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Citation
Ping, Y., Tsunoda, S. (2011). Inactivity-induced increase in nAChRs upregulates Shal K(+) channels to stabilize synaptic potentials.  Nat. Neurosci. 15(1): 90--97.
FlyBase ID
FBrf0217106
Publication Type
Research paper
Abstract

Long-term synaptic changes, which are essential for learning and memory, are dependent on homeostatic mechanisms that stabilize neural activity. Homeostatic responses have also been implicated in pathological conditions, including nicotine addiction. Although multiple homeostatic pathways have been described, little is known about how compensatory responses are tuned to prevent them from overshooting their optimal range of activity. We found that prolonged inhibition of nicotinic acetylcholine receptors (nAChRs), the major excitatory receptors in the Drosophila CNS, resulted in a homeostatic increase in the Drosophila α7 (Dα7)-nAChR. This response then induced an increase in the transient A-type K(+) current carried by Shaker cognate L (Shal; also known as voltage-gated K(+) channel 4, Kv4) channels. Although increasing Dα7-nAChRs boosted miniature excitatory postsynaptic currents, the ensuing increase in Shal channels served to stabilize postsynaptic potentials. These data identify a previously unknown mechanism for fine tuning the homeostatic response.

PubMed ID
PubMed Central ID
PMC3888491 (PMC) (EuropePMC)
Related Publication(s)
Note

Homeostatic plasticity in Drosophila central neurons, and implications in human diseases.
Ping and Tsunoda, 2012, Fly 6(3): 153--157 [FBrf0221677]

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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Nat. Neurosci.
    Title
    Nature Neuroscience
    Publication Year
    1998-
    ISBN/ISSN
    1097-6256
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