Synaptic organization of GABAergic amacrine cells in the salamander retina

Abstract

The synaptic organization of GABA-immunoreactive (GABA-IR) amacrine cells in the inner plexiform layer (IPL) of salamander retina was studied with the use of postembedding immuno-electron microscopy. A total of 457 GABA-IR amacrine synapses, with identified postsynaptic elements, were analyzed on photomontages of electron micrographs covering 3,618 microm2 of the IPL. GABA-IR amacrine synapses were distributed throughout the IPL, with a small peak at the proximal margin of sublamina a. The majority of the output targets (81%) were GABA(-) neurons. Most of the contacts were simple synapses with one postsynaptic element identified as a process of an amacrine cell (55%), bipolar cell (19%) or ganglion cell (26%), and serial synapses were very rare. Of the 89 postsynaptic bipolar terminals, 63% participated in a reciprocal feedback synapse with the same presynaptic GABA-IR amacrine profile. There appeared to be no preference between GABA-IR amacrine contacts with rod- or cone-dominated bipolar cells (9.1% vs. 8.9%) or in the total number of amacrine synapses in sublaminas a and b (52% vs. 47%). The preponderance of amacrine cell input to bipolar cells in the OFF layer was derived from GABA-IR cells. These findings provide ultrastructural support to the existing physiological studies regarding the functional roles of the GABAergic amacrine cells in this species. Our results have added to the data base demonstrating that, in contrast to mammals, GABA-IR amacrine cells in amphibians and other nonmammals contact other amacrine cells more frequently, suggesting greater involvement of GABAergic amacrine cells in modulating lateral inhibitory pathways.

Retinal Ganglion Cells Can Rapidly Change Polarity from Off to On

“…However, an image shift in the periphery stimulates a second amacrine cell (labeled A 1 ), and this neuron in turn suppresses the Off bipolar input through an inhibitory synapse. In addition A 1 inhibits A 2 [30], which transiently relieves the suppression of the On bipolar inputs. If the synapse from A 1 to A 2 desensitizes rapidly, then disinhibition of the On pathway would be more transient than suppression of the Off pathway, as observed.…”

Mechanisms Underlying Lateral GABAergic Feedback onto Rod Bipolar Cells in Rat Retina

“…In addition to contacting bipolar cell terminals and ganglion cell dendrites, amacrine cells also contact other amacrine cells (Dowling and Boycott, 1966; Dowling and Werblin, 1969; Zhang et al, 2004), primarily via GABA A R-mediated synapses (Zhang et al, 1997; Fletcher et al, 1998; Wassle et al, 1998; Eggers and Lukasiewicz, 2009). Although such “serial inhibition” (Zhang et al, 1997) was not evident in our recordings, we cannot exclude the possibility that amacrine-amacrine signaling may have influenced the results of some pharmacological manipulations.…”

On the functional role of gamma synchronization in the retinogeniculate system of the cat

“…GABAergic interneurons are known to play a critical role in the generation and control of gamma-band oscillations (Buzsáki and Wang, 2012; Cardin et al, 2009; Chen et al, 2017; Tiesinga and Sejnowski, 2009; Veit et al, 2017). In the vertebrate retina, many amacrine cells release GABA (Pourcho and Goebel, 1983; Yang, 2004), providing inhibitory inputs to bipolar cell terminals, retinal ganglion cells, and other amacrine cells (Diamond, 2017; Franke and Baden, 2017; Zhang and McCall, 2012; Zhang et al, 2004). Volatile anesthetics, such as halothane and isoflurane, among their various excitability control functions, primarily potentiate GABAA receptor activity (Franks, 2008; Sousa et al, 2000).…”