Final answer:
The statement about the G protein Golf and cGMP-gated sodium channels is false. In olfaction, Golf activates mechanisms leading to the opening of cAMP-gated channels for depolarization. In vision, the G protein transducin leads to the closure of cGMP-gated channels, causing hyperpolarization.
Step-by-step explanation:
The statement that the G protein Golf stimulates the opening of cGMP-gated sodium channels, which depolarizes the olfactory receptor neuron, is false. In the olfactory system, Golf typically activates adenylate cyclase, increasing the production of cAMP, not cGMP. The increase in cAMP opens cAMP-gated sodium channels, leading to depolarization of the olfactory receptor neuron. By contrast, in the visual system, as mentioned in Figure 27.20 and 36.21, the G-protein transducin is activated by light, which leads to the activation of phosphodiesterase, the conversion of cGMP to GMP, and the subsequent closure of cGMP-gated sodium channels, resulting in hyperpolarization.
In a classical nerve impulse scenario, the influx of Na+ through voltage-gated sodium channels, as described by both option a and option c, leads to depolarization of the membrane. The process can form a positive feedback loop where more sodium channels open in response to the initial sodium influx, as mentioned in option c. However, in the context given, the reference to ligand-gated and mechanically gated channels explains how different stimuli can initiate the opening of sodium channels.