Control of Synapse Number by Glia

Ullian, Erik M.; Sapperstein, Stephanie K.; Christopherson, Karen S.; Barres, Ben A.

doi:10.1126/science.291.5504.657

Cited by 1,225 publications

(910 citation statements)

References 21 publications

Supporting

Mentioning

856

Contrasting

Unclassified

Order By: Relevance

“…These behavioral studies argue for the involvement of LIF in postnatal brain development at least in part through alterations in glia. The importance of astrocytes and morphological contacts formed between astrocytic processes and synapses is apparent as astrocytes and astrocyte-conditioned media promote synapse formation (Pfrieger and Barres, 1997;Ullian et al, 2001) and both LTP and LTD are affected by astrocytes acting through several mechanisms. Astrocytes directly regulate NMDA-receptor-dependent LTP and plasticity through glial-derived D-serine (Yang et al, 2003;Panatier et al, 2006), ATP and adenosine (Pascual et al, 2005;Fields and Burnstock, 2006), glutamate reuptake and release (Haydon and Carmignoto, 2006) and extracellular K + handling (Wallraff et al, 2006;Djukic et al, 2007;Ge and Duan, 2007).…”

Section: Discussionmentioning

confidence: 99%

Activity-dependent neuron–glial signaling by ATP and leukemia-inhibitory factor promotes hippocampal glial cell development

Cohen

Fields

2008

Neuron Glia Biol.

View full text Add to dashboard Cite

Activity-dependent signaling between neurons and astrocytes contributes to experience-dependent plasticity and development of the nervous system. However, mechanisms responsible for neuronglial interactions and the releasable factors that underlie these processes are not well understood. The pro-inflammatory cytokine, leukemia-inhibitory factor (LIF), is transiently expressed postnatally by glial cells in the hippocampus and rapidly up-regulated by enhanced neural activity following seizures. To test the hypothesis that spontaneous neural activity regulates glial development in hippocampus via LIF signaling, we blocked spontaneous activity with the sodium channel blocker tetrodotoxin (TTX) in mixed hippocampal cell cultures in combination with blockers of LIF and purinergic signaling. TTX decreased the number of GFAP-expressing astrocytes in hippocampal cell culture. Furthermore, blocking purinergic signaling by P2Y receptors contributed to reduced numbers of astrocytes. Blocking activity or purinergic signaling in the presence of function-blocking antibodies to LIF did not further decrease the number of astrocytes. Moreover, hippocampal cell cultures prepared from LIF −/− mice had reduced numbers of astrocytes and activity-dependent neuron-glial signaling promoting differentiation of astrocytes was absent. The results show that endogenous LIF is required for normal development of hippocampal astrocytes, and this process is regulated by spontaneous neural impulse activity through the release of ATP.

show abstract

Section: Discussionmentioning

confidence: 99%

Activity-dependent neuron–glial signaling by ATP and leukemia-inhibitory factor promotes hippocampal glial cell development

Cohen

Fields

2008

Neuron Glia Biol.

View full text Add to dashboard Cite

show abstract

“…Retinal ganglion cells grown in the absence of astrocytes show dramatically decreased number of synapses as well as a large decrease in the pool of functional synapses (Ullian et al, 2001). The presence of nAChRs on glial cells suggests a potential role for the receptors in formation of functional synapses.…”

Section: Possible Physiologic Roles For Nachrs On Nonexcitable Cellsmentioning

confidence: 99%

Nicotinic receptor signaling in nonexcitable cells

2002

View full text Add to dashboard Cite

ABSTRACT:The finding that neuronal nicotinic acetylcholine receptors (nAChRs) are present in nonneuronal cells both within and outside the nervous system raises some interesting issues. The mechanisms underlying receptor signaling and its downstream consequences in these cells remain to be elucidated. Factors controlling the release of acetylcholine and the extent of its diffusion are likely to be different for these cells than for traditional neuronal synapses. Recent advances on the physiologic functions of some of these cell types have provided a better insight into possible functional roles for nAChRs in nonexcitable cells. The presence of nAChRs on these cells also implies a broader scope for the actions of nicotine that needs to be considered from a clinical viewpoint. Revealing the potential physiologic roles for nAChRs on nonexcitable cells is likely to provide a more complete understanding of cholinergic signaling.

show abstract

“…Astrocytes induce a dramatic increase in synapse formation, and in spontaneous synaptic activity in cultured retinal ganglion cells (Pfrieger and Barres, 1997). Astrocytes also increase the number of functional synapses on CNS neurons sevenfold, and are required for maintenance of synapses in vitro (Ullian et al, 2001). Further experiments show that cholesterol derived from CNS glia is sufficient to facilitate synapse formation (Mauch et al, 2001).…”

Section: Glia-another Source Of Extrinsic Regulatory Signalsmentioning

confidence: 99%

Regulatory mechanisms that govern nicotinic synapse formation in neurons

et al. 2002

View full text Add to dashboard Cite

Individual cholinoceptive neurons express high levels of different neuronal nicotinic acetylcholine receptor (nAChR) subtypes, and target them to the appropriate synaptic regions for proper function. This review focuses on the intercellular and intracellular processes that regulate nAChR expression in vertebrate peripheral nervous system (PNS) and central nervous system (CNS) neurons. Specifically, we discuss the cellular and molecular mechanisms that govern the induction and maintenance of nAChR expression-innervation, target tissue interactions, soluble factors, and activity. We define the regulatory principles of interneuronal nicotinic synapse differentiation that have emerged from these studies. We also discuss the molecular players that target nAChRs to the surface membrane and the interneuronal synapse.

show abstract

Control of Synapse Number by Glia

Cited by 1,225 publications

References 21 publications

Activity-dependent neuron–glial signaling by ATP and leukemia-inhibitory factor promotes hippocampal glial cell development

Activity-dependent neuron–glial signaling by ATP and leukemia-inhibitory factor promotes hippocampal glial cell development

Nicotinic receptor signaling in nonexcitable cells

Regulatory mechanisms that govern nicotinic synapse formation in neurons

Contact Info

Product

Resources

About