Okay, let's tackle this question about rod cells and their permeability to sodium and potassium when exposed to light. First, I need to remember the basic physiology of photoreceptor cells. Rod cells are involved in low-light vision and use rhodopsin for detecting light. When light hits rhodopsin, it triggers a cascade involving transducin and phosphodiesterase (PDE), which breaks down cGMP.

Under normal, dark conditions, rod cells have a high concentration of cGMP. This cGMP keeps sodium channels open, allowing sodium ions to flow into the cell. This makes the rod cell depolarized in the dark. The depolarization leads to the release of neurotransmitters like glutamate, which affects bipolar cells in the retina.

When light is present, rhodopsin activates PDE, which reduces cGMP levels. Lower cGMP causes the sodium channels to close, leading to hyperpolarization of the rod cell. Hyperpolarization decreases the release of glutamate. So, in the light, sodium permeability decreases, and potassium channels might open, allowing potassium to leave the cell, contributing to hyperpolarization.

Now, looking at the options, the correct answer should state that sodium permeability decreases and potassium permeability increases in the presence of light. The other options might suggest the opposite or confuse the roles of sodium and potassium. For example, if an option says sodium increases in light, that's wrong. Similarly, if potassium permeability decreases, that's incorrect because potassium channels open to aid hyperpolarization.

The clinical pearl here is that in the dark, rod cells are depolarized due to sodium influx, and light causes hyperpolarization by closing sodium channels and opening potassium channels. This is a classic example of how photoreceptors function differently from other neurons, where resting state is depolarized and light causes hyperpolarization.

**Core Concept**
Rod photoreceptors undergo light-induced hyperpolarization due to changes in ion permeability. In darkness, cyclic GMP (cGMP) maintains open sodium channels, allowing Na⁺ influx. Light activates phosphodiesterase (PDE), degrading cGMP and closing Na⁺ channels while opening K⁺ channels.

**Why the Correct Answer is Right**
In response to light, rod cells **decrease sodium permeability** (Na⁺ channels close) and **increase potassium permeability** (K⁺ channels open). This causes hyperpolarization, reducing neurotransmitter release. The cGMP-dependent mechanism is central to phototransduction in rods, distinguishing their "dark current" from other excitable cells.

**Why Each Wrong Option is Incorrect**
**Option A:** (If it states increased Na⁺ permeability) Incorrect—light closes Na⁺ channels, reducing influx.
**Option B:** (If it states decreased K⁺ permeability) Incorrect—light opens K⁺ channels to enhance efflux.
**Option C:** (If it claims both permeabilities decrease) Incorrect—K⁺ permeability specifically increases during light.

**Clinical Pearl / High-Yield Fact**
Rod cells are *depolarized in darkness* and *hyperpolarized by light*, opposite to typical neurons. This "dark current" is sustained by Na⁺ influx through cGMP-gated channels, which close when cGMP degrades in light.

✓ Correct Answer: C. Decreased sodium permeability, no change in potassium permeability