期刊
JOURNAL OF NEUROSCIENCE
卷 28, 期 16, 页码 4136-4150出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4274-07.2008
关键词
A2 amacrine cell; circuitry; whole-cell recording; patch clamp; retinal; Y-cell
资金
- NEI NIH HHS [R01 EY014454-04, T32 EY013934, R01 EY014454, P30 EY007003, F31 EY007003, EY14454, EY07003, T32-EY13934] Funding Source: Medline
- NINDS NIH HHS [T32 NS076401] Funding Source: Medline
Cone signals divide into parallel ON and OFF bipolar cell pathways, which respond to objects brighter or darker than the background and release glutamate onto the corresponding type of ganglion cell. It is assumed that ganglion cell excitatory responses are driven by these bipolar cell synapses. Here, we report an additional mechanism: OFF ganglion cells were driven in part by the removal of synaptic inhibition (disinhibition). The disinhibition played a relatively large role in driving responses at low contrasts. The disinhibition persisted in the presence of CNQX and D-AP-5. Furthermore, the CNQX/D-AP-5-resistant response was blocked by L-AP-4, meclofenamic acid, quinine, or strychnine but not by bicuculline. Thus, the disinhibition circuit was driven by the ON pathway and required gap junctions and glycine receptors but not ionotropic glutamate or GABA(A) receptors. These properties implicate the AII amacrine cell, better known for its role in rod vision, as a critical circuit element through the following pathway: cone -> ON cone bipolar cell -> AII cell -> OFF ganglion cell. Rods could also drive this circuit through their gap junctions with cones. Thus, to light decrement, AII cells, driven by electrical synapses with ON cone bipolar cells, would hyperpolarize and reduce glycine release to excite OFF ganglion cells. To light increment, the AII circuit would directly inhibit OFF ganglion cells. These results show a new role for disinhibition in the retina and suggest a new role for the AII amacrine cell in daylight vision.
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