PUBLICATION

Dopaminergic modulation of mitral cells and odor responses in the zebrafish olfactory bulb

Authors
Bundschuh, S.T., Zhu, P., Schärer, Y.P., and Friedrich, R.W.
ID
ZDB-PUB-120522-3
Date
2012
Source
The Journal of neuroscience : the official journal of the Society for Neuroscience   32(20): 6830-6840 (Journal)
Registered Authors
Bundschuh, Sebastian, Friedrich, Rainer
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Dopamine/pharmacology
  • Dopamine/physiology*
  • Dopamine D2 Receptor Antagonists
  • In Vitro Techniques
  • Interneurons/physiology
  • Membrane Potentials/drug effects
  • Membrane Potentials/physiology
  • Models, Neurological
  • Molecular Imaging/methods
  • Olfactory Bulb/drug effects
  • Olfactory Bulb/physiology*
  • Olfactory Perception/physiology*
  • Olfactory Receptor Neurons/physiology*
  • Patch-Clamp Techniques/methods
  • Photic Stimulation/methods
  • Receptors, Dopamine D2/physiology*
  • Rhodopsin/genetics
  • Rhodopsin/metabolism
  • Stimulation, Chemical
  • Time Factors
  • Zebrafish
PubMed
22593052 Full text @ J. Neurosci.
Abstract

In the olfactory bulb, the modulatory neurotransmitter dopamine (DA) is coexpressed with GABA by local interneurons, but its role in odor processing remains obscure. We examined functions of DA mediated by D2-like receptors in the olfactory bulb of adult zebrafish by pharmacology, whole-cell recordings, calcium imaging, and optogenetics. Bath application of DA had no detectable effect on odorant-evoked sensory input. DA directly hyperpolarized mitral cells (MCs) via D2-like receptors and slightly increased their response gain. Consistent with this effect on input–output functions of MCs, small odorant responses were suppressed, whereas strong responses were enhanced in the presence of DA. These effects increased the root-mean-square contrast of population activity patterns but did not reduce their correlations. Optical stimulation of interneurons expressing channelrhodopsin-2 evoked fast GABAergic inhibitory currents in mitral cells but failed to activate D2 receptor-mediated currents when stimuli were short. Prolonged stimulus trains, however, activated a slow hyperpolarizing current that was blocked by an antagonist of D2-like receptors. GABA and DA are therefore both released from interneurons by electrical activity and hyperpolarize MCs, but D2-dependent dopaminergic effects occur on slower timescales. Additional effects of DA may be mediated by D1-like receptors. These results indicate that DA acts on D2-like receptors via asynchronous release and/or volume transmission and implicate DA in the slow adaptation of circuit function. The shift of the membrane potential away from spike threshold could adapt mitral cells to background input without compromising their sensitivity.

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