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Neurophysiology Flashcards

1
Q

How many neurons and synapses are found in the brain?

A

10^11 neurons, and 10^15 synapses

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2
Q

What is a synapse? What are the types of synapse?

A

Connection between neurons
- Chemical synapse: neurotransmitter transmission
- Electrical synapse: action potential transmission (gap junction)

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3
Q

What is the brain for? How did we come about this theory?

A

The brain is for movement. In order to move, search or interact. See this function in the sea squirt which eats its own brain for nutrient later in life once it has found its permanent spot. Tells us it needs its brain to move around, but once it is immobile, doesn’t need anymore.

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4
Q

What are the cells in the nervous system?

A
  • Nerve cells (aka neurons): do information processing, and are electrically excitable. - communicate through action potentials
  • Glial cells (aka glial): support operation of neurons by maintaining brain environment.
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5
Q

Describe Glia

A
  • 10x more numerous than neurons
  • More than just ‘glue’ that holds neurons together:
    Supply backup glucose from glycogen, remove neurotransmitters, remove ammonia (a byproduct of metabolism), take up K+, and provides myeline sheaths for axon, to aid information transmission
    *Some research suggests glia may do some information computation - do not understand the brain very well even now, you can find exceptions everywhere
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6
Q

What is the location on a neuron that receives input?

A

Dendrites - receive from many neurons

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7
Q

Where does output come from neuron?

A

Axon terminal - release neurotransmitters

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8
Q

What is an EPSP?

A

Excitatory post-synaptic potential (Depolarization) - transient increase in permeability to Na+/K+
Towards threshold

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9
Q

What is an IPSP?

A

Inhibitory post-synaptic potential (Hyperpolarization - usually)
Transient increase in permeability to Cl-/K+
Move away from threshold
*K+ channels open up in both EPSP and IPSP - not the driver, Cl- and Na+ move toward their equilibrium

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10
Q

How much are single EPSP/ IPSPs?

A

Approximately 1 mV

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11
Q

What are the differences from the neuromuscular junction?

A
  • There are many transmitters in the CNS (only acetylcholine)
  • In the CNS an EPSP at a single synapse is < 1 mV (need many incoming action potentials to summate before the membrane is depolarized to the threshold level and an action potential is generated in the post-synaptic neuron. At the NMJ one action potential in an alpha motorneuron produces end plate potential that is about 70 mV in size, always reaches threshold)
  • Central synapses are excitatory or inhibitory (at the NMJ there is only excitation).
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12
Q

Describe the two types of summation of post-synaptic potentials

A
  • Spatial summation: if receive EPSP from multiple pre-synaptic neurons at once get summation
  • Temporal summation: if EPSPs are fired very quickly close together, these will cause summation - if they are slow, can return back to equalized state, get no summation
    *no refractory period
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13
Q

What is the mechanism of an EPSP?

A

Action potential opens calcium channels (voltage gated) causes vesicle holding neurotransmitters to move to synapse (exocytosis) - released and cross synapse (diffuse). Some will influence receptors (ionotropic receptors) on post-synaptic neurons - causes opening of AMPA allowing sodium to flow in which causes EPSP.

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14
Q

Describe and list some neurotransmitters

A

100 + different neurotransmitters and neuromodulators
- Acetylcholine (ACh; Alzheimers, ANS)
- Biogenic Amines (Dopamine - Parkinson’s, Norepinephrine - Sleep/ Arousal, ANS, Serotonin)
- Amino acids (Glutamate, GABA)
- Neuropeptides (act as modulators, often at metabolic receptors)
- Other (e.g. Nitric acid)

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15
Q

What are the main neurotransmitters in the CNS?

A
  • Glutamate - most common excitatory neurotransmitter
  • GABA - widespread inhibitory neurotransmitter
  • Glycine - inhibitory transmitter in the spinal cord and brainstem
  • Strychnine - Glycine antagonist (not a neurotransmitter but neutralizes Glycine, reduces inhibitory effect)
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16
Q

Describe presynaptic inhibition and facilitation

A

A means to tune presynaptic inputs - doesn’t go to the synapse but instead to the axon of the presynaptic neuron (axo-axonic)
e.g. - Normal: AP= 4 vesicles = 1 mV EPSP
- Presynaptic inhibition: AP= 2 vesicles = 0.5 mV (decreased Ca+2)
- Presynaptic facilitation: AP= 8 vesicles= 2 mV (increased Ca+2) - instead of inhibitory, spits out excitatory factors - change how many Ca channels are open

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17
Q

Describe synaptic plasticity and its processes - second messengers?

A

NMDA receptors open (ionotropic) when there is lots of neurotransmitter (harder to open)0, they allow mostly Ca++ to enter, then lead to 2nd messengers. Similarly, G-protein receptors (metabotropic) also lead to production of second messengers.
- These increase sensitivty of AMPA channels (causes bigger EPSPs), insert channels (more AMPA), and make new channels (synthesize new AMPA, prepare to insert more).
*NMDA and G-protein channels/ receptors are minimally involved in EPSP generation directly but cause increased sensitivity through second messengers.

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18
Q

Describe the AMPA receptor

A
  • Glutamate-gated ion channels (ionotropic)
  • High conductance to Na+ (causes excitatory post-synaptic potential, leads to depolarization of the post-synaptic neuron)
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19
Q

Describe the NMDA receptor

A
  • Glutamate-gated ion channels (ionotropic)
  • For low glutamate, little conductance to Na+ and Ca2+
  • For high glutamate, high conductance to Ca2+ (mechanism thought to underlie synaptic plasticity)
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20
Q

Describe the mechanism of long-term potentiation

A
  • Presynaptic: changed Ca2+ channel - increased Ca2+ entry
  • Postsynaptic: increased sensitivity of existing AMPA ion channels, insertion of existing AMPA ion channels in membrane, and synthesis of new AMPA ion channels
  • memory at cell - process involving persistent strengthening of synapses that leads to a long-lasting increase in signal transmission
  • can also have long-term depression (opposite effects)
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21
Q

How do we get the outside world into the brain?

A

Photons of light, sound waves or environmental stimuli are transduced (encoded) into language the brain can understand = patterns of action potentials - brain decodes this information.

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22
Q

What is an adequate stimulus?

A

Form of energy that receptor is most sensitive to.
- rods in eye are sensitive to pressure in eye so punch to eye can be perceived as flash of light.

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23
Q

What are sensory receptors?

A

Specialized endings in nerves that are sensitive (tuned) to one form of environmental energy

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24
Q

What is transduction?

A

How the energy is turned into spikes.

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25
Q

What are the different transduction mechanisms?

A
  • Mechanical (skin, muscles, tendons, etc.): physical forces stretch open ion channels (sound is mechanically transduced - bend hair cells in ear)
  • Temperature: hot and cold act on specific receptors to open ion channels
  • Chemical (nociceptors): tissue damage (e.g. bruise) releases chemicals that bind to receptors and open channels
  • Light: photon absorption closes ion channel
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26
Q

What are generator/ receptor potentials?

A
  • Cause depolarization due to increased permeability to Na+/ K+ (like EPSP)
  • Local and non-propagated, graded in proportion to the stimulus
  • Can sum and will cause action potential if neuron reaches threshold
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27
Q

Describe adaptation

A
  • How fast after stimulation does the receptor return to baseline levels? (give measure of what is changing)
  • How fast does it adapt to a constant stimulus? (feel initial press, but don’t keep responding over time)
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28
Q

What are the two core types of receptors?

A
  • Slow adapting (SA) - continue responding (constant feedback to stimulus)
  • Rapidly or fast adapting (RA/FA)
  • different receptors use different stimulus coding schemes (frequency vs population coding)
    *different receptors encode different stimulus features (SA = amount of skin indentation, RA = skin motion)
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29
Q

Describe frequency coding

A

Intensity of stimulus is encoded in the number of APs a neuron generates. e.g. more AP = more intense stimulus
*involved in slow adapting receptors but not rapidly adapting
- Not in rapidly adapting because it stops responding to continuous stimuli - this isn’t always true though, can have to varying degree

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30
Q

Describe population coding

A

Intensity measure based on which neurons are activated. e.g. more neurons activated = more intense stimulus
*involved in both slow and rapidly adapting receptors2

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31
Q

What is the Pacinian corpuscle?

A

The most sensitive mechanoreceptor
- Detects vibration (very sensitive to vibration) and skin motion when hand moves across an object or when an object slips
- Extremely fast adapting receptor
- Appreciation of fine textures
- Responds to fast pressure not slow
* fast pressure causes onion parts to lock to each other and can’t slip so it is felt
*slow = energy causes the parts to slip relative to each other - not felt

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32
Q

How do we achieve fine sensory ability?

A
  • Different populations of receptors with different modalities
  • Different rates of adaptation
  • Different thresholds
    *Tactile sensation has a large role in manual dexterity. If we lose textile sensation = lose manual dexterity.
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33
Q

What are the receptors of the glabrous skin? Kinds and what these respond to?

A

Hairless skin - high sensitivity to touch (e.g. palm, genitals, inside mouth.
4 kinds of receptors - defined according to their response to stimuli:
1. Type 1 fast adapting (change in fingertip forces, fine forms, moving stimuli, friction) e.g Meissner
2. Type 1 slow adapting (fingertip forces, fine forms, edge contours, texture) e.g. Merkel
3. Type 2 fast adapting (transient events, vibration) e.g. Pacinian
4. Type 2 slow adapting (tissue strain) e.g. Ruffini
- Types named according to the size of the region to which they respond. Type 1 is very small regions, type 2 includes very large receptive regions. Can have overlapping response territories.

34
Q

Axon diameter relation to conduction velocity

A

Greater axon diameter = greater conduction velocity
*alpha axon = fastest
*C = slowest

35
Q

What is the receptive field?

A

Location where adequate stimulus will increase or decrease the firing rate of a neuron

36
Q

What is innervation density?

A

Number of receptors in a given area
*small receptive fields and high innervation density yields high sensory acuity

37
Q

Describe the dorsal columns

A
  • Mammals, highest development in primates
  • Fine touch, proprioception, and vibration
  • Small receptive fields (greater sensitivity) type 1
  • One modality per neuron
  • Faithful transmission, fast conduction
  • Contralateral
38
Q

Describe the spintothalamic

A
  • Phylogenetically old system
  • Pain, temperature, crude touch, itch
  • Larger receptive fields
  • Convergence of modalities
  • Afferent information is contralateral
39
Q

Describe the somatotopic organization

A

Not proportional - a lot of innervation + processing power = more representation. Surface of somatosensory cortex. Shows the representation of where + how much of different areas of the body are found in the somatosensory cortex.

40
Q

Describe the plasticity of the somatotopic organization

A
  • Somatotopic organization is present at birth
  • Size of region is modified with use (e.g. braille, musci, juggling, etc.)
  • Possible mechanism - dormant synapses (remove inhibition / increase excitation)
    *For example, if someone had their hand amputated, as time went on, there would start to be encroachment of flanking areas of the cortex when hand used to be represented, other areas could expand with training.
41
Q

Describe columnar organization

A
  • Group of many thousands of neurons that are highly interconnected (structure is 200-800 microns in diameter, highly conserved organization across the cortex)
  • In somatosensory cortex, each column is modality pure and has similar receptive field
  • Most columns (90%) from dorsal columns.
    *depth of cortical surface - consistent responses along the column
42
Q

Describe the reconstruction of somatosensory inputs

A
  • Reconstruction begins at somatosensory cortex (analysis of object properties - smoothness, edges, temp, direction of movement - integration across neurons of many types)
  • Higher order reconstruction continues in the posterior parietal cortex
43
Q

What occurs when there is a lesion in posterior parietal cortex?

A

Disorder in the appreciation of sensory input from the left side of the body or of external space
e.g. don’t see left side of field, not in control of hand - alien hand syndrome, don’t appreciate that your hand is a part of your body

44
Q

What are rods?

A
  • Critical for night vision
  • Peripheral retina (to see something clearly at night, don’t want to look directly at it
  • Sensitive faint light (more pigment, convergence, 100:1)
  • No sensitivity to colour
  • Relatively few rods in the fovea (mostly cones)
45
Q

What are cones?

A
  • Critical for day vision
  • Concentrated in fovea (acute visual inputs) - thumb nail at arm’s length
  • Greater acuity/ sharper image (less convergence of cones onto bipolar cells, 6:1)
  • Bright light
  • Colour vision
46
Q

What is the transduction of light?

A

When light hits rhodopsin, it changes conformation

47
Q

How do we get action potentials in the dark?

A

Neurotransmitter glutamate is released in the dark, not in the light.

48
Q

Describe the receptive field direct mechanism with dark in center of vision

A

Darkness in centre = cone depolarized, glutamate released, opens diff ion channels causes:
- On-center bipolar cell hyperpolarized and transmitter release decreased + firing of on-center ganglion cell decreased
- Off-center bipolar cell depolarized and transmitter release increased + firing of off-center ganglion cell increased

49
Q

Describe the receptive field direct mechanism with light in center of vision

A

Light in center = cone hyperpolarized, glutamate release decreased, causes:
- On-center bipolar cell depolarized and transmitter release increased + firing of on-center ganglion cell increased
- Off-center bipolar cell hyperpolarized and transmitter released decreased + firing of off-center ganglion cell decreased

50
Q

Describe the receptive field indirect mechanism with dark in surround vision

A

Cone depolarized and glutamate release increased, horizontal cell activated, GABA released (inhibitory neurotransmitter) - less glutamate release in direct pathway, causes presynaptic inhibition for direct pathway - controls how much glutamate is released - with less glutamate released, makes it seem like direct view is brighter (in comparison to surround)

51
Q

Describe the receptive field indirect mechanism with light in surround vision

A

Cone hyperpolarized, glutamate release decreased, activity of horizontal cell decreased, glutamate release increased in direct pathway, appears darker in direct view.

52
Q

Describe the information processing in visual cortex

A

Pathway from retina to lateral geniculate (thalamus) to visual cortex refines visual information and performs advanced feature extraction.
- Ganglion cells - see changes in light, get edges “neural image”, cannot exhibit edge sensitivity on own ->
- Simple cells - sensitive to the orientation of edges

53
Q

Describe the primary visual cortex organization

A
  • Retinotopic map with crossing fibers (similar to somatosensory organization) - lesions are tool for neurologists
    -> left hemifield ends up in right visual cortex (inside of left eye, outside of right eye)
    -> right hemifield ends up in left visual cortex (inside of right eye, outside of left eye)

-Columnar organization: orientation column, ocular dominance column, hyper-column (2 dimensions) - similar in same column (same as somatosensory)

54
Q

Describe higher visual cortex

A

Higher cortical areas put picture back together
- one outcome of lesion in higher areas of the visual cortex is prosopagnosia
- prosopagnosia is the inability to recognize familiar faces “face blindness”, can’t discriminate, failure in temporal cortex which has facial awareness

55
Q

Describe transduction of the auditory system

A
  • Cochlea deconstructs sound into difference frequency components
  • Hair cells transduce vibrations into action potentials
    Vibrates the bones of the ear, causing hair cells to move and open ion channels
56
Q

Describe the cochlea
What is place code?

A
  • Snail like structure
  • Higher frequency response closer to the base (hair cells are shorter + stiffer closer to base)
  • Lower frequency opposite end to base (longer + less stiff hair cells respond to lower frequencies
    *higher frequency has peak occur faster, early along the cochlea, while lower frequency takes longer - further distance to reach peak in cochlea - why the cochlea has frequency response the way it does
    Place code: location of where the hair cells are on cochlea determines frequency they respond to - depending on which auditory nerve is activated tells you what the frequency of the stimulus is
57
Q

Describe the response of hair cells (stereocilia) during an action potential

A
  1. Variations in air pressure (i.e. sound)
  2. Motion of the stapes (bones in ear)
  3. Motion of endolymph fluid (fluid high in potassium) in the cochlea (propagate waves in the fluid)
  4. Motion of the basilar membrane
  5. Motion of hair cells
  6. Increased permeability of hair cells to K+ (open potassium channels)
  7. Depolarization
  8. Opening of voltage-gated Ca2+ channels
  9. Release of excitatory neurotransmitter
  10. Action potentials in the auditory nerve (generated in afferent nerve, goes through auditory pathway)
58
Q

Describe signalling intensity

A
  • Increase in frequency of firing of afferents (say 10 afferents discharging at base (stapes) end of cochlea, 100 APs/s = 10,000 Hz sound. If not 200 APs/s = 10,000 Hz sound, but louder
    *frequency coding
  • Increase in number of afferents firing (louder sound, amplitude travelling wave increases, larger amplitude, now 20 afferents discharging, still 10,000 Hz sound but louder)
    *population coding
59
Q

Describe sound localization

A

Two mechanism for localizing sound (intensity, timing)
- Which ear is getting louder sound (more intensity)
- Which ear is getting sound first (timing- sound propagates relatively slowly)

60
Q

Describe the auditory cortex and its organization

A
  • Tonotonic organization (map) -diff frequencies remain organized or seperated
  • Columnar organization
    *with the loss of hair cells, can become deaf or reduce hearing capacity
61
Q

What occurs if there is a lesion in the auditory cortex?

A
  • Deficit in localizing sound
  • Deficit in recognizing sound patterns (recognizing language)
  • Not deafness on one or both sides (most deafness arises from problems in the periphery - e.g. hairs)
62
Q

Describe the cochlear implant

A

Contains a microphone and stimulating electrodes. Microphone transfers to frequency spectrum in the electrodes, stimulates afferent fibers along the cochlea - APs same as actual hearing.
*want to place early in life for plasticity - allow the auditory cortex to adapt to new kind of signals

63
Q

Describe the vestibular system

A
  • Position and motion of head in space
  • Rotational (semicircular canals tells information about rotation of head) and linear (e.g. translational - walking)
  • located in inner ear - mechanism for sensing acceleration
64
Q

Describe the parts of the Semi circular canal:
- Cupula
- Endolymph
- Hair cells
- Utricle (otoliths horizontal)
- Saccule (otoliths vertical)
- Otoliths (Otoconia)

A

-Semi circular canal is a rigid structure which moves with head immediately
-Cupula is a gelatinous wedge in the corner of the semi circular canal, contains hair cells
-Endolymph fluid lags behind due to inertia (lagging movements, causes forces to apply to cupula, causes motional bending / displacement of hair cells
-When hair cells are deformed = depolarization (crista ampullaris) -ampula = swelling
-Utricle (otoliths horizontal), when lying down, oriented with gravity
-Saccule (otoliths vertical), in-line with gravitational force, gives orientation relative to gravity (otoconia pull down)
-Otoliths (Otoconia) - crystals of CaCO3, creates inertial mismatch, crystals lag behind with gelatinous wedge, bend hair cells, gives info about gravitational force

65
Q

Further describe the semicircular canals (rotation)

A
  • Three orthogonal fluid-filled structure
  • Ampula = swelling in the canals
  • Cupula = gelatinous wedge that interupts the canal
  • Hair cells are embedded in the cupula and attached to basal layer.
  • When the head moves, the endolymph lags behind and thus pushes on the cupula, which in turn moves the hair
  • If you keep moving, eventually the fluid catches up and the hairs return to straight ( can only signal changes in head orientation - not absolute head orientation)
66
Q

Further describe Otoliths (linear)

A
  • Utricle and Saccule, oriented horizontally (x2) and vertically respectively
  • Have gelatinous mass, this time filled with Otoconia (calcium carbonate crystals)
  • The gelatinous mass again filled with hair cells
  • If moving, the otoconia lag behind and thus deflect the hair cells
  • Because of the otoconia, the hair cells in the saccule can provide constant information about gravity (absolute orientation)
67
Q

Describe benign positional vertigo

A
  • Commonly occurs after head trauma or infection of vestibular apparatus
  • Characterized by sudden attacks of vertigo and nausea produced by turning the head to certain positions
  • Due to distortion of endolymph flow by debris in semicircular canals (e.g. otolith crystals - flow into semi circular canal and impact cupula, feel more movement)
  • Can be cured (at least temporarily) by moving the person through a series of maneuvers that clear the debris (often recurring)
    *vertigo after a spinning ride for example is caused by the after affect of getting endolymph fluid caught up to movement (inertia) - still moving in a circle
68
Q

Describe the transduction of the vestibular system

A

Have a main hair (longer than others) called Kinocilium, helps with directional information, e.g. distinguish moving left/ right
- resting = 90 spikes/ sec
- bent right = depolarize, 180 spikes/sec (excitation)
- bent left = hyperpolarization, 10 spikes/sec (inhibition)

69
Q

Describe vestibular pathways

A
  • Sense equilibrium/ orientation in space (train, car lights, imax - feel like your moving on train when you see train next to you moving)
  • Vestibular postural reflexes (fall, balance, bike, blindfolded cat, decerebrate frog (can still self-right themselves, no access to cortex)
70
Q

What happens when you remove the gravitational effect? What is the postural reflex?

A

Pigeon tries to fly but has no orientation of what is up or down -> flies upside down

71
Q

What is the vestibular ocular reflex?

A
  • Keeps eyes on target when head moves
    eyes counter role to head to keep focus/ gaze
    *VOR - adjusts to keep gaze stable
    *Saccade - recentres eye in socket
72
Q

What is Nystagmus?

A

Involuntary and rapid eye movements whereby person is unable to maintain fixation on target even without head movement
-> non functional VOR can cause, multiple other causes as well

73
Q

What are the 4 classes of eye movements?

A
  1. Saccades - rapid step like shifts in gaze, 250,000 saccades per day (lose information between saccades - would have jumps around, shuts off signal between saccades, why it has to be rapid)
  2. Smooth pursuit - tracking movements of slower objects (can’t self generate without a stimulus)
  3. Vestibular Ocular Reflex (VOR)
  4. Vergence - eyes turn together (cross eyed when stimulus comes close to you)
74
Q

What is muscle spindle?

A

Mechanosensitive receptor wraps around intrafusal muscle fiber
- Proprioception (sense of body’s configuration in space)
- Very fast conduction velocity (do not want delayed feedback)
- Driver by vibration to produce illusion of movement
- Embedded in muscle themselves - in all skeletal muscles
- Numerous in small muscles with fine control (neck, hand), fewer in quad e.g. bicep has ~ 300 spindles
-> primary spindle = velocity of muscle stretch - most responsive during stretch, then returns to normal + very strongly reduces activation during release of stretch (completely quiet)
-> secondary spindle = length of muscle - how stretched - no burst during stretch but increase in firing overall + during release continues firing but slowly reduces in frequency.

75
Q

What are the kinds of muscle fibers?

A

2 kinds of muscle fibers:
1. Extrafusal: actually generate muscle force, alpha motor neuron innervates extrafusal muscle fiber, generates movement (contraction)
2. Intrafusal: doesn’t generate much muscle force, when extrafusal contracts/ changes shape, the intrafusal changes shape along with it

76
Q

What are the 4 types of muscle receptors?

A
  • Free nerve endings (pain, pressure, temperature)
  • Golgi tendon organ (in series with muscle - sits in tendon, senses forces the muscle is generating)
  • Muscle spindle in primary ending (group Ia afferent, in parallel)
  • Muscle spindle in secondary ending (group II afferent, in parallel)
    *muscle spindle can’t tell you about force
77
Q

Describe the golgi tendon organ (GTO)

A
  • Innervated by fine branches of single Ib axon that intertwines with collagen fibers
  • Contraction of muscle stretches the capsule which compresses the Ib nerve endings (GTO) and opens mechanically sensitive ion channels
  • Sensitive mostly to tension in muscle caused by muscle contraction
  • Reflec called Ib inhibitory reflex which tries to ensure you don’t damage a muscle under hard contraction
78
Q

Further describe primary and secondary muscle spindle

A
  • Primary muscle spindle (Ia) responds to the dynamic and static phases of muscle stretch (changes)
  • Secondary muscle spindles (II) respond mostly to the static phase
    They both sense both velocity and length it is just that Ia is much more biased to velocity while II is biased towards length
    *These are for passive stretch of muscle - uncommon = someone moving you rather than you moving your muscle
79
Q

What is alpha-gamma co activation?

A

Stimulate both alpha and gamma at once. Alpha generates extrafusal muscle force, while gamma generates intrafusal muscle. This keeps intrafusal taunt while extrafusal is floppy
- If working correctly there should be no response change in APs - telling the nervous system whether the movement is progressing as expected or not - if something goes wrong, e.g. bump into something during movement, the length of intrafusal + extrafusal will be different, critical information sent to brain through change in response.

80
Q

Describe elbow flexion

A
  • Increase in biceps Ia afferent activity because of alpha-gamma coactivation to keep spindle operating in its sensitive range (if movement goes too slow or too fast there will be a change in biceps Ia discharge that will be sent to the CNS)
  • Increase in triceps Ia activity because muscle is being stretched (this activity is proportional to the length and velocity of stretch - passive stretch due to bicep)
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Human Physiology (13 decks)

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