Conduction velocity is faster when axons are myelinated and have a larger diameter because myelin enables saltatory conduction and a bigger diameter lowers internal resistance to current flow. Preganglionic autonomic fibers are typically both myelinated and relatively large compared with postganglionic fibers, so they conduct signals more rapidly. If the fibers were unmyelinated or smaller, the signal would propagate more slowly. Therefore, being myelinated and larger leads to faster conduction velocity.

Receptor potentials are graded changes in membrane potential at the sensory ending that can summate over time or across space. The key idea is that an action potential is fired only when this integrated depolarization reaches a threshold at the trigger zone, activating voltage-gated channels. If the receptor potentials do not reach this threshold, no action potential is produced. Therefore, the generation of action potentials depends on receptor potentials summing to threshold. This captures why summation matters: it’s not just any summation that matters, but reaching the critical threshold that triggers the all-or-none spike. The other statements conflict with this view: action potentials rely on receptor-driven depolarization to reach threshold, receptor potentials can influence CNS signaling by driving these spikes, and relying on summation to reach threshold aligns with how sensory information is encoded and transmitted.

Chemical nociceptors respond to chemical signals indicating tissue damage. They are activated by chemicals such as extreme pH (very acidic or basic conditions), high extracellular potassium released from damaged cells, and inflammatory mediators like bradykinin, histamine, and prostaglandins. Plant irritants, such as capsaicin from chili peppers, can also activate these receptors. When these chemical cues bind to receptors on the nociceptor, they cause it to fire and signal pain, which is why this set of stimuli fits chemical nociception. In contrast, mechanical pressure triggers mechanical nociceptors, temperature changes engage thermal nociceptors, and electrical fields are not typical activators for chemical nociceptors.

Special senses rely on receptor cells that act as transducers, turning a stimulus into chemical signals that drive the associated sensory neurons. The receptor cell, upon stimulation, releases neurotransmitter at a synapse with the sensory neuron. This neurotransmitter binds to receptors on the sensory neuron, causing it to depolarize and fire action potentials (or adjust its firing rate). This is how vision, hearing, balance, taste, and smell transmit information to the nervous system. For example, hair cells in the inner ear release glutamate onto afferent fibers that carry the signal to the brain; photoreceptors modulate their neurotransmitter release in response to light onto downstream neurons; taste receptor cells release ATP onto gustatory fibers; olfactory receptor neurons release neurotransmitter onto olfactory bulb neurons. Hormonal signaling, direct electrical coupling, or signaling without neurotransmitter release do not describe the usual local communication between receptor cells and their sensory neurons in these systems.