Authors: Yong Ping and Susan Tsunoda

Yong Ping

Department of Biomedical Sciences; Colorado State University; Fort Collins, CO USA

Susan Tsunoda

Corresponding author: susan.tsunoda@colostate.edu
Department of Biomedical Sciences; Colorado State University; Fort Collins, CO USA

Abstract:
Synaptic homeostasis is a form of neuronal plasticity that stabilizes activity of neural networks. Both presynaptic and postsynaptic effects are well documented in response to activity changes. The electrical signaling machinery of individual neurons, or intrinsic properties, have also been implicated in this plasticity. How synaptic and intrinsic changes are coordinated, however, is still a puzzle. A recent study by Ping and Tsunoda shows both synaptic and intrinsic changes in Drosophila central neurons in response to prolonged inactivity.¹ Changes include the upregulation of Dα7 nicotinic acetylcholine receptors (nAChRs) and Shal (K_v4) potassium channels. This work has two noteworthy findings. First, although mediated by different receptors, synaptic homeostasis in the central nervous system (CNS) is conserved across species. This is perhaps the most direct demonstration that nAChRs mediate synaptic homeostasis. Changes in the expression of nAChRs have long been noted during development, as well as during pathological conditions, such as nicotine addiction² and Alzheimer disease.³ The second interesting finding is the relationship between synaptic and intrinsic plasticity: nAChRs are upregulated immediately, subsequently triggering a rapid increase in Shal K⁺ channels. This novel mechanism regulates synaptic homeostasis to stabilize synaptic potentials. This study sets the stage for Drosophila central neurons as a model for cholinergic synaptic homeostasis, its regulation and role in disease.

Extra View to:
Y Ping, S Tsunoda. Inactivity-induced increase in nAChRs upregulates Shal K(+) channels to stabilize synaptic potentials. Nat Neurosci 2012; 15: 90-7
PMID: 22081160 DOI: 10.1038/nn.2969

Received: March 30, 2012; Accepted: May 15, 2012

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