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Light hits photoreceptors (rods and cones)
Photopigments inside rods and cones are activated
Photopigment structure
Consists of opsin (protein) and retinal (vitamin A-derived lipid)
Photopigment in rods
Rhodopsin = rod opsin + retinal
Effect of light on rhodopsin
Isomerization: shape changes, bleaching (color change), opsin and retinal separate
Ion channel changes in photoreceptors
Light causes Na⁺ channels to close, K⁺ channels stay open → hyperpolarization
Ca²⁺ effect in light
Ca²⁺ channels close, reducing neurotransmitter release
Glutamate in the dark
Photoreceptors release glutamate continuously (inhibitory via mGluRs)
Glutamate in light
Less glutamate released → less inhibition of bipolar cells
Activation of bipolar cells
Disinhibition activates ON bipolar cells → more glutamate released (excitatory)
Ganglion cell stimulation
Ganglion cells fire action potentials → form optic nerve → send signal to brain
ON bipolar cells in light
Disinhibited by less glutamate → depolarize and activate
OFF bipolar cells in light
Lose excitatory glutamate → hyperpolarize and become inactive
Dark state photoreceptors
Depolarized → release glutamate → inhibit ON bipolar cells, excite OFF bipolar cells
Light state photoreceptors
Hyperpolarized → reduce glutamate → ON bipolar cells activate, OFF bipolar cells silent
Sound wave path
Outer ear → tympanic membrane → ossicles → oval window → cochlear fluid
Basilar membrane response
Fluid waves move basilar membrane → hair cells in Organ of Corti activated
Hair cell cilia
Bending of cilia opens mechanically gated ion channels
Ion entry into hair cells
K⁺ and Ca²⁺ enter due to high K⁺ in cochlear fluid → depolarization
Hair cell neurotransmitter release
Depolarization causes glutamate release
Activation of auditory nerve
Spiral ganglion neurons (CN VIII) activated by neurotransmitter
Auditory pathway to brain
Auditory nerve → cochlear nucleus → superior olive → inferior colliculus → MGN → auditory cortex
Mechanoreceptors
Respond to mechanical pressure/stretch via ion channels
Merkel’s disks
Texture/form; slow adapting, small receptive field
Meissner’s corpuscles
Light touch; fast adapting, small receptive field
Ruffini endings
Skin stretch; slow adapting, large receptive field
Pacinian corpuscles
Vibration; fast adapting, large receptive field
Temperature receptors
Warm = TRPV1–4; Cool = TRPM8
Pain (nociceptors)
Free nerve endings detect mechanical, thermal, chemical damage
Action potentials in somatosensation
Depolarization → AP travels via dorsal root to spinal cord
Touch pathway
Dorsal column-medial lemniscus → thalamus → somatosensory cortex
Pain/temp pathway
Spinothalamic tract → thalamus → somatosensory cortex
Taste detection
Taste molecules in saliva bind to receptors in taste buds
Salty taste
Na⁺ enters ion channels → depolarization → AP
Sour taste
H⁺ enters channels → depolarization
Sweet receptors
T1R2 + T1R3 (GPCRs)
Umami receptors
T1R1 + T1R3 (GPCRs)
Bitter receptors
T2R (GPCRs)
GPCR cascade in taste
Activates G-protein (gustducin) → 2nd messenger → ion channels open → depolarization
Neurotransmission in taste
Depolarized receptor cells release ATP (not typical neurotransmitters)
Taste pathway
Facial (VII), Glossopharyngeal (IX), Vagus (X) → NST → thalamus → gustatory cortex
Odorant detection
Odorant binds GPCR on cilia of olfactory receptor neuron
Golf protein cascade
Odorant → Golf → adenylate cyclase → ↑cAMP → Na⁺ channels open → depolarization
Action potential path in smell
AP travels through cribriform plate → olfactory bulb
Synapse location in bulb
Olfactory neuron axons synapse at glomeruli onto mitral cells
Olfactory pathways
Mitral cell axons project to amygdala, piriform, entorhinal, and orbitofrontal cortices
Unique feature of olfaction
Only sense that bypasses thalamus and connects directly to limbic system