exam 2 study guide deck COPY COPY Flashcards
- What type of physical energy is transduced into electrochemical signals by specialized sensory neurons in each of our five primary sensory systems?
Vision: photons
Audition: sound waves
Somatosensation: pressure, vibration, heat/ cold
Taste/ Smell:chemicals
- Describe how neurons in the retina transduce light energy (photons/light waves) from the environment into electrochemical signals in the brain.
a. What does each type of photoreceptor cell respond to, and how are the different types distributed in the retina?
Rods: low-light vision ( no detail or color)
Many rods → a few bipolar cells → ganglion cells
Cones: high light vision (detail and color RGB color)
Each cone → bipolar cells → ganglion cells
b. What are the 3 major layers of neurons that make up the retina, and what is the direction and type of communication between these neurons and to the brain? (i.e., how does light ultimately become an action potential?)
back front
Photoreceptor → Bipolar cells → Ganglion cells
First photoreceptors transduce light sends signals too bipolar cells, then they send signals to ganglion cells
- In DARK, Na+ channels are OPEN (sodium goes in and is excitatory), photoreceptors depolarized and releasing glutamate and excites the bipolar cell (an inhibitory cell) decreases firing to retinal ganglion cells to the LGN .
- LIGHT activates “rhodopsin” receptor> Na+ channels close > hyperpolarization of photoreceptor > glutamate release to bipolar cell is less which means the inhibitory bipolar cell fires less and it means more Aps to the RGC and then more to the LGN
c. What is the most common cause of color-blindness?
Due to genetics, the most common type of color blindness is red-green (8%)
- Explain how visual information from right and left eyes compared to right and left visual fields gets into the brain.
Everything from the left visual field goes to the right hemisphere even if it’s picked up by the right eye and vise versa
- Describe the “major” and “minor” pathways of visual information processing from retinal ganglion cells to brain.
Major: Retina → LGN → Primary visual cortex (occipital lobe) → secondary visual pathway –> assoc. (ventral/ dorsal)
Minor: Retina → Superior colliculus (midbrain tectum) → Post parietal lobe
- Explain at least one mechanism by which our brains process visual information to sharpen our perception of edges (e.g., enhance our ability to visually distinguish foreground from background objects).
Lateral inhibition: retinal and LGN: neurons firing maximally to the bright side of a given edge inhibit the firing of adjacent neurons- sharpening our edge perception
Center- surround firing: vision neurons [retina (some r. Ganglion cells), LGN, primary visual cortex] are excited or inhibited depending on where in their receptive field light hits: in an “on-center” or “off-center” manner fire most strongly to contrast edges
- What types of simple stimuli do individual primary visual cortex (V1) neurons respond to?
Simple cells: simple lines
- Input from only one eye
- Rectangular receptive fields with “on/off” areas
- Fire maximally to straight edge of particular orientations
Complex Cells: lines but also movement
- Particular orientation and movement direction
- Input from either eye or both (binocularity → depth perception)
- Explain the change in visual perception that may be caused by single-hemisphere vs. dual-hemisphere damage to primary visual cortex (V1), and explain why people with extensive, dual-hemisphere V1 damage may still show rudimentary, visually guided behavior, albeit “unconsciously.” What is this phenomenon called?
V1 damage; “scotoma” = area of blindness
- One hemisphere = one visual field
- Both hemispheres = “cortical blindness” may experience “blindsight” – due to intact superior colliculus- to- posterior parietal lobe pathway
Note: retinal damage (e.g due to glaucoma, injury) can also produce scotomas; how to test whether a scotoma is due to eye or brain damage?
- What is meant by “dorsal stream” and “ventral stream” in the visual system? What visual dysfunction is associated with dorsal vs. ventral stream brain damage?
Ventral (WHAT) stream (occipitall > inferotemporal cortex): what am I looking at? (Conscious ID of objects, people)
Dorsal (WHERE/HOW) stream (occipital> posterior parietal cortex): where is this object in relation to my body, and how do I adjust my body relative to it? (Visually guided touch/movement, learned but largely unconscious
Dorsal stream damage: Dusrupted visually guided movement (case A.T)
Ventral stream damage: disrupted form / shape perception (case D.F)
- Describe the specific disturbances of visual perception that are associated with damage to secondary visual cortex areas V4 and V5, compared to inferior temporal lobe (=inferotemporal cortex) vs. posterior parietal lobe. What are the various visual agnosias called, specifically? Make sure you can identify on brain drawings the area associated with each type of visual deficit.
V4 Damage in secondary visual cortex in the occipital lobe: loss of normal color vision “achromatopsia”
V5 Damage in secondary visual cortex in the occipital lobe: motion blindness “akinetopsia”
Agnosias: Ventral Stream damage
Object agnosia implicated in the same areas below: inability o recognize previously familiar objects
Prosopagnosia ventral stream damage and it runs from occipital lobe secondary visual cortex to the inferotemporal lobe (damage to the infero temporal cortex or genetics which affect 2.5% of all people): inability to recognize faces
- Compare/contrast the pathways from sensory nerve ending in the PNS to brain for visual vs. auditory vs. somatosensory systems. Is the somatosensory system “crossed” (i.e., does information from one side of the body get sent to the opposite side of the brain)?
Somatosensory:
Somatosensory. Nerves → Thalamus (VPN) → primary somatosensory cortex (anterior p. lobe) → secondary somatosensory cortex (just posterior of the primary in the parietal) → assoc. Cortex (p.p. Cortex, PFC) Total crossing
Visual:
Retina → Thalamus (LGN) → primary visual cortex → secondary visual cortex → assoc. Cortex (ventral (inferotemporal) and dorsal streams (posterior parietal) Total crossing
Audition:
Inner ear → hindbrain (medulla) → inferior colliculi → thalamus (MGN) → primary auditory cortex (dorsal temporal) → secondary auditory cortex (temporal)→ assoc. Cortex: (p.p. Cortex (WHERE), PreFrontalCortex (WHAT) temporal (Visualize) Partial crossing
Yes, the somatosensory system is crossed
- Somatosensation is composed of what 3 sub-types of somatosensory systems? Where are the sensory nerve endings in each sub-system, and what does each of these sub-systems enable you to detect? (come up with some of your own examples)
Exteroceptive System: nerve endings in the skin, detect touch, temp and pain. (touching a hot stove) CONCIOUS
Proprioceptive System: nerve endings in muscles, tendons, and joints, provide body position/ balance info
( → cerebellum, largely unconscious) (when you are playing sports and you keep your balance even though there is a lot of jostling) MOSTLY UNCONCIUS
Interoceptive System: Nerve endings in organs (gut, lungs, heart, bladder) (when you are hungry you feel it) SOMETIMES CONCIOUS
- What types of sensory nerves (named for their specialized nerve endings, called “receptors”) are there in the exteroceptive somatosensory system, and what type of physical stimulus causes each of them to fire?
Mechanoreceptors: the deformation of nerve endings open Na+ channels → depolarization
Rapid adaption to constant pressure. Which is why you no longer feel your clothes on you after dressing
Thermoreceptors: fire in response to cold or heat; have cation channels that are temp- sensitive opens sodium channels.
Painful stimuli (nociceptors):Pressure tearing, bruising) Can be sensitive to pressure or heat. Fires when tissue damage may occur. Temperature (burning hot, or freezing cold)Hot also fires to capsaicin; cold also fires to menthol feeling cold
- Explain how mechanoreceptors vs. thermoreceptors transduce physical stimuli (e.g., pressure vs. temperature) into electrochemical signals. In other words, what causes these nerve endings to depolarize?
Mechanoreceptors: the deformation of nerve endings open Na+ channels → depolarization
Rapid adaption to constant pressure. Which is why you no longer feel your clothes on you after dressing
Thermoreceptors: fire in response to cold or heat; have cation channels that are temp- sensitive.
- Explain how the number of somatosensory nerve endings and number of primary somatosensory (S1) neurons relate to how sensitive different parts of your body are to touch. How is the primary somatosensory cortex organized?
Homunculus, more nerve ending on the mouth and tongue, hands, feet, genitals than the rest of the body.
- Describe how limited vs. extensive damage to somatosensory nerve endings in skin, vs. spinal cord damage at different levels, vs. single hemisphere damage to VPN or primary somatosensory cortex can affect one’s somatosensory experiences and abilities.
Damage to Sensory nerve endings: your brain would do completion when you see someone touch you.
Damage Spinal cord: the higher the damage the more conscious perception you lose, the more loss you will have in the body., also loss of feeling
Damage to VPN on one side: you would not feel things coming from the opposite side
Damage to primary somatosensory cortex: distorted or changed sensation from the other side, they can tell they have something in their hand but can’t tell what it is Restricted → mostly touch discrimination. More extensive → cannot identify objects by touch w/ opposite hand
- Describe what substantial damage to right posterior parietal lobe causes (what is the syndrome called, and what are the symptoms?). Contrast this syndrome with what happens when a person sustains damage to their left posterior parietal lobe (see Ch. 8 lecture notes).
· If R p. parietal lobe: Asomatognosia (contralateral neglect or spatial neglect): cannot perceive L side of self and world - a somatosensory and visual deficit and they are not usually aware of their deficit so it has some cognitive deficit.
Left-hemisphere: no change in consciousness, but APRAXIA - difficulty miming familiar movement (particularly when out of context) …
And/or difficulty performing visually guided movements like juggling.
- Describe the flow of information from sensory cortices to frontal lobe association and motor cortices, as well as the flow of movement information out of the brain to the muscles.
Visual, somatosensory, auditory cortex converge on >
Post parietal association cortex (Integrate sensory info) >
Prefrontal assoc cortex (plan movement)>
Pre motor secondary cortex (plan movement) >
Primary motor cortex posterior frontal (execute the movement) > down the spinal chord and out to the muscles
SN/basal ganglia/thalamus, cerebellum (these loop to eachother)
- What is the function of secondary motor cortex, and what are “mirror neurons” that have been described in this area of the brains of animals?
Prefrontal association cortex > secondary motor cortex
Secondary motor cortex neurons fire when we are imagining a movement.
“mirror neurons”: also fire when watching someone else move- helps us understand others actions? (social cognition)
Dammage: delayed movement? (few cases)
Secondary Motor Cortex: an area of the cerebral cortex that receives much of its input from assoc. Cortex and sends much of its output to the primary motor cortex
Mirror Neurons: fire when a individual performs a particular goal-directed hand movement or when they observe the same goal-directed movement performed by another.
- Explain how the primary motor cortex is organized, and what movement deficits would be most likely to result from damage to this part of the brain.
Primary motor cortex
Initiation of conscious (goal directed) movement
Damage > speed, accuracy, force of directed movement decrease (complete paralysis usu. Decrease within weaks after stroke; pre motor cortex also signals sub cortical movee=ment areas)
Bell’s palsy: loss of facial motor nerve function
Damage: decrease in speed, accuracy, force of directed movement, (complete paralysis tends to wane after stroke; premotor cortex also signals subcortical movement areas of the brain)
- Describe the role of the basal ganglia in movement, and how movement may be changed by damage to this brain area (particularly in Huntington’s disease – also see Ch. 10).
Modulates cortical output in a loop with thalamus; active during habitual movement
Damage: uncontrolled (excess) movement (Huntington’s disease)… dysfunction also implicated in Tourette’s disorder (involuntary repetitive movements, “tics”
Basal ganglia: modulates primary motor cortex output in a loop w/ thalamus; facilitates habitual movement While inhibiting excess movement. Basal ganglia is lateral to thalami
Damage> uncontrolled excess movement E.G huntingtons disease.
Basal ganglia Inhibits > thalamus> motor cortex> loops back to basal ganglia
… Dysfunction also implicated in tourrettes syndrome (involuntary, repetitive movements or vocalizations, “tics”), and OCD
Substantia nigra: Projects to basal ganglia (releases DA) >> modulates speed of movement
Age related loss of SN neurons= Parkinsons disease (resting tremor, slowed movement, starting/stopping difficulty); ~ 10 mil people (most common neurological disorder)
Cases early onset include 10%
- Describe the role of the cerebellum in movement, and how movement may be changed by damage to this brain area.
Cerebellum: compares/monitors neural signals from motor and somatosensory cortices, integrates w/vestibular signals (from inner ear) .. enables you to perform movement sequences that require precise timing, balance
Demo: finger to nose cerebellar exam.
Ataxia (uncoordinated movement); “wide stance” walking & turning
Difficulty executing movement sequence smoothly (w/optimal turning)
Comparison/ monitoring of neural signals from motor and somatosensory cortices and vestibular system → enabling you to learn movement sequences that require precise timing and balance
- Ataxia: Uncoordinated movement, wide stance, walking a turning difficulty executing movement sequences smoothly (nose to finger)
- Describe the symptoms of Parkinson’s disease, and explain the anatomical/physiological cause of this disease (in terms of changes in neural communication in the brain). Also see Ch. 10.
Cause: Age-related loss of SN neurons in the substantia nigra
Symptoms: Resting tremor and slowed movement
- Describe the direct vs. indirect movement pathways (brain to body). Do motor pathways from primary motor cortex cross to the other side of the body?
Descending pathways: partly crossed (is crossed for our purposes) Direct pathways (independent movement of limbs, digits): primary motor cortex\> Spinal cord motor neurons \> muscles
Indirect pathways (posture + whole body movements): e.g., synapse in vestibular nucleus(medulla)>> spinal cord motor neurons> muscles
Direct pathway: (independent movement of limbs, digits): primary motor cortex → motor neurons → muscles
Indirect pathway: (posture and whole-body movement) Synapses in midbrain (superior colliculus), vestibular nucleus (medulla), etc. → spinal cord → muscles
They are partly crossed
- Explain how the knee-jerk and biceps stretch reflexes work, including the “reciprocal innervation” that helps make the reflex efficient. Make sure you can draw and label these simple spinal circuits, including the various types of neurons involved in each, the direction of signaling, whether synapses are excitatory or inhibitory, and what nt’s are released at each synapse.
A. Spinal sensorimotor Circuits
Stretch reflexes: muscle/tendon stretch causes sensory neuron in muscle to fire> activates motor neuron that terminates on the same muscle causing muscle contraction
a. Knee jerk reflex
b. Biceps stretch reflex
- Explain how the pain withdrawal reflex works. Make sure you can draw and label this simple spinal circuit, including the various types of neurons, the direction of signaling, whether synapses are excitatory or inhibitory, and what nt’s are released at each synapse. When you encounter a painful stimulus, which occurs first, limb withdrawal or the verbal “ouch”? Why?
Pain withdrawal reflex: pain thermoreceptor (sensory n.) > (+) Interneuron > (+) motor neuron > motor neuron > muscle contracts (withdraw limb)
Withdrawal happens before the ouch.
Pain thermoreceptor (sensory n.) → excites interneuron → excites motor neuron → muscle contract (withdraw limb)
The limb withdrawal happens first because it is a much simpler circuit only three neurons long if you said ouch first you would already be hurt badly.
- What are two ways that tumors are classified, and which are the most dangerous (most difficult to treat)?
Benign vs malignant (difficult to treat)
Encapsulated vs infiltrating (difficult to treat)
- Name and describe two types of stroke (what happens to the blood vessel?), and explain what happens to neurons in the brain when stroke occurs, and why.
Hemorrhagic: aneurysm bursts, weak spot on vessel causes a bulge
Ischemic: vessel blockage, the vessel stays intact but there is a blood clot
- Describe two types of closed head injury. What is “CTE” and who is at greatest risk of developing it?
Contusion: bruising (bleeding) increase in pressure on neurons
Concussion: disrupted consciousness after a blow to the head
CTE: caused by repeated head trauma, due to lack of scar tissue accumulation, progressive neuron loss, symptoms: headache, attention problems, memory loss, confusion, mood disturbance, dementia
football players?
- Explain what epilepsy is, and some differences in types.
Epilepsy: chronic seizures, too much electrical activity
Focal (one part of the brain)
Generalized (whole brain)
Convulsive (muscles rigid or contracting)
Not convulsive (absence seizures)
- What are some treatments for epilepsy, and how do they work?
Drugs that decrease neural firing:
- GABA agonists
- Drugs that alter Na+ channel firing
- CBD
- Vagus (parasympathetic nerve stimulator: emits regular pulses to decrease neural firing)
- Brain surgery: remove of focal area
- What is MS (and why is it called that)? What is the most common type of treatment for MS?
Multiple Sclerosis: autoimmune disease, demyelinating disease; development of scar tissue (lesions) in CNS; diagnosis is usually in 20s- 30s
Treatment: immunosuppressant drugs to decrease the immune system attack on myelin
- What is Alzheimer’s disease? Why do people with Alzheimer’s have learning and memory problems, and also sometimes emotional outbursts?
Alzheimer’s disease: progressive dementia due to neurofibrillary tangles (excessive tau protein), amyloid plaques (scar tissue) → neuron loss
Most prevalent in amygdala and hippocampus and PFC, which are major areas for memory and emotions
- What are the most common motor symptoms of Parkinson’s disease, particularly in early-to-middle stages? What are some treatments for Parkinson’s disease, and how are they believed to work (and what are the side-effects, if any)?
Symptoms:
- Slowed movement
- Muscle rigidity
- Asymmetric resting tremor (losing substantia nigra neurons, more on one side than the other)
- Tremor is decreased when directed reach is made (switch from indirect to direct motor pathway)
Treatment:
- DA agonist
- L-dopa (DA precursor, increase DA synthesis)
- MAO inhibitors (prevent the breakdown of DA)
- Deep brain stimulation
- Stem cell therapy (inject DA progenitor cells into the brain) … still experimental
- Explain what caused the Parkinsonian symptoms of the heroin users in the video, “The Case of the Frozen Addict” (1986). How did this “detective story” lead to breakthroughs in Parkinson’s research and therapy?
The drug MPTP seemed to affect the substantia nigra
They are better candidates than actual Parkinson’s patients because they are younger and have more potential for recovery
