Visual Neuroscience

Research Articles

Genetic targeting and physiological features of VGLUT3+ amacrine cells

WILLIAM N. GRIMESa1*, REBECCA P. SEALa2*, NICHOLAS OESCHa1*, ROBERT H. EDWARDSa3 and JEFFREY S. DIAMONDa1 c1

a1 Synaptic Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland

a2 Department of Neurobiology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania

a3 Departments of Physiology and Neurology, School of Medicine, University of California, San Francisco, California

Abstract

Amacrine cells constitute a diverse class of interneurons that contribute to visual signal processing in the inner retina, but surprisingly, little is known about the physiology of most amacrine cell subtypes. Here, we have taken advantage of the sparse expression of vesicular glutamate transporter 3 (VGLUT3) in the mammalian retina to target the expression of yellow fluorescent protein (YFP) to a unique population of amacrine cells using a new transgenic mouse line. Electrophysiological recordings made from YFP-positive (VGLUT3+) amacrine cells provide the first functional data regarding the active membrane properties and synaptic connections of this recently identified cell type. We found that VGLUT3+ amacrine cells receive direct synaptic input from bipolar cells via both N-methyl-d-aspartate receptors (NMDARs) and non-NMDARs. Voltage-gated sodium channels amplified these excitatory inputs but repetitive spiking was never observed. VGLUT3+ amacrine cells responded transiently to both light increments (ON response) and decrements (OFF response); ON responses consisted exclusively of inhibitory inputs, while OFF responses comprised both excitatory and inhibitory components, although the inhibitory conductance was larger in amplitude and longer in time course. The physiological properties and anatomical features of the VGLUT3+ amacrine cells suggest that this bistratified interneuron may play a role in disinhibitory signaling and/or crossover inhibition between parallel pathways in the retina.

(Received May 03 2011)

(Accepted July 15 2011)

(Online publication August 25 2011)

Correspondence:

c1 Address correspondence and reprint requests to: Dr. Jeffrey S. Diamond, Synaptic Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, Building 35, Room 3C-1000, Bethesda, MD 20892-3701. E-mail: diamondj@ninds.nih.gov

Footnotes

* These authors contributed equally.