Lecture 3

Neural Pathways of Vision

• Effect of Light on ON/OFF Pathways:

  • Absence of Light: Photoreceptor is depolarized.

  • Presence of Light:

    • Photoreceptor hyperpolarizes.

    • cGMP is broken down by cGMP-dependent phosphodiesterase.

    • Cytoplasmic concentration of cGMP decreases.

    • Cation channels close.

  • Photoreceptor cell hyperpolarization leads to decreased glutamate release.

  • ON Pathway: Decreased glutamate release from photoreceptor reduces inhibition on bipolar cell, causing it to depolarize and release more glutamate, leading to ganglion cell depolarization and action potentials.

  • OFF Pathway: Reduced excitation of OFF bipolar cell due to decreased glutamate release from photoreceptor causes bipolar cell to hyperpolarize, releasing less glutamate, resulting in ganglion cell hyperpolarization and fewer action potentials.

Neural Pathways of Vision Details

• Light signals are converted into action potentials through photoreceptor, bipolar, and ganglion cell interaction.

• Photoreceptor and bipolar cells undergo graded responses; lack voltage-gated sodium channels needed for action potential generation.

• Ganglion cells have voltage-gated sodium channels and are the first cells in the pathway where action potentials can be initiated.

• Photoreceptors interact with bipolar and ganglion cells via ON and OFF pathways.

• In both pathways, photoreceptors are depolarized in the absence of light, releasing glutamate.

• Light hyperpolarizes photoreceptor cells, decreasing glutamate release.

• Presence of light reduces cGMP via activation of cGMP-dependent phosphodiesterase, hyperpolarizing the cell.

• Hyperpolarization of photoreceptor cells reduces glutamate release onto bipolar cells.

• Key Differences:

  • ON pathway bipolar cells spontaneously depolarize without input; OFF pathway bipolar cells hyperpolarize.

  • Glutamate receptors of ON pathway bipolar cells are inhibitory; glutamate receptors of OFF pathway bipolar cells are excitatory.

• Glutamate on ON pathway bipolar cells binds to metabotropic receptors, causing cGMP breakdown, hyperpolarizing the bipolar cell, preventing glutamate release onto ganglion cells.

• Absence of Light: Photoreceptor depolarized due to cGMP binding to cation channels, allowing sodium and calcium to enter the cell, releasing glutamate onto the ON bipolar cell, which hyperpolarizes, decreasing its glutamate release onto the ganglion cells; no action potentials are generated in ON ganglion cells.

• Presence of Light: Photoreceptor hyperpolarized as cGMP is broken down, reducing glutamate release, removing inhibition on ON bipolar cells, which release glutamate onto ganglion cells, causing action potentials.

OFF Pathway Functionality

• OFF pathway bipolar cells have ionotropic glutamate receptors (nonselective cation channels).

• Glutamate binding depolarizes the bipolar cell, stimulating glutamate release onto the ganglion cells, generating action potentials.

• OFF pathway generates action potentials in the absence of light.

• Coexistence of ON and OFF pathways improves image resolution by enhancing contrast perception at edges or borders.

Visual Pathways and Fields

• Visual cortex is located in the occipital lobe.

• Left Eye:

  • Information from the lateral field of view hits the nasal retina, crosses at the optic chiasm to the contralateral side, synapses in the lateral geniculate nucleus, and goes to the visual cortex.

  • Information from the medial field of view hits the temporal retina, does not cross at the optic chiasm (stays ipsilateral), synapses in the lateral geniculate nucleus, and goes to the visual cortex.

• Visual information from each eye goes to both sides of the brain.

• Lateral field of view → nasal retina → contralateral side at optic chiasm → lateral geniculate nucleus → visual cortex.

• Medial field of view → temporal retina → ipsilateral side → lateral geniculate nucleus → visual cortex.

Hearing and Sound

• Pinna: The external ear.

• Temporal Lobe: Contains the auditory cortex.

• Sound energy is transmitted through gaseous, liquid, or solid media by molecular vibration; air is the most common medium.

• Sound:

  • Tuning fork example: Striking the fork creates zones of compression (tightly packed air molecules) and rarefaction (fewer air molecules).

  • Compression and rarefaction ripple outward, transmitting sound.

  • Amplitude (Volume/Loudness): Determined by the number of air molecules in a zone of compression or the difference between pressure in compression and rarefaction zones.

  • Frequency (Pitch): Determined by the distance between compression zones or the number of compression/rarefaction zones in a given time; faster vibration means higher pitch.

  • Anything disturbing molecules can be a sound source.

  • Hearing occurs when compression and rarefaction zones hit the ear.

Anatomy of the Ear and Sound Transmission

• Pinna (Earlobe): External ear.

• Outer ear and external auditory canal funnel compression and rarefaction zones towards the middle and inner ear.

• Air molecules in compression and rarefaction zones travel along the auditory canal and hit the tympanic membrane (eardrum).

• Tympanic Membrane: Vibrates in and out at an amplitude and frequency consistent with the sound.

  • Increased volume means greater displacement of the tympanic membrane.

  • Increased frequency means faster tympanic membrane movement.

• Cochlea: Inner ear.

• Tympanic membrane is attached to three bones in the middle ear: malleus, incus, and stapes.

• Bones act as levers and amplify sound.

• Small tympanic membrane movements are amplified by the malleus, incus, and stapes.

• Amplification is needed because the outer and middle ear are air-filled, while the inner ear (containing sensory receptors) is fluid-filled.

• Vibrations pass from air to fluid.

• Skeletal muscles (tensor tympani and stapedius) attached to malleus and stapes contract to dampen bone movement and protect the inner ear from loud sounds.

  • Malleus: Tensor tympani muscle.

  • Stapes: Stapedius muscle.

• Muscles protect from ongoing loud sounds, but not sudden loud noises.

• Stapes terminates on the oval window of the cochlea.

• The stapes pushes against the oval window, causing fluid movement within the inner ear.

• Tympanic membrane moves → 3 bones amplify the movement, with the stapes pushing against the inner ear and causing movement of fluid within the inner ear

Sound Transmission in the Ear

• When sound becomes too loud, the stapedius muscle and the tensor tympani muscles contract and dampen the movements of the bone.

• Cochlea: Inner ear, divided into three compartments: scala vestibuli, scala tympani, and cochlear duct.

• Scala vestibuli and scala tympani contain perilymph.

• Cochlear duct contains endolymph and houses the sensory receptors for the auditory system.

• Sound waves move the tympanic membrane → move middle ear bones → stapes pushes against the oval window → perilymph movement towards the helicotrema → perilymph movement down across the cochlear duct (from scala vestibuli to scala tympani).

• Fluid movement activates sensory receptors in the cochlear duct.

Cochlea & the Organ of Corti

• The compartments of the cochlea (inner ear): scala vestibuli, scala tympani and cochlear duct.

• Cochlear duct: where the sensory receptors for the auditory system are located.

• Sensory receptors for the auditory system are known as hair cells.

• Hair cells are located in the cochlear duct on a structure known as the Organ of Corti: a specialized sensory epithelium that allows for the transduction of sound vibrations into neural signals.

• Hair cells have stereocilia protruding from them at their tips.

• 2 anatomically separate groups of hair cells; a single row of inner hair cells and three rows of outer hair cells.

• The stereocilia of the single row of inner hair cells extend into the endolymph and transduce pressure waves caused by fluid movement in the cochlear duct into receptor potentials.

• The stereocilia of the 3 rows of outer hair cells are attached to the tectorial membrane.

• At the bottom, each outer hair cell is attached to the basilar membrane.

• Different regions of the basilar membrane vibrate maximally at different frequencies.

• The hair cells in the region of peak vibration of the basilar membrane undergo the most mechanical deformation; this information is sent to the CNS, which interprets the pattern of hair cell stimulation as a sound of a particular frequency.

• Different sound frequencies are detected along the length of the Organ of Corti.

• Vestibulocochlear nerve takes auditory information from the ear towards the brain.

• Tympanic membrane vibrates based on the characteristics of the sound → activates the malleus, incus and stapes in the middle ear → pushes against the oval window and amplifies the movements → pushes the perilymph down across the cochlear duct → when fluid is pushed down, the basilar membrane moves up and down based on the amplitude and the frequency of the sounds → the hair cells move back and forth.

Hair Cells of the Organ of Corti

• The hair cells move back and forth when the basilar membrane moves.

• Remember, the stereocilia of the outer hair cells are attached to the tectorial membrane at the top.

• When the stereocilia move, a mechanically-gated potassium channel opens.

• This is how the auditory receptors are activated and how they depolarize.

• When the basilar membrane moves, the hair cells move back and forth and the stereocilia bend.

• When the stereocilia are bent towards the tallest member of a bundle, mechanically-gated cation channels open, allowing potassium to flow down its concentration gradient through the channel.

• In the ear, there is little potassium in a hair cell as opposed to the extracellular space.

• When the mechanically-gated potassium channel is opened, potassium flows down its concentration gradient into the cell.

• Once potassium has flowed into the cell, the hair cell depolarizes due to the inward movement of positively charged potassium.

• This generates graded potentials in the hair cell.

• The neurotransmitter glutamate is released onto the afferent neurons.

• The afferent neurons make up the vestibulocochlear nerve.

• If enough glutamate is released to bring the afferent neurons to threshold, action potentials are generated in the vestibulocochlear nerve and travel back towards the brain.

• Bending of the hair cells in the opposite direction closes the channels, allowing the cell to rapidly repolarize.

• As sound waves vibrate the basilar membrane, the stereocilia are bent back and forth, and the membrane potential of the hair cell rapidly oscillates, leading to bursts of neurotransmitter being released onto afferent neurons.

Neural Pathways in Hearing

• Cochlear nerve fibers synapse with interneurons in the brainstem.

• From the brainstem information is transmitted by a multineuron pathway to the thalamus and then to the auditory cortex in the temporal lobe.

Restoration of Hearing

• Hearing aids and cochlear implants.

• Hearing Aids: Auditory machinery in the ear is not as sensitive.

  • An amplifier which is placed in the auditory canal which activates the existing auditory machinery.

  • Amplifies existing sounds.

  • Hearing aids are restricted to the outer ear component and can be turned up and down in volume.

• Cochlear Implant: People have damage to certain components of the outer, middle or inner ear.

  • Machinery of the ear simply does not work.

  • A speaker put on the outside of the head which picks up noises and transduces them into electrical impulses.

  • Electrodes go from the speaker down to the vestibulocochlear nerve and send electrical impulses to the vestibulocochlear nerve dependent on the features of the sound that the receiver is picking up.

  • The receiver is on the outside of the head; takes in auditory information and bypasses the outer, middle, and inner ear; directly electrically stimulates the vestibulocochlear nerve to take information from the vestibulocochlear nerve to the cortex which accurately represents the features of the sound.