Figure 10

Schematic model showing possible mechanisms for the neuroprotective effects of α7-nAChR activation. Excessive activation of postsynaptic NMDA receptors produces a sustained depolarizing influx of Ca²⁺ in RGCs that eventually leads to neurodegeneration. In our study, the activation of presynaptic α7-nAChR by PNU-282987 increased GABA release from presynaptic GABAergic amacrine cells. Thus, the activation of GABA_A receptors can attenuate the activity of excitatory NMDARs. RGC, retinal ganglion cell; nAChR, nicotinic acetylcholine receptor; GAD, glutamic acid decarboxylase; L-VDCC, L-type voltage-dependent Ca²⁺ channels.