Senses - Lecture Flashcards

(46 cards)

1
Q

What effects interpretation of sensory information

A

Sensory signals are relayed from the receptor to a specific neuron in the CNS. Projection pathways carry information concerning specific sensations to specific destinations in the CNS

  1. Modality (Type of Stimulus):
    • What it is: The kind of stimulus (e.g., light, sound, pressure, chemical)
    • How it is encoded:
      • Determined by the type of receptor activated (e.g., photoreceptor, mechanoreceptor, nociceptor).
      • Each receptor sends its signal through a dedicated neural pathway—called a labeled line—to the brain.
      • Even when multiple modalities (e.g., pain and temperature) project to overlapping regions (like the somatosensory cortex), the brain distinguishes them based on which labeled line was activated.
    • Example:
      • Photoreceptors → visual cortex = light
      • Nociceptors and thermoreceptors → spinothalamic tract → somatosensory cortex = pain or heat
  2. Location:
    • What it is: Where the stimulus is coming from
    • How encoded: Determined by which nerve fibers are activated and their corresponding brain region (sensory homunculus, for example)
    • Receptive fields help determine resolution—smaller fields = greater localization (e.g., fingertips)
  3. Intensity:
    • What it is: Strength of the stimulus
    • How encoded: By firing frequency of the neuron and number of neurons recruited (temporal and spatial summation)
    • Stronger stimuli = higher firing rate + more neurons recruited
  4. Duration:
    • What it is: How long the stimulus lasts
    • How encoded: Based on changes in firing over time
    • Receptors can be:
      • Phasic: Rapidly adapt (e.g., smell); fire at beginning/end
      • Tonic: Slowly adapt or not at all (e.g., pain); maintain firing
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2
Q

Ways to classify sensory organs

A
  1. By Modality (Stimulus Type):
    • Thermoreceptors – detect temperature
    • Photoreceptors – detect light
    • Nociceptors – detect pain
    • Chemoreceptors – detect chemicals (smell, taste)
    • Mechanoreceptors – detect pressure, vibration, stretch (proprioceptor, tactil receptors, baroreceptors, visceral mechanoreceptors).
  2. By Origin of Stimulus:
    • Exteroceptors: Detect external stimuli (e.g., skin, eyes, ears)
    • Interoceptors: Detect internal stimuli (e.g., stretch in GI tract)
    • Proprioceptors: Detect body position and movement (e.g., muscles, tendons)
  3. By Distribution in the Body:
    • General (somatosensory) senses: Widely distributed (e.g., touch, pressure, temperature, proprioception)
    • Special senses: Limited to head (e.g., vision, hearing, taste, smell, equilibrium)
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3
Q

List Receptors of General Senses, base function and general location

A
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4
Q

General characteristic of sensory receptor

A

Sensory receptors transduce stimulus energy, generate receptor potentials, and may lead to conscious or unconscious sensations.

  • Transduction:
    • Sensory receptors act as transducers, converting one form of energy (e.g., light, heat, pressure, chemical) into electrical signals (nerve impulses)
    • This is the fundamental function of all sensory receptors
  • Receptor Potential:
    • A local electrical change in the receptor cell membrane caused by a stimulus
    • May lead to the release of neurotransmitters (in non-neuronal receptors) or trigger action potentials (in sensory neurons), which then transmit signals to the CNS
  • Sensation:
    • The subjective awareness of a stimulus
    • Not all incoming signals reach conscious perception
      • Many are filtered out by the reticular formation / thalamus to prevent sensory overload
      • Some are processed unconsciously (e.g., blood pH, body temperature)
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5
Q

Define receptive field

A

A specific region of sensory space in which an appropriate stimulus can drive an electrical response in a sensory neuron

  • Function:
    Determines how precisely a stimulus can be located (spatial resolution)
  • Size Variation:
    • Small receptive fields → allow fine spatial discrimination (e.g., fingertips, lips)
    • Large receptive fields → allow poor localization (e.g., back, thighs)
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6
Q

Describe Somatosensory Projection Pathway

A

Pathway by which somesthetic sensory signals (e.g., touch, pressure, pain, temperature, proprioception) travel from receptors to the primary somatosensory cortex of the brain

  • Involves Three Neurons:
  1. First-order neuron (afferent neuron):
    • From body → enters spinal cord via dorsal root of spinal nerves -> cell is dorsal root ganglion
    • From head → enters brainstem (pons or medulla) via cranial nerves (mainly CN V) -> cell is cranial ganglion
    • Large, myelinated axons for touch, pressure, proprioception
    • Small, unmyelinated axons for pain, temperature
  2. Second-order neuron:
    • Nucleus in spinal cord or brainstem - depends on specific tract
    • Decussates (crosses midline) to the opposite side in spinal cord, medulla, brainstem
    • Ascends to and ends in the thalamus
    • Exception: Proprioception signals end in the cerebellum
  3. Third-order neuron:
    • From thalamus to primary somatosensory cortex in the cerebrum

Summary: Receptor → 1st-order neuron → decussation → 2nd-order neuron → thalamus → 3rd-order neuron → somatosensory cortex

cuneate fasciculus and gracile fasciculus part of posterior-column medial lemniscus tract

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7
Q

Sensory Adaptation

A

A decrease in sensitivity to a constant stimulus over time. Can occur at the receptor level or within the central nervous system (CNS).

Two Types of Adaptation:

  1. Peripheral Adaptation
    • Occurs at the sensory receptor
    • Receptors respond strongly at first, then reduce signaling even if the stimulus continues
    • Sensory adaptation is the reduced responsiveness of a receptor to a sustained stimulus.
      Phasic receptors adapt quickly and signal changes (respond at stimulus onset and / or offset, while tonic receptors adapt slowly and signal duration. Some tonic receptors may never fully adapt
    • Example: Smell of perfume fades after initial exposure
  2. Central Adaptation
    • Occurs within the CNS (e.g., reticular formation, thalamus)
    • Sensory signals may still arrive, but the brain filters them out
    • Leads to loss of conscious awareness of the stimulus
    • Example: Stop feeling your clothes after putting them on
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8
Q

Describe the Types and Mechanisms of Pain

A

Two clinical categories of pain.
1. Neuropathic: injuries to nerves, spinal cord, meninges, or brain: Stabing, burning, tingling, electrical.
2. Nociceptive pain - stems from tissue injury, detected by nociceptors. Detection includes mechanical injury, thermal extremems, chemical mediators released from injured cells.

Nociceptive Pain is further subdivided into.
1. Visceral Pain: arises from internal organs, diffuse, dull, hard to locate. Caused by stretch, ischemia (reduced blood flow), chemical irritation.
2. Deep somatic pain: arises from bones, joints, muslces and related sources.
3.Superficial somatic pain: arises in skin.

Pain is mediated by two types of nerve fibers.
1. Fast pain: imemediate sharp pain. mediated by mylinated nerve fibers. Also called discriminative pain.
2. Slow pain. Delayed, burning / aching fee. Hard to locate.

Inured tissues release chemicals that stimulate pain fibers.
- Bradykinin - most potent pain stimulus known. Makes us aware of injury and activates cascade or reactions that promote healing
- Histamine, prostaglandin, and serotonins also sitmulate nociceptros

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9
Q

Projection Pathway for Pain

A

1. First-Order Neuron (Afferent):
- Detects pain via nociceptors in skin, muscles, joints, or organs
- Cell body in dorsal root ganglion (for body) or cranial sensory ganglia. Major cranial nerves involved are trigeminal, facial, glossopharyngeal, and vagus
- Enters the dorsal horn of spinal cord (body) or brainstem (cranial nerves) and synapses with second-order neuron.

2. Second-Order Neuron:
- Decussates (crosses midline) in the spinal cord (body) or brainstem (head). Cell body is in the dorsal horn or brainstem
- Ascends via one of the following tracts:

  • Spinothalamic Tract
    • An ascending sensory pathway that transmits sharp, localized pain, temperature, and crude touch
    • Carries input from both somatic and some visceral sources, especially when the pain is sharp and well localized
    • Origin: Second-order neurons in the dorsal horn (especially lamina I and V)
    • Decussates in the anterior white commissure of the spinal cord
    • Ascends to the ventral posterolateral (VPL) nucleus of the thalamus
    • Projects to the primary somatosensory cortex for conscious perception
  • Spinoreticular Tract
    • An ascending sensory pathway that transmits dull, aching, or poorly localized pain, from both somatic and visceral structures
    • Particularly involved in the emotional and motivational aspects of pain
    • Origin: Second-order neurons in the dorsal horn
    • Ascends bilaterally to the reticular formation in the brainstem
    • From there, signals are relayed to the intralaminar nuclei of the thalamus and the limbic system
    • Associated with pain-related arousal, attention, and emotional response
  • Trigeminal Lemniscus (Head/Face)
    • Carries pain and temperature sensation from the face and head
    • First-order neurons enter the brainstem and descend before synapsing in the medulla
    • Second-order neurons cross the midline and ascend through the brainstem to reach the thalamus
    • Final projections go to the primary somatosensory cortex for conscious perception

3. Third-Order Neuron:
- From Spinothalamic and Trigeminal Lemniscus pathways:
- Arises in the thalamus
- VPL for body
- VPM for face/head
- Projects to the primary somatosensory cortex (S1) for conscious perception of pain

  • From Spinoreticular pathway:
    • signals are relayed to the thalamus
    • From the intralaminar nuclei of the thalamus, signals project to the limbic system, hypothalamus, and widespread cortical areas (not just the somatosensory cortex)
    • These projections influence emotional response, attention, and autonomic reactions to pain
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10
Q

Referred Pain

A

Pain perceived at a location different from its actual source — usually on the body surface rather than from an internal organ.

  • Mechanism:
    • Visceral and somatic sensory fibers converge onto the same second-order neurons in the dorsal horn of the spinal cord
    • These neurons send signals up the same labeled line to the brain
    • The brain interprets the signal based on the labeled line’s usual source — typically somatic structures
    • Because the CNS cannot differentiate the true origin, visceral pain is misinterpreted as somatic
  • Example – Heart Attack:
    • Pain from the heart (viscera) is referred to the left shoulder and arm
    • This is because T1–T5 spinal segments receive input from both the heart and left upper limb
    • The brain interprets the signal as coming from the limb
Pain pathways are organized by pain type (sharp, dull, emotional), not strictly by pain origin.
There is no pain tract that carries only visceral or only somatic input — they share tracts through convergence in the spinal cord.
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11
Q

Endogenous Opioids

A

bind to the same receptors (mu, delta, kappa) as drugs like morphine

  • Types:
    • Enkephalins – small peptides with high affinity for delta receptors; mediate spinal pain gating and also regulate emotion, stress, and reward in the brain
    • Endorphins – larger peptides (e.g., β-endorphin) released during pain and exercise; promote analgesia and euphoria, especially via mu receptors
    • Dynorphins – bind mostly to kappa receptors; involved in aversive states, pain regulation, and stress
  • Sources:
    • Found in the CNS, pituitary gland, adrenal medulla, and digestive tract
  • Functions:
    • Inhibit pain transmission in the spinal cord (spinal gating)
    • Modulate mood, reward, and stress response in higher brain centers
    • Can produce analgesia, calm, or dysphoria depending on receptor type and location
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12
Q

Pain modulation Pathway

A

The brain can inhibit pain signals through a descending analgesic pathway and spinal gating mechanisms.

  • Pathway Steps:
    1. Cerebral cortex and hypothalamus detect pain and activate descending signals
    2. Signal travels to midbrain
    3. Midbrain relays signal to medulla oblongata
    4. Some descending analgesic fibers from the medulla secrete serotonin onto inhibitory spinal interneurons in the dorsal horn.
    5. Spinal interneurons secrete enkephalins, which block pain transmission by:
      - Postsynaptic inhibition of second-order pain neurons
      - (Possibly also) presynaptic inhibition of first-order pain fibers
    6. Other descending analgesic fibers synapse directly on first-order pain fibers, blocking transmission via presynaptic inhibition
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13
Q

Define Spinal Gating

A

Spinal gating is a mechanism by which pain signals are inhibited at the level of the spinal cord, preventing them from reaching the brain.

Mechanisms of Spinal Gating:

  1. Descending Analgesic Pathway
    • descending analgesic fibers from medulla (specifically nucleus raphe magnus of reticular formation) activate
      a. inhibitory interneurons in the spinal cord (release seratonin) which release enkephalines by means of postsynaptic inhibition of second order pain neuron
      b. Synapse directly on first-order pain fiers blocking pain transmision via presynaptic inhibition.
  2. Somatic Mechanoreceptor Activation
    • Rubbing, shaking, or moving the painful area activates touch receptors
    • These signals stimulate inhibitory interneurons in the spinal cord
    • The interneurons dampen the pain signal by suppressing second-order neurons
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14
Q

Lingual Papillae

A
  • Fungiform papillae – scattered, contain taste buds
  • Vallate (circumvallate) papillae – large, arranged in a V-shape at back of tongue; contain numerous taste buds
  • Foliate papillae – ridges on the sides of tongue; taste buds present, especially in children
  • Filiform papillae – most numerous; no taste buds; aid in texture sensing and food manipulation
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15
Q

Structure taste bud

A
  • Location:
    Embedded within lingual papillae (especially vallate, fungiform, and foliate)

Main Cell Types:

  1. Taste Cells (Gustatory Cells):
    • Not neurons, but epithelial cells with microvilli (taste hairs) projecting into the taste pore
    • Taste hairs detect tastants (chemicals)
    • Synapse with sensory nerve fibers at their base
  2. Supporting Cells:
    • Look similar to taste cells
    • Do not have taste hairs or synaptic vesicles
    • Likely provide structural support
  3. Basal Cells:
    • Stem cells that divide to replace taste cells (lifespan: ~40–60 days)
    • Also give rise to supporting cells

Additional Structures:
- Taste Pore: Opening on the epithelial surface through which taste hairs extend
- Sensory Fibers: Carry signals from taste cells to the brain via cranial nerves

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16
Q

Mechanisms of Taste Cell Activation

A

Each taste modality is triggered when a dissolved tastant binds or passes through structures on the taste cell, causing a chain reaction that ends in neurotransmitter release to a sensory neuron.

1. Salty (Na⁺):
- Tastant Sodium ions (Na⁺) from salty substances (e.g., table salt)
- Mechanism: Na⁺ enters through ion channels
- Effect Depolarization → Ca²⁺ influx → neurotransmitter release

2. Sour (H⁺):
- Tastant: Hydrogen ions (H⁺) from acidic foods (e.g., citrus)
- Mechanism: H⁺ enters through ion channels
- Effect Depolarization → Ca²⁺ influx → neurotransmitter release

3. Sweet:
- Tastant: Sugars (e.g., glucose, sucrose) dissolved in saliva
- Mechanism: Sugar binds to a sweet receptor (G-protein-coupled) on the taste cell
- Effect: Activates G-proteincAMP cascade → closes K⁺ channels → depolarization → neurotransmitter release

4. Umami:
- Tastant: Amino acids, especially glutamate (e.g., in meats, broths)
- Mechanism: Glutamate binds to umami receptor (G-protein-coupled)
- Effect: Activates G-proteincAMP cascade → closes K⁺ channels → depolarization → neurotransmitter release

5. Bitter:
- Tastant: Bitter alkaloids (e.g., caffeine, quinine)
- Mechanism: Binds to bitter receptor (G-protein-coupled)
- Effect: Activates G-proteincAMP cascadeCa²⁺ released from internal stores → neurotransmitter release

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17
Q

Projection pathway for taste

A
Taste cell → Cranial nerve (CN VII / IX / X) → Medulla (solitary nucleus) → Thalamus (VPM) → Primary gustatory cortex (insula & frontal operculum)
  1. Primary Neurons – Cranial Nerves (PNS):
    • Facial nerve (CN VII): Taste from anterior 2/3 of tongue
    • Glossopharyngeal nerve (CN IX): Taste from posterior 1/3 of tongue
    • Vagus nerve (CN X): Taste from epiglottis, palate, pharynx
      → All carry taste input to the nucleus of the solitary tract in the medulla
  2. Secondary Neurons – Medulla (Brainstem):
    • Cell bodies in the solitary nucleus
    • Ascend ipsilaterally via the central tegmental tract
    • Synapse in the ventral posteromedial (VPM) nucleus of the thalamus
  3. Tertiary Neurons – Thalamus to Cortex:
    • Project to the primary gustatory cortex in the insula and frontal operculum
    • Perception of taste occurs here

Additional Projections:
- Branches to the hypothalamus (autonomic response: salivation, hunger)
- Branches to the amygdala (emotional response to taste)
- Local brainstem reflex circuits (e.g., gag, swallowing)

Orbitofrontal Cortex (Frontal Lobe):
- Combines taste, smell, texture, and appearance into overall flavor
- Contributes to liking/disliking food
- Association center for taste

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18
Q

Olfactory Epithelium

A
  • Location:
    Found in the superior region of the nasal cavity.
  • Key Cell Types:
    1. Olfactory receptor cells – bipolar neurons with olfactory hairs (cilia) that detect odorants
    2. Supporting cells – columnar cells that support and nourish receptor cells
    3. Basal cells – stem cells that replace olfactory neurons (which live ~60 days)
    4. Olfactory glands (Bowman’s glands) – secrete mucus that dissolves odorants
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19
Q

Mechanism of Olfactory Receptor Activation

A
  • Step 1:
    Odorant molecules (chemicals in air) dissolve in mucus of the olfactory epithelium
  • Step 2:
    Odorant binds to a G-protein-coupled receptor (GPCR) on the olfactory cilia of receptor cells
  • Step 3:
    Activates G-protein → increases cAMP
    → cAMP opens Na⁺ and Ca²⁺ channels → depolarization -> receptor potential -> action potential
  • Step 4:
    Action potential travels along the axon of the olfactory receptor neuron, through the cribriform plate, to the olfactory bulb
20
Q

Olfactory projection pathway

A
  • Primary Neurons:
    • Olfactory receptor cells in the olfactory epithelium detect odorants
    • Their axons form cranial nerve I (olfactory nerve) and pass through the cribriform plate
    • Synapse in the olfactory bulb
  • Secondary Neurons:
    • Located in the olfactory bulb (mitral and tufted cells)
    • Their axons form the olfactory tract
    • Project caudally to the primary olfactory cortex and other targets — bypassing the thalamus initially
  • Tertiary Processing Centers:
    • Primary olfactory cortex (temporal lobe): conscious perception of odors and relays signals onward
    • Amygdala, hippocampus, insula, and hypothalamus: assign emotional, visceral, and memory-linked responses to odor
    • Signals cross to the contralateral temporal lobe for bilateral processing - After primary olfactory cortex receives input from one side, it relays that information to the contralateral (opposite side) temporal lobe via commissural fibers
    • Orbitofrontal cortex - information from lambic system vis thalamus. integrates smell with taste, texture, and satiety → overall flavor evaluation. Association center for smell.
  • Feedback Modulation:
    • Orbitofrontal cortex and limbic regions send feedback to the olfactory bulb
    • This modulates perception of odors depending on internal state (e.g., hunger vs satiety)
21
Q

Lacrimal Apparatus and tear flow pathway

A
  • Function: Produces and drains tears to clean, protect, and moisten the eye
  • Tear Production:
    • Lacrimal gland (superolateral orbit) continuously secretes tears
    • Tears contain bactericidal enzymes (like lysozyme), aid in O₂/CO₂ diffusion, and flush away debris
  • Tear Flow Pathway:
    1. Tears spread across the eye surface
    2. Drain through lacrimal puncta (on medial eyelids)
    3. Enter lacrimal canaliculilacrimal sac
    4. Flow into the nasolacrimal duct
    5. Exit into inferior nasal meatus, explaining runny nose during crying
22
Q

Palpebrae - Function and key structures

A

The palpebrae maintain eye moisture and protection through blinking, structural support, and oil secretion.

  • Function:
    • Protect the eye from injury, debris, and excessive light
    • Blink reflex spreads tears to moisten cornea and clear particles
    • Help with sleep by closing eye and blocking stimuli
  • Key Structures:
    • Orbicularis oculi muscle: enables blinking and closing the eyelids - facial nerve
    • Tarsal plate: stiff connective tissue that gives eyelid shape
    • Tarsal glands (Meibomian): secrete oily substance to slow tear evaporation
    • Eyelashes: trap and deflect airborne particles
23
Q

Conjunctiva – Structure and Function

A

The conjunctiva is a thin, clear membrane that protects your eye. It covers the inside of your eyelid and the white of your eye (the sclera).

The conjunctiva creates the mucus layer that forms part of your tears.

The conjunctiva keeps your eye lubricated and prevents irritants from getting in. It works with a few glands to create your tears and protects the white part of your eyes from damage.

pink eye (conjunctivitis)

24
Q

Extrinsic Eye Muscles – Actions, Innervation, and Deficits

A
  • Superior oblique
    • Nerve: Trochlear (IV)
    • Movement: Internal rotation, slight depression
  • Superior rectus
    • Nerve: Oculomotor (III)
    • Movement: Rolls eye up
  • Lateral rectus
    • Nerve: Abducens (VI)
    • Movement: Rolls eye laterally
  • Medial rectus
    • Nerve: Oculomotor (III)
    • Movement: Rolls eye medially
  • Inferior oblique
    • Nerve: Oculomotor (III)
    • Movement: External rotation, slight elevation
  • Inferior rectus
    • Nerve: Oculomotor (III)
    • Movement: Rolls eye down
25
intrinsic eye muscles
- **Ciliary muscle** - *Function:* Changes lens shape for focusing (accommodation) - *Innervation:* Parasympathetic fibers of **Oculomotor nerve (CN III)** - *Contracts:* Loosens suspensory ligaments → lens becomes rounder → **near vision** - *Relaxes:* Tightens ligaments → lens flattens → **distance vision** - **Sphincter pupillae** (circular muscle) - *Function:* Constricts pupil (miosis) in bright light - *Innervation:* Parasympathetic fibers from **Oculomotor nerve** - *Contracts:* Constricts pupil (miosis) → in bright light - **Dilator pupillae** (radial muscle) - *Function:* Dilates pupil (mydriasis) in low light or sympathetic activation - *Innervation:* **Sympathetic** fibers from **superior cervical ganglion** - *Contracts:* Dilates pupil (mydriasis) → in low light or sympathetic state - *Innervation:* Sympathetic (superior cervical ganglion)
26
Emmetropia
- State of relaxed vision when viewing distant objects (≥ 20 ft / ~6 m) - Ciliary muscles relaxed → suspensory ligaments taut → lens flattens - Light focuses directly on retina without accommodation
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Convergence
- Inward movement of both eyes to focus on near object - Ensures light from object hits same spot on both retinas - Uses medial rectus muscles (CN III – Oculomotor nerve)
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Lens accommodation
- Adjustment of lens curvature to focus on **near objects** - **Ciliary muscles contract** → suspensory ligaments **relax** → lens becomes **thicker and rounder** - This shape change increases **refractive power** for close-up focus - Controlled by **parasympathetic fibers of CN III** (oculomotor) via the **ciliary ganglion** - Requires **increased parasympathetic input** - *At rest (in the absence of parasympathetic stimulation), the lens remains in its natural **flattened** or **"emmetropic"** state for **distance vision***
29
Pupillary miosis
- Constriction of the pupil to enhance **near focus** and reduce **spherical aberration** - Caused by contraction of the **sphincter pupillae** (circular muscle of the iris) - Controlled by **parasympathetic fibers from CN III** via the **ciliary ganglion** - Occurs with **increased parasympathetic input** during accommodation for near vision ``` Parasympathetic control is stimulus-driven, not emotional-state-driven. If your eyes need to focus on a near object, the parasympathetic system activates the ciliary muscle and sphincter pupillae, even if you're stressed. Sympathetic tone may be elevated, but the parasympathetic pathway still engages locally when near vision is required. ```
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Near response
- Group of adjustments that allow the eyes to focus on nearby objects - Involves three coordinated actions 1. **Convergence of eyes** - *Muscles:* **Medial rectus muscles** (one in each eye) - *Innervation:* **Somatic motor fibers of CN III (oculomotor)** - *Control:* **Voluntary**, not autonomic - Function: Eyes turn medially to align visual axes with the near object, ensuring focus on the fovea of each retina 2. **Constriction of pupil (miosis)** - *Muscle:* **Sphincter pupillae** (circular muscle of iris) - *Innervation:* **Parasympathetic fibers of CN III** via **ciliary ganglion** - Function: Reduces peripheral light rays, minimizes spherical aberration, improves clarity 3. **Accommodation of lens** - *Muscle:* **Ciliary muscle** - *Innervation:* **Parasympathetic fibers of CN III** via **ciliary ganglion** - Function: Ciliary muscle contracts → suspensory ligaments relax → lens becomes **rounder** → increased refraction for near focus > The **entire near response** is coordinated by the **oculomotor nerve (CN III)** and is driven by **parasympathetic activation**.
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Visual Accommodation
- **Myopia (nearsightedness)** - Eye is too long or cornea too curved - Light focuses *in front* of retina → distant objects appear blurry - Corrected with *concave (diverging)* lenses - **Hyperopia (farsightedness)** - Eye is too short or cornea too flat - Light focuses *behind* retina → near objects appear blurry - Corrected with *convex (converging)* lenses
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Aqueous Humor: Flow and Function
- *Production:* - Secreted by **ciliary body epithelium** into the **posterior chamber**. Serous fluid. - *Flow pathway:* 1. Posterior chamber 2. Through the **pupil** 3. Into the **anterior chamber** 4. Drains into the **canal of Schlemm** (scleral venous sinus) 5. Enters **venous circulation** - *Function:* - **Maintains intraocular pressure (IOP):** - Helps preserve the eye’s shape and keeps the cornea properly curved for light refraction - **Provides nutrients:** - Delivers oxygen and nutrients (especially glucose, amino acids) to **avascular structures** like the **cornea** and **lens** - **Removes waste products:** - Carries away metabolic byproducts from the cornea and lens - **Optical clarity:** - Maintains a **clear optical path** for light to reach the retina - *Clinical Note:* - Impaired drainage leads to increased pressure → **glaucoma**
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Posterior Cavity and Vitreous Humor
- *Vitreous humor:* Gelatinous substance in the posterior cavity between lens and retina - *Functions:* - Maintains intraocular pressure - Supports the shape of the eye - Presses retina against choroid, allowing nutrient diffusion - Stabilizes position of lens and retina - *Clinical note:* - Loss of pressure can lead to **retinal detachment** The vitreous humor is formed during development and is not replenished like aqueous humor. It plays structural and optical roles but is essentially permanent in the adult eye
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Tunics of Eye
- **Fibrous Tunic** - **Sclera** - Provides structural support and protection - Serves as attachment site for extrinsic eye muscles - **Cornea** - Transparent and curved to refract (bend) light into the eye - Allows light to enter the anterior eye - high innervated - one of the highest nerve densities in the body - Is protective - **Vascular Tunic (Uvea)** - **Choroid** - Highly vascularized; supplies nutrients and oxygen to retina - Pigmented to absorb stray light and prevent reflection inside eye - **Ciliary Body** - Contains **ciliary muscle** that control the shape of the lens (accommodation) - Secretes and reabsorbs aqueous humor into the anterior cavity - **Iris** - Pigmented part of eyes. Consists of blood vessels, pigments an smooth muscles. - Contains **smooth muscles** that adjust pupil diameter to regulate light entry - sphincter and dilator pupillae - **Neural Tunic (Retina)** - **Pigmented Layer** - Absorbs stray light and prevents image distortion - Supports and nourishes photoreceptors - **Neural Layer** - Contains photoreceptors (rods and cones) that detect light - Converts light into neural signals sent via the optic nerve
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Retina structure
The **retina** (neural tunic) has two layers: - **Pigmented epithelium**: Outer layer that absorbs stray light, supports photoreceptor metabolism, and continually regenerates photopigments. - **Neural layer**: Inner layer containing photoreceptors and neurons for visual signal processing. - *Photoreceptors*: - **Rods**: Specialized for **low-light (scotopic) vision**; do not detect color. - **Cones**: Specialized for **color vision** and **sharp detail** in bright light. - Each has an *outer segment* with light-sensitive discs and an *inner segment* with mitochondria and organelles. - *Synaptic pathway*: 1. **Rods/cones** detect light and generate **receptor potentials** (not action potentials). 2. Signal passes to **bipolar cells** 3. Then to **ganglion cells**, which generate action potentials that travel via the **optic nerve**. (first-order neurons). - *Support and anchoring*: - Retina is firmly attached only at the **optic disc** (posteriorly) and **ora serrata** (anteriorly). - Aqueous humor and vitreous body help press retina against the choroid to maintain contact.
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Distribution of rods and cones in the retina
- *Macula lutea*: Central region of retina with **high cone concentration** for detailed, color vision. - *Fovea centralis* (center of macula): - Contains **only cones** (100% cones). - Site of **greatest visual acuity** and **sharpest image** formation. - Best color and detail vision occurs when an object is focused here. - *Optic disc*: - Contains **no rods or cones**. - Location where ganglion cell axons exit the eye to form the **optic nerve**. - Known as the **blind spot** — no vision occurs if an image lands here. - The brain "fills in" missing information, and constant small eye movements (Microsaccades) help prevent gaps in perception. - *Peripheral retina*: - Contains **more rods** than cones. - Specialized for **low-light vision** and motion detection, but lower resolution.
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Non Receptor cells of the retina
- **Bipolar cells** - *Function:* *Intermediate (relay) neurons* in the retina; receive input from photoreceptors and transmit to ganglion cells - *Synapse on:* Ganglion cells - *Note:* **High convergence with rods** (many rods → one bipolar cell); **little to no convergence with cones** (1:1 ratio enhances visual acuity) - **Ganglion cells** - *Function:* **First-order neurons** of the visual pathway proper; their axons form the **optic nerve (CN II)** and carry signals to the brain - *Axons form:* **Optic nerve (CN II)** - *Note:* More convergence from rod pathways than cone pathways - **Horizontal cells** - *Function:* Connect photoreceptors laterally - **Amacrine cells** - *Function:* Connect bipolar cells and ganglion cells laterally Enhance perception of contrast, edges of objcts, and changes in light intensity
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Lens – Role in Vision
- *Function:* - Transmits light from the pupil to the retina - Focuses **inverted image** onto photoreceptors of retina - Changes shape for accommodation (focusing near vs far) - *Structure:* - Made of **concentric layers** of transparent cells - Suspended by **suspensory ligaments** behind iris - *Accommodation:* - **Ciliary muscles contract** → lens rounds → near vision - **Ciliary muscles relax** → lens flattens → distance vision - *Pathway of light:* - Passes through **cornea → anterior cavity → pupil → lens** - Lens focuses light on retina → photoreceptors depolarize → signal sent via **CN II (optic nerve)** - *Photoreceptor activation:* - **Cones** need bright light → color vision - **Rods** activate in low light → grayscale night vision (cones deactivate) - *Clinical note:* - **Cataract** = clouding of lens → blurred vision - Caused by aging, UV, diabetes, smoking
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**Structure of Rods and Cones**
- *Pigment Epithelium:* - Located behind photoreceptors - Absorbs stray light to prevent reflection - Engulfs and recycles shed outer segment discs - Stores vitamin A needed for retinal regeneration - *Outer Segment:* - Contains **membrane discs** stacked in cylindrical shape - Discs contain **visual pigments**: - **Rods:** rhodopsin (opsin + retinal) - **Cones:** photopsin (opsin + retinal) - Retinal undergoes cis → trans isomerization upon light exposure (bleaching) - *Inner Segment:* - Contains nucleus and organelles (mitochondria, Golgi apparatus) - Responsible for ATP production and protein synthesis (including photopigments) - *Synaptic Terminal:* - Forms synapse with **bipolar cells** (first-order neurons) - *Photopigments:* - **Rhodopsin (rods):** absorbs at ~500 nm; highly sensitive to dim light - **Photopsin (cones):** three variants absorbing short (420 nm), medium (531 nm), and long (558 nm) wavelengths for color vision
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Bleaching
- **Bleaching** is the light-induced breakdown of a photopigment after it absorbs a photon. - Specifically, **retinal** changes from the *cis* to *trans* form, causing it to dissociate from **opsin**. - This reaction renders the opsin temporarily **nonfunctional** for detecting more light. - *Why It's Important:* - Bleaching is necessary to **trigger a visual signal**: Bleaching stops glutamate release from photoreceptors, lifting inhibition on ON bipolar cells and triggering their activation. The visual signal is phasic — the bipolar and ganglion cells respond to changes in glutamate, not its continued absence. - However, once bleached, the pigment **cannot respond to light** again until retinal is converted back to the *cis* form and rebinds to opsin — this is the **recovery** or **regeneration** phase. - *Physiological Significance:* - Prevents continuous stimulation — each pigment must reset before detecting light again. - Explains **why vision adapts slowly in darkness** (rods must regenerate rhodopsin). - Explains **color fade in bright light** (cones bleach faster than they regenerate). - *Time to Regenerate:* - **Cones:** recover in **90 seconds** → why bright-light vision returns quickly - **Rods:** take **5 to 10 minutes** or longer → explains slow *dark adaptation* - Rods are highly sensitive but recover slowly after bleaching - *Overall Role in Vision:* - Ensures **visual sensitivity adapts** to changing light conditions - Underlies **light and dark adaptation** and protects photoreceptors from overstimulation ``` Only a fraction of photopigments are bleached at any given time. While some photoreceptors are being stimulated and bleached, others are recovering and being recharged by the retinal pigment epithelium (RPE). The RPE absorbs stray light and recycles retinal from the trans → cis form. Rods and cones don’t all fire at once — you have millions of them, and they operate in overlapping fields, so even if one is in the middle of bleaching and recovery, nearby ones are active and feeding your brain the visual signal. Meanwhile, your eyes constantly move (microsaccades) — this prevents any single photoreceptor from being locked into continuous activation or bleaching. ```
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**Color vision**
based on the stimulation of three types of **cone photoreceptors**, each containing a different type of **photopsin** that absorbs light at different wavelengths: - **Short-wavelength (S) cones**: peak at **420 nm** (blue light) - **Medium-wavelength (M) cones**: peak at **531 nm** (green light) - **Long-wavelength (L) cones**: peak at **558 nm** (red light) - *Color perception* arises from the **relative activation** of these three cone types; the brain interprets the **ratio of activity** to generate the perceived hue. - Example: Equal activation of red + green cones → perception of **yellow**. - Blue-green light (~500 nm) → activates both **blue and green cones** to varying degrees. - **Rods** do not contribute to color vision; they are active in low light and peak at ~**500 nm**. - Light must fall within **400–750 nm** to be detected: - <400 nm: **damaging** to cells (UV) - >750 nm: **not energetic** enough (infrared)
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color blindness
- **Color blindness** is a genetic or acquired condition in which one or more types of **cone photoreceptors** are missing or nonfunctional. - Most common form: **red-green color blindness** - Caused by **absence or malfunction** of **L (red)** or **M (green)** cones - Individuals have difficulty distinguishing reds from greens - **Blue-yellow color blindness** (rare): - Caused by lack of **S (blue)** cones - Impairs blue-yellow discrimination - **Total color blindness (monochromacy)**: - Extremely rare - No functional cones → vision relies on rods only → **black-and-white vision**
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Dual Vision system
- **Rods** and **cones** provide **complementary functions**—you can't have a cell that is both highly sensitive and high resolution. - **Rods** - High **sensitivity** to light (activated by very little light) - Enable **night vision** (scotopic vision) - Located mostly in **peripheral retina** - Exhibit **high convergence**: multiple rods synapse on fewer bipolar/ganglion cells → increased sensitivity but **low resolution** - Monochrome vision (no color) - **Cones** - Require **bright light** to activate - Densely packed in **fovea centralis** - Exhibit **low convergence**: one-to-one or few-to-one signaling → **high resolution**, precise spatial detail - Enable **color vision** and **sharp focus** (photopic vision) - *Why both?* - **Rods** give us **sensitivity** to detect light in dim conditions - **Cones** give us **acuity and color**, but only when light is sufficient - A single type of cell cannot do both due to trade-off between **sensitivity** and **spatial precision**, so a **dual system** is essential
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Light and Dark Adaptation
**Light adaptation** (e.g., stepping into sunlight): - **Pupils constrict** to reduce light entry - **Photopigments (esp. rhodopsin)** bleach faster than they can regenerate - **Retinas overstimulated**, causing discomfort and temporary reduced acuity - **Color vision and sharpness** reduced for ~5–10 minutes until cones adjust **Dark adaptation** (e.g., lights off): - **Pupils dilate** to allow more light in - **Rhodopsin in rods regenerates slowly** (~20–30 minutes) - Rods gradually take over from cones, restoring **night vision**
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Stereoscopic Vision
The ability to perceive **depth and three-dimensional structure** by comparing slightly different views from the **left and right eyes**. - *Mechanism:* - Each eye views the same object from a **slightly different angle** (binocular disparity). - The brain uses this disparity to compute **depth and relative distance**.
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Visual Pathway
- *1. Retina:* - **Photoreceptors** (rods & cones) detect light → stimulate **bipolar cells** → activate **retinal ganglion cells**. - Their axons form the **optic nerve (CN II)**. - *2. Optic Nerve → Optic Chiasm:* - Right and left optic nerves converge at the **optic chiasm**, where fibers undergo **hemidecussation** (nasal retinal fibers cross; temporal do not). - This results in the right cerebral hemisphere processing the left visual field, and vice versa. - *The brain processes visual input from the same side it controls motor output toward (contralateral control).* - *3. Optic Tracts:* - MOST fibers from the optic tract synapse in the **posterior nucleus** of the thalamus **thalamus**. - A smaller number branch off to other midbrain structures involved in visual reflexes, including the **superior colliculi** (midbrain) and the **pretectal area** (midbrain). - *4. Thalamus to Cortex:* - **third-order neurons** in the posterior nuclei project via the **optic radiations** to the **primary visual cortex (V1)** in the **occipital lobe**. - V1 interprets basic visual features such as edges, contrast, and orientation. - *Other Targets:* - **Pretectal area**: Receives direct input from retinal ganglion cells → controls the **pupillary light reflex** -> parasympathetic CNIII - **Superior colliculi**: Coordinate reflexive eye and head movements in response to visual stimuli. - **Ventral stream**: V1 → temporal lobe → object recognition & visual memory (“what” pathway). - **Dorsal stream**: V1 → parietal lobe → spatial relationships & motion tracking (“where/how” pathway).