Advanced Somatosensory and Visual Pathways Quiz

DRG neurons contain three major ending types: encapsulated receptors for touch and vibration, proprioceptors for muscle stretch and tension, and free nerve endings for pain and temperature. These endings determine which modality each neuron transduces.

Mechanosensing channels like Piezo produce inward cation currents when the membrane is displaced. Voltage-clamp recordings show stretch-evoked depolarizations, and Piezo knockouts lose mechanosensitivity, proving these channels specifically transduce mechanical stimuli.

SA neurons fire continuously during sustained pressure, whereas RA neurons fire only at stimulus onset and offset. These differing adaptation profiles explain why RA fibers encode vibration while SA fibers encode constant stretch or pressure.

TRP channels detect thermal and chemical stimuli by allowing cation influx into DRG neurons. TRPV1 detects heat and capsaicin, TRPM8 detects cooling, and TRPA1 detects irritants. ASICs and P2X channels also contribute to pain signaling.

The somatosensory cortex contains parallel somatotopic maps of the body surface and orthogonal maps for modality-specific columns. These organizational layouts allow precise spatial coding of tactile stimuli.

Phantom limb pain arises from cortical remapping after amputation. Mirror box therapy provides visual feedback that reshapes cortical maps, reducing pain via top-down modulation of sensory representations.

Pain is modulated by descending pathways from the PAG to the RVM to the dorsal horn, where endogenous opioids inhibit nociceptive transmission. This system shapes pain perception centrally, reducing ascending signals.

Itch is transmitted by C-fiber pruriceptors projecting to the dorsal horn and spinothalamic tract. Receptors include histamine H1/H4, PAR2, TRPV1, TRPA1, and Mrgpr, enabling responses to chemical and inflammatory pruritogens.

TRPM8 channels respond to menthol and cooling, whereas TRPV1 responds to capsaicin and heat. These channels are key contributors to temperature-dependent nociception.

Pain transduction relies on TRP channels, ASICs, and P2X receptors, all of which depolarize nociceptors in response to heat, acid, irritants, or ATP. These channels form key entry points for pain signals.

Taste buds sit on fungiform, foliate, and circumvallate papillae; filiform papillae lack taste buds. Taste cells include Type II (sweet, bitter, umami), Type III (sour), and Type I (support/salty).

Chorda tympani axons respond to several tastants, showing overlapping tuning. This supports population coding, where taste is encoded by combined responses rather than strict labeled lines.

Salty stimuli use ENaC channels; sour uses proton-gated channels like OTOP1; sweet uses T1R2+T1R3, umami uses T1R1+T1R3, and bitter uses T2R GPCRs. Bitter, sweet, and umami share the GPCR→PLC→IP₃→TRPM5 cascade.

Each olfactory neuron expresses only one odorant receptor gene. Neurons expressing the same receptor converge onto the same glomerulus, creating combinatorial coding for odor identity.

Anosmia is the loss of smell sensitivity, resulting from receptor dysfunction, nasal obstruction, or neural damage.

Olfactory pathways begin with OSNs projecting to bulb glomeruli, then to piriform cortex, then thalamus, and finally orbitofrontal cortex. These stages enable odor discrimination and conscious perception.

Each glomerulus receives many axons, but all originate from neurons expressing the same receptor. This pattern supports spatial encoding of odors across glomerular maps.

Species with higher olfactory sensitivity have more odorant receptors and larger olfactory bulbs. Dogs far exceed humans in receptor number, correlating with superior odor detection.

Corneal layers include epithelium, Bowman’s membrane, stroma, Descemet’s membrane, and endothelium. LASIK reshapes the stroma to adjust optical focusing.

Retinal neurons include rods, cones, bipolar cells, horizontal cells, amacrine cells, and ganglion cells. These layers transform light into neural signals.

RP affects rods first in peripheral retina, progressing in children; macular degeneration affects foveal cones in older adults. This explains their distinct visual deficits.

Light converts 11-cis retinal to all-trans, activating opsins and transducin. PDE reduces cGMP, closing Na⁺/Ca²⁺ channels and hyperpolarizing the cell. Cones adapt faster due to rapid pigment regeneration.

ON bipolar cells use mGluR6 and depolarize in light; OFF cells use AMPA/kainate and depolarize in dark. This divergence underlies center on/off pathways.

Center responses arise from direct photoreceptor→bipolar→ganglion pathways, while surround signals arise from horizontal-cell inhibition, producing center–surround receptive fields.

Protanopia and deuteranopia result from loss of L and M opsins. These are the most common forms of dichromacy, affecting red–green perception.

Gene therapy restoring L/M opsins in primates shows circuitry can incorporate new photopigments, implying genetically predetermined pathways can be functionally rescued.

The LGN has segregated ipsilateral and contralateral layers. Lesions before the chiasm affect one eye; lesions after affect visual fields. Inferior retina maps superior fields and vice versa.