Format

Send to:

Choose Destination
See comment in PubMed Commons below
Curr Biol. 2013 Jul 8;23(13):1202-8. doi: 10.1016/j.cub.2013.05.016. Epub 2013 Jun 13.

Transient and specific inactivation of Drosophila neurons in vivo using a native ligand-gated ion channel.

Author information

  • 1Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.

Abstract

A key tool in neuroscience is the ability to transiently inactivate specific neurons on timescales of milliseconds to minutes. In Drosophila, there are two available techniques for accomplishing this (shibire(ts) and halorhodopsin [1-3]), but both have shortcomings [4-9]. Here we describe a complementary technique using a native histamine-gated chloride channel (Ort). Ort is the receptor at the first synapse in the visual system. It forms large-conductance homomeric channels that desensitize only modestly in response to ligand [10]. Many regions of the CNS are devoid of histaminergic neurons [11, 12], raising the possibility that Ort could be used to artificially inactivate specific neurons in these regions. To test this idea, we performed in vivo whole-cell recordings from antennal lobe neurons misexpressing Ort. In these neurons, histamine produced a rapid and reversible drop in input resistance, clamping the membrane potential below spike threshold and virtually abolishing spontaneous and odor-evoked activity. Every neuron type in this brain region could be inactivated in this manner. Neurons that did not misexpress Ort showed negligible responses to histamine. Ort also performed favorably in comparison to the available alternative effector transgenes. Thus, Ort misexpression is a useful tool for probing functional connectivity among Drosophila neurons.

Copyright © 2013 Elsevier Ltd. All rights reserved.

PMID:
23770187
[PubMed - indexed for MEDLINE]
PMCID:
PMC3725270
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk