glutamatergic Neuronssupporting

confidence: 72%

“…For instance, an increasing body of evidence suggests that both VGLUT1 and VGLUT2 colocalize in synapses of a select subset of neurons. VGLUT1 and VGAT (Kao et al, 2004;Gó mez-Lira et al, 2005), and VGLUT2 and VGAT (Ottem et al, 2004), were found to colocalize by immunofluorescence microscopy. In addition, both VGLUT2 and VGAT were detected in a subset of presynaptic terminals in the rat hippocampus using postembedding immunogold electron microscopy (Boulland et al, 2009).…”

Section: Introductionmentioning

confidence: 93%

“…The cytosolic content of electrophysiologically identified granule cells and interneurons was extracted as previously described (Gó mez-Lira et al, 2005), applying gentle negative pressure with the pipette, and placed in a PCR tube containing the following: 8 l of buffer 5ϫ (One-Step RT-PCR Kit, Qiagen), 1.6 l of dNTPs (final concentration 10 mM; One-…”

Section: Single-cell Pcrmentioning

confidence: 99%

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Synaptic and Vesicular Coexistence of VGLUT and VGAT in Selected Excitatory and Inhibitory Synapses

Zander¹,

Münster-Wandowski²,

Brunk³

et al. 2010

J. Neurosci.

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130

136

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The segregation between vesicular glutamate and GABA storage and release forms the molecular foundation between excitatory and inhibitory neurons and guarantees the precise function of neuronal networks. Using immunoisolation of synaptic vesicles, we now show that VGLUT2 and VGAT, and also VGLUT1 and VGLUT2, coexist in a sizeable pool of vesicles. VGAT immunoisolates transport glutamate in addition to GABA. Furthermore, VGLUT activity enhances uptake of GABA and monoamines. Postembedding immunogold double labeling revealed that VGLUT1, VGLUT2, and VGAT coexist in mossy fiber terminals of the hippocampal CA3 area. Similarly, cerebellar mossy fiber terminals harbor VGLUT1, VGLUT2, and VGAT, while parallel and climbing fiber terminals exclusively contain VGLUT1 or VGLUT2, respectively. VGLUT2 was also observed in cerebellar GABAergic basket cells terminals. We conclude that the synaptic coexistence of vesicular glutamate and GABA transporters allows for corelease of both glutamate and GABA from selected nerve terminals, which may prevent systemic overexcitability by downregulating synaptic activity. Furthermore, our data suggest that VGLUT enhances transmitter storage in nonglutamatergic neurons. Thus, synaptic and vesicular coexistence of VGLUT and VGAT is more widespread than previously anticipated, putatively influencing fine-tuning and control of synaptic plasticity.

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Section: Vgat In Glutamatergic Neuronssupporting

confidence: 72%

Section: Introductionmentioning

confidence: 93%

Section: Single-cell Pcrmentioning

confidence: 99%

See 1 more Smart Citation

Synaptic and Vesicular Coexistence of VGLUT and VGAT in Selected Excitatory and Inhibitory Synapses

Zander¹,

Münster-Wandowski²,

Brunk³

et al. 2010

J. Neurosci.

Self Cite

130

136

View full text Add to dashboard Cite

show abstract

“…However, different treatments, such as sustained synaptic activity or direct activation of glutamate receptors or BDNF administration, can rescue the developmental phenotype. This form of plasticity is not limited to the developmental critical period (5). These findings demonstrate an activity-dependent regulation of the matching of transmitters and their receptors in defining the identity of recently formed synapses.…”

mentioning

confidence: 71%

Transmitter-receptor mismatch in GABAergic synapses in the absence of activity

Cesa

Morando

Strata

2008

Proc. Natl. Acad. Sci. U.S.A.

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Competition among different axons to reach the somatodendritic region of the target neuron is an important event during development to achieve the final architecture typical of the mature brain. Trasmitter-receptor matching is a critical step for the signaling between neurons. In the cerebellar cortex, there is a persistent competition between the two glutamatergic inputs, the parallel fibers and the climbing fibers, for the innervation of the Purkinje cells. The activity of the latter input is necessary to maintain its own synaptic contacts on the proximal dendritic domain and to confine the parallel fibers in the distal one. Here, we show that climbing fiber activity also limits the distribution of the GABAergic input in the proximal domain. In addition, blocking the activity by tetrodotoxin infusion in Wistar rat cerebellum, a synapse made by GABAergic terminals onto the recently formed Purkinje cell spines appear in the proximal dendrites. The density of GABAergic terminals is increased, and unexpected double symmetric/asymmetric postsynaptic densities add to the typical symmetric phenotype of the GABAergic shaft synapses. Moreover, glutamate receptors appear in these ectopic synapses even in the absence of glutamate transmitter inside the presynaptic terminal and close to GABA receptors. These results suggest that the Purkinje cell has an intrinsic tendency to develop postsynaptic assemblies of excitatory types, including glutamate receptors, over the entire dendritic territory. GABA receptors are induced in these assemblies when contacted by GABAergic terminals, thus leading to the formation of hybrid synapses.cerebellum ͉ GABA receptor ͉ spinogenesis ͉ synaptic plasticity

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“…Nevertheless, it is well known that a neuron can store and presumably release the different sets of transmitters from individual axon endings [25]. The neurotransmitter choice of the neurons depends on programmed and environmental factors, and this process is neither limited by a critical period nor restricted by their insertion in a network [26]. Calcium transient patterns plays a key role in the differentiation of neural precursor cells, and their frequency may specify neuronal morphology and acquisition of neurotransmitter phenotype [27].…”

Section: B Synaptogenesismentioning

confidence: 99%

Morpholess Neurons Compromise the Development of Cortical Connectivity

Gafarov

Khusnutdinov²,

Galimyanov³

2009

J. Integr. Neurosci.

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It is currently accepted that cortical maps are dynamic constructions that are altered in response to external input. Experience-dependent structural changes in cortical microcurcuts lead to changes of activity, i.e. to changes in information encoded. Specific patterns of external stimulation can lead to creation of new synaptic connections between neurons. The calcium influxes controlled by neuronal activity regulate the processes of neurotrophic factors released by neurons, growth cones movement and synapse differentiation in developing neural systems. We propose a model for description and investigation of the activity dependent development of neural networks. The dynamics of the network parameters (activity, diffusion of axon guidance chemicals, growth cone position) is described by a closed set of differential equations. The model presented here describes the development of neural networks under the assumption of activity dependent axon guidance molecules. Numerical simulation shows that morpholess neurons compromise the development of cortical connectivity. I. INTRODUCTIONNeural networks are not constant structures. Modification in neural nets leads to changes in mapping of input signal to output. The most explored type of neural plasticity is synaptic plasticity. Synaptic plasticity deals with modifications of connection strength between neurons. It is an activity dependent process, and synaptic efficacy modifications depend on activity of postsynaptic and presynaptic neurons [1,2]. The second type of plasticity is known as structural plasticity. Structural plasticity deals with anatomical structure of neurons, and connections between neurons. The anatomical structures of neurons are subject to variation, and new connections between neurons can be established or deleted [3] in the course of development of neuron net. Structural plasticity as well as synaptic plasticity is a permanent and activity dependent process. Because it is an activity dependent process it can be the basis of learning. Activity-dependent modifications of neural circuits lead to changes in activity pattern of whole network. The geometrical properties of neurons should be considered in the theoretical investigations of structural plasticity of neural netsworks. The network must be considered as a system of neurons in three dimensional neuropil where neurons communicate with each other. The geometrical properties of neurons and the neuropil where neurons are constituent elements of networks. The neural networks generate activity patterns which depend on the intrinsic state of individual neuron and external influences on the system. This activity influences structural plasticity process. An external signal changes the activity pattern and leads to creation of new connections i.e. network will be modified according to external information.The neurons without connections can be considered a system of neurons in three dimensional space. At the beginning, the neurons interact only by emission of chemicals. Even no connections between neuron...

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Programmed and Induced Phenotype of the Hippocampal Granule Cells

Cited by 81 publications

References 51 publications

Synaptic and Vesicular Coexistence of VGLUT and VGAT in Selected Excitatory and Inhibitory Synapses

Synaptic and Vesicular Coexistence of VGLUT and VGAT in Selected Excitatory and Inhibitory Synapses

Transmitter-receptor mismatch in GABAergic synapses in the absence of activity

Morpholess Neurons Compromise the Development of Cortical Connectivity

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