Visual Neuroscience



Functional polarity of dendrites and axons of primate A1 amacrine cells


CHRISTOPHER M.  DAVENPORT  a1 c1 , PETER B.  DETWILER  a2 and DENNIS M.  DACEY  a3
a1 Neurobiology and Behavior Graduate Program, University of Washington, Seattle, Washington
a2 Department of Physiology and Biophysics, University of Washington, Seattle, Washington
a3 Department of Biological Structure, University of Washington, Seattle, Washington

Article author query
davenport cm   [Google Scholar] 
detwiler pb   [Google Scholar] 
dacey dm   [Google Scholar] 
 

Abstract

The A1 cell is an axon-bearing amacrine cell of the primate retina with a diffusely stratified, moderately branched dendritic tree ([similar]400 [mu]m diameter). Axons arise from proximal dendrites forming a second concentric, larger arborization (>4 mm diameter) of thin processes with bouton-like swellings along their length. A1 cells are ON-OFF transient cells that fire a brief high frequency burst of action potentials in response to light (Stafford & Dacey, 1997). It has been hypothesized that A1 cells receive local input to their dendrites, with action potentials propagating output via the axons across the retina, serving a global inhibitory function. To explore this hypothesis we recorded intracellularly from A1 cells in an in vitro macaque monkey retina preparation. A1 cells have an antagonistic center-surround receptive field structure for the ON and OFF components of the light response. Blocking the ON pathway with L-AP4 eliminated ON center responses but not OFF center responses or ON or OFF surround responses. Blocking GABAergic inhibition with picrotoxin increased response amplitudes without affecting receptive field structure. TTX abolished action potentials, with little effect on the sub-threshold light response or basic receptive field structure. We also used multi-photon laser scanning microscopy to record light-induced calcium transients in morphologically identified dendrites and axons of A1 cells. TTX completely abolished such calcium transients in the axons but not in the dendrites. Together these results support the current model of A1 function, whereby the dendritic tree receives synaptic input that determines the center-surround receptive field; and action potentials arise in the axons, which propagate away from the dendritic field across the retina.

(Received October 23 2006)
(Accepted December 16 2006)


Key Words: Retina; Amacrine; Calcium; Receptive Field; Axon.

Correspondence:
c1 Address Correspondence and reprint requests to: Christopher M. Davenport, Department of Physiology and Biophysics, Box 357290, Seattle, WA 98195. E-mail: daven@u.washington.edu