Inhibitory synapses in the developing auditory system are glutamatergic

Gillespie, Deda C.; G, Kim; Kandler, Karl

doi:10.1038/nn1397

Cited by 205 publications

(207 citation statements)

References 49 publications

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“…Activity-dependent modification of inhibitory synaptic strength must be non-Hebbian, however, because the interaction between an inhibitory neuron and its target prevents them from firing together. Mechanisms that may underlie inhibitory plasticity will be discussed, including the possibility that it is limited to the early period when GABA/glycine release is excitatory (BenAri, 2002) or that corelease of another substance alters synapses that produce inhibition (Gillespie et al, 2005). Alternatively, inhibitory synapses may decline in strength through long-term depression (Kotak et al, 2001;Chang et al, 2003), or an as-yet undiscovered mechanism may be responsible.…”

Section: Discussionmentioning

confidence: 99%

Developmental Plasticity of Inhibitory Circuitry

et al. 2006

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In 1949, Donald Hebb proposed a mechanism for use-dependent synaptic plasticity, suggesting that input neurons that reliably activate their postsynaptic target will strengthen their connections (Hebb, 1949). Since then, studies of use-dependent plasticity during development have been almost entirely focused on excitatory synapses, particularly those incorporating NMDA receptors (NMDARs). Neural circuits depend heavily on inhibition, however. Although there have been several in vitro studies of possible synaptic mechanisms underlying inhibitory plasticity Alger, 1992, 1994;Komatsu, 1994;Kano, 1995;Zilberter, 2000;Kreitzer and Regehr, 2001;Wilson and Nicoll, 2001;Kilman et al., 2002;Maffei et al., 2006), little is known at the systems level about use-dependent plasticity of inhibitory synapses. The realization that "inhibitory" neurotransmitters often depolarize immature neurons (Ben-Ari, 2002) further complicates the picture. This issue is important because clinical treatments for epilepsy, sensory dysfunction, or brain damage need to be informed by an understanding of both excitatory and inhibitory components of the circuits they are aimed at influencing. This mini-symposium, presented at the 36th Annual Meeting of the Society for Neuroscience, will address the roles and mechanisms of inhibitory synaptic plasticity during development of the mammalian CNS, using primarily in vivo approaches to examine circuit-level plasticity in a wide array of model systems. The goal of the mini-symposium is to bring this important research area into the spotlight and to encourage other investigators to participate in developing a better understanding of this underappreciated issue. Inhibitory plasticity in motor systemsThe transient presence of episodic bursts of spontaneous network activity (SNA) is observed throughout the developing CNS. In the spinal cord, SNA is important for axon guidance, motoneuron survival, neurochemical expression, and joint and muscle development . Despite its importance, the role of SNA in the maturation of spinal connectivity is poorly understood. In the laboratory of Peter Wenner, co-chair of the mini-symposium, postdoctoral fellow Carlos Gonzalez-Islas has been investigating the role of SNA in homeostatic plasticity within the embryonic chick spinal cord. Despite significant developmental challenges to the production of SNA, it is clear that the network is capable of maintaining its activity levels (Chub and O'Donovan, 1998). Wenner and Gonzalez-Islas hypothesized that SNA is maintained through compensatory changes in synaptic strength. To test this hypothesis, they reduced network activity with lidocaine for 2 d in ovo. This increased the strength of both glutamatergic synapses and immature, depolarizing GABAergic synapses (Gonzalez-Islas and Wenner, 2006) and accelerated the modulation of GABAergic synaptic strength normally observed between episodes of SNA. Together, these compensatory responses appeared to increase the excitability of the embryonic spinal cord in an attempt to maintain approp...

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Section: Discussionmentioning

confidence: 99%

Developmental Plasticity of Inhibitory Circuitry

et al. 2006

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“…In the mature mammalian CNS, VGLUT1 and VGLUT2 appear in essentially nonoverlapping distributions, although they are coexpressed in some neurons during development (Fremeau et al, 2004a). VGLUT3 is found in scattered locations in the CNS of rats including the lateral superior olive and other auditory nuclei (Gillespie et al, 2005;Deng et al, 2007). It has also been detected in amacrine cells of the retina in rodents and humans (Johnson et al, 2004;Haverkamp et al, 2004;Gong et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Vesicular Glutamate Transporter 3 Is Required for Synaptic Transmission in Zebrafish Hair Cells

Obholzer¹,

Wolfson²,

Trapani³

et al. 2008

J. Neurosci.

300

355

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“…Although a number of cases have been described (Holton, 1959;Schwarzer and Sperk, 1995;Jonas et al, 1998;Gutierrez, 2000;Yang et al, 2002;Borodinsky et al, 2004;Trudeau, 2004;Gillespie et al, 2005), the ability of some of these neurons to release two classical neurotransmitters has attracted less attention. The recent characterization of vesicular glutamate transporters 1-3 (VGluT1-VGlutT3) has renewed attention on neuronal populations that release glutamate (Trudeau, 2004).…”

Section: Introductionmentioning

confidence: 99%

Developmental and Target-Dependent Regulation of Vesicular Glutamate Transporter Expression by Dopamine Neurons

Mendez

Bourque²,

Bo³

et al. 2008

Journal of Neuroscience

116

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Mesencephalic dopamine (DA) neurons have been suggested to use glutamate as a cotransmitter. Here, we suggest a mechanism for this form of cotransmission by showing that a subset of DA neurons both in vitro and in vivo expresses vesicular glutamate transporter 2 (VGluT2). Expression of VGluT2 decreases with age. Moreover, when DA neurons are grown in isolation using a microculture system, there is a marked upregulation of VGluT2 expression. We provide evidence that expression of this transporter is normally repressed through a contact-dependent interaction with GABA and other DA neurons, thus providing a partial explanation for the highly restricted expression of VGluT2 in DA neurons in vivo. Our results demonstrate that the neurotransmitter phenotype of DA neurons is both developmentally and dynamically regulated. These findings may have implications for a better understanding of the fast synaptic action of DA neurons as well as basal ganglia circuitry.

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Inhibitory synapses in the developing auditory system are glutamatergic

Cited by 205 publications

References 49 publications

Developmental Plasticity of Inhibitory Circuitry

Developmental Plasticity of Inhibitory Circuitry

Vesicular Glutamate Transporter 3 Is Required for Synaptic Transmission in Zebrafish Hair Cells

Developmental and Target-Dependent Regulation of Vesicular Glutamate Transporter Expression by Dopamine Neurons

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