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Neurobiology 523 > Unit 2 > Flashcards

Unit 2 Flashcards

1
Q

What is taste for?

A
  1. Distinguish between food and poison
  2. Distinguish between different types of food
  3. Important for the control of feeding (e.g., GI hormones)
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2
Q

five basic tastes

A
  1. Saltiness
  2. Sourness
  3. Sweetness
  4. Bitterness
  5. Umami
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3
Q

What is the name for a chemical stimuli of taste?

A

tastant

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4
Q

tastant of saltiness

A

NaCl

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5
Q

tastant of sourness

A

proton (H+)

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6
Q

tastant of sweetness

A

sugar, sucrose

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7
Q

tastant of bitterness

A

quinine, K+ ion, caffeine

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8
Q

tastant of umami

A

monosodium glutamate (MSG)

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9
Q

How many taste buds do we have?

A

2000-5000

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10
Q

basic structure of taste system

A

each papilla has taste buds, and taste buds have several taste receptor cells that synapse with gustatory axons

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11
Q

taste receptor cells (TRCs)

A

respond to tastants, about 50-150 in a single taste bud; synapse onto gustatory afferent axons

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12
Q

receptor potential

A

stimulus-induced change in the membrane potential of a sensory receptor

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13
Q

receptor potential in response to tastants

A

tastants depolarize taste receptor cells via ion channels (salty, sour) or GPCRs (bitter, sweet, umami), stimulating neurotransmitter release

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14
Q

Can gustatory afferent axons respond to more than one basic taste?

A

Yes, gustatory afferent axons can respond to more than one basic taste

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15
Q

sensory transduction

A

the process by which an environmental stimulus causes an electrical response (receptor potential) in a sensory receptor cell

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16
Q

saltiness taste receptor

A

Na+ channel (ion channel)

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17
Q

sourness taste receptor

A

H+ channel and K+ channel (ion channels)

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18
Q

sweetness taste receptor

A

T1R2 + T1R3 (dimer GPCRs)

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19
Q

bitterness taste receptor

A

T2R; 25 types (dimer GPCRs)

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20
Q

umami taste receptor

A

T1R1 + T1R3 (dimer GPCRs)

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21
Q

What neurotransmitter is released in response to saltiness?

A

serotonin

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22
Q

saltiness detection cascade

A

salty tastant activates special Na+-selective channel in salt-sensitive TRCs, causing Na+ to enter and depolarize the cell, Ca2+ to flow into the presynaptic terminal, and serotonin NT to be released into the synaptic cleft to gustatory axons

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23
Q

What neurotransmitter is released in response to sourness?

A

serotonin

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24
Q

sourness detection cascade

A

sour tastant activates H+ channel and blocks K+ channel, causing H+ (and Na+) to enter (and inhibit K+ from leaving) and depolarize the cell, Ca2+ to flow into the presynaptic terminal, and serotonin NT to be released into the synaptic cleft to gustatory axons

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25
Q

bitterness, sweetness, umami detection cascade

A

tastant activates GPCR, triggering the PLC->IP3->Ca2+ cascade, depolarizing the cell and initiating the release of ATP NT into the synaptic cleft to gustatory axons

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26
Q

What neurotransmitter is released in response to bitterness?

A

ATP

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27
Q

What neurotransmitter is released in response to umami?

A

ATP

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28
Q

What neurotransmitter is released in response to sweetness?

A

ATP

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29
Q

central taste pathway

A
  1. Taste receptor cells
  2. Gustatory nucleus (pathways diverge from here)
  3. VPM of thalamus
  4. Gustatory cortex
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30
Q

What is smell for?

A

warns of harmful substances, combines with taste for identifying foods; detection of pheromones, which communicate reproductive behavior, territorial boundaries, and signal aggression

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31
Q

What is the name for a chemical stimuli of smell?

A

odorant

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32
Q

anosmia

A

inability to smell

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33
Q

What is the organ of smell?

A

olfactory epithelium

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34
Q

olfactory receptor neurons (ORNs)

A

have GPCR odorant receptors (cAMP) that depolarize in response to activation by odorants; each ORN expresses a single odorant receptor, but can be activated by many odorants

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35
Q

scent detection cascade (olfactory transduction)

A
  1. Odorants bind to GPCRs
  2. Golf subunit activates AC, and cAMP level increases
  3. cAMP-gated cation channels open, causing an influx of Na+ and Ca2+
  4. Ca2+-activated Cl- channels open, Cl- leaves cell
  5. Cell becomes depolarized and fires action potential
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36
Q

What is unique about olfactory transduction and Cl-?

A

Cl- is more concentrated inside the cell, and when Ca2+-activated Cl- channels open, Cl- leaves the cell, depolarizing it

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37
Q

How many genes encode odorant receptors?

A

many hundreds of genes encode odorant receptors

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38
Q

How many odorant receptors does each ORN express?

A

a single odorant receptor is expressed by each ORN (but each ORN can be activated by many odorants due to broad tuning)

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39
Q

broad tuning of ORN

A

idea that each ORN can detect multiple types of odorants (despite the fact that a single odorant receptor is expressed by each ORN)

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40
Q

olfactory bulb

A

has ~2000 glomeruli that synapse with ORNs to create a sensory map (each glomeruli receives input from one type of ORN)

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41
Q

combinatorial activation of ORNs

A

odorants are represented by combinatorial activation of ORNs, meaning multiple ORNs activate in response to a given odorant

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42
Q

glomeruli

A

~2000 facets of olfactory bulb that synapse with ORNs to create a sensory map; each glomeruli receives input from one type of ORN

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43
Q

sensory map

A

orderly arrangement of neurons that correlate with certain features of the environment; glomeruli create a sensory map by receiving input from one type of ORN

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44
Q

central olfactory pathway

A
  1. Olfactory receptor cells (olfactory epithelium)
  2. Glumeruli
  3. 2nd order olfactory neuron (synapses to ORNs on glomeruli)
  4. Olfactory cortex

unique in that passage through thalamus first is not necessary

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45
Q

complete olfactory transduction cascade

A
  1. Odorants bind to GPCR (cAMP) odorant receptors on ORNs in the olfactory epithelium
  2. Golf subunit activates AC, cAMP levels rise, and cAMP-gated channels open, allowing for an influx of Na+ and Ca2+
  3. Ca2+-activated Cl- channels open, and Cl- leaves the cell, causing further depolarization and causing an action potential to fire
  4. Action potentials from the same ORN type propogate to a single glomeruli on the olfactory bulb, where they synapse with 2nd order olfactory neurons
  5. 2nd order olfactory neurons propogate action potential to olfactory cortex
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46
Q

Technical Tuesday: calcium imaging to visualize neuron activity

A

GCaMPs are a class of genetically encoded Ca2+ indicators; Ca2+ binds to GCaMP during periods of high neural activity, causing flourescence

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47
Q

olfactory population coding

A

a large number of neurons specify the properties of a single stimulus; different smells cause activation in different regions of olfactory bulb and olfactory cortex; olfactory system uses temporal coding for population coding

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48
Q

olfactory temporal coding

A

the olfactory system uses temporal coding, where the timing of spikes caused by different odorants carries information about those odorants

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49
Q

2 categories of memory

A
  1. Declarative (explicit) - memory of facts and events
  2. Nondeclarative (implicit) - memory for skills, habits, and others that don’t have a conscious component
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50
Q

flow of sensory info into long-term memory

A
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51
Q

memory acquisition

A

conversion of sensory information into a short-term memory

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52
Q

memory consolidation

A

conversion of a short-term memory into a long-term memory

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53
Q

Where is memory stored within neural circuits?

A

distributed memory storage - unique pattern or ratio of activity of neuronal network where memory is distributed and no single neuron represents a specific memory

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54
Q

cellular basis of memory

A

modification of synaptic strengths forms memory; sensory info “shapes” synapses, forming memories

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55
Q

synaptic plasticity

A

changes in the strengths of synaptic connections in response to experience and neuronal activity

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56
Q

What biologically strengthens synaptic connections?

A
  1. synaptic potentiation (increased efficiency)
  2. formation of new synapses
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57
Q

What biologically weakens synaptic connections?

A
  1. synaptic depression (decreased efficiency)
  2. elimination of existing synapses
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58
Q

CA3 –> CA1 synapse

A

synapse in the hippocampus where the CA1 neuron receives input from the CA3 neuron; extremely important for understanding LTP/LDP and overall synaptic plasticity

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59
Q

Long-Term Potentiation (LTP)

A

a long-lasting increase in the effectiveness of synaptic transmission that is induced by learning (i.e., memory formation); shown by increased EPSP amplitude in CA1

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60
Q

Hebb’s rule

A

synaptic potentiation (increased efficiency) results when presynaptic activity correlated with strong activation of postsynaptic neuron; i.e., neurons firing synchronously leads to synaptic potentiation

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61
Q

tetanic stimulation

A

artificial stimulation that can induce LTP or LDP; high frequency stimulation can induce a very strong EPSP, while low frequency stimulation can induce an extremely weak EPSP (below baseline)

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62
Q

What is required for NMDA receptor activation?

A

Both depolarization AND glutamate needed to activate and allow Ca2+ influx; Mg2+ blocks the channel at certain negative Vm, even if glutamate binds

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63
Q

How does the NMDA receptor act as a co-incidence detector?

A

Ca2+ entry though NMDA receptor specifically signals that pre- and postsynaptic neurons are active at the same time

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64
Q

How is LTP acheived? (mechanisms of LTP in CA1)

A

Ca2+ enters postsynaptic terminal through NMDA receptors and activates CaMKII, which acheives LTP by:
1. Increasing effectiveness of existing AMPA receptors via phosphorlyation
2. Upregulating AMPA receptors

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65
Q

BCM theory

A

synaptic depression (synaptic efficiency) results when presynaptic activity is correlated with a weak depolarization of a postsynaptic neuron; i.e., weak depolarization leads to neurons firing asynchronously which leads to synaptic depression

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66
Q

2 rules of bidirectional plasticity

A
  1. Synapses during strong depolarization of postsynaptic neuron causes LTP (Hebb’s rule)
  2. Synapses during weak depolarization of postsynaptic neuron causes LTD (BCM theory)
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67
Q

How is LTD acheived? (mechanisms of LTD in CA1)

A
  1. Increase of protein phosphatase activity
  2. Dephosphorlyation of AMPA receptors on the membrane
  3. Removal of existing AMPA receptors
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68
Q

How can Ca2+ trigger both LTP and LTD in CA1?

A

Ca2+ influx activates CaMKII, which leads to phosphorylation (LTP)
Lack of Ca2+ activates phosphatase, which leads to dephosphorylation (LTD)

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69
Q

What constitutes stable synaptic transmission (memory)?

A

AMPA receptors are replaced, maintaining the same number; LTP and LTD disrupt this equilibrium

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70
Q

complete early phase LTP cascade

A
  1. In the presence of both glutamate and depolarization, NMDA receptors activate, letting glutamate and Ca2+ into the cell
  2. Ca2+ influx activates CaMKII, which phosphorylates to increase effectiveness of existing AMPA receptors and to insert new AMPA receptors into the membrane (lower amounts of Ca2+ do the opposite in LTD)
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71
Q

Why is phosphorylstion insufficient as long-term memory consolidation mechanism?

A
  1. Phosphorylation of a protein is not permanent (memories would be erased
  2. Protein molecules themselves are not permanent
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72
Q

2 methods of memory consolidation

A
  1. Permanently active CaMKII; once activated, autophosphorylation will keep kinases on permanently
  2. New protein synthesis via cAMP, PKA, and CREB
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73
Q

complete late phase LTP cascade (memory consolidation)

A
  1. Ca2+ from early phase stimulates AC to convert ATP to cAMP
  2. cAMP activates PKA
  3. PKA phosphorylates CREB
  4. CREB causes gene expression (new protein synthesis)
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74
Q

CREB-1 vs. CREB-2

A

CREB-2 is a repressor of gene expression, while CREB-1 is an activator of gene expression (leading to memory consolidation via new protein synthesis)

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75
Q

synaptic remodeling

A

formation or demolition of synapses during learning and memory

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76
Q

Technical Tuesday: optogenetics

A

utilization of light and to activate (channelrhodopsins (ChRs)) and inactivate (Halorhodopsin) neurons and control neuron activity

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77
Q

channelrhodopsins (ChRs) (from Technical Tuesday)

A

subfamily of light-gated cation channels that are activated by blue light to activate neurons

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78
Q

halorhodopsins (from Technical Tuesday)

A

Cl- pump activated by yellow-light to inactivate neurons (move chlorine ions into the cell, reducing membrane potential)

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79
Q

What are sounds?

A

sounds are audible variations in the air pressure; basically every object moves the air, creating sound

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80
Q

sound cycle

A

distance between successive compressed patches of air; peak to peak, trough to trough

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81
Q

sound frequency

A

number of cycles per second; determines pitch

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82
Q

What is the audible sound range for humans?

A

20 Hz - 20000 Hz

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83
Q

pitch

A

high pitch = high frequency
low pitch = low frequency

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84
Q

intensity (amplitude)

A

defines loudness; high intensity (high amplitude) louder than low intensity (low amplitude)

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85
Q

structural components of the outer ear

A
  1. Pinna - funnel/visible
  2. Auditory canal - entry into ear
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86
Q

structural components of the middle ear

A
  1. Ossicles - small bones
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87
Q

structural components of the inner ear

A
  1. Cochlea - where sound is converted into signals
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88
Q

tympanic membrane (eardrum)

A

where sounds are converted into membrane vibration

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89
Q

central auditory pathway

A
  1. Sound wave
  2. Tympanic membrane (eardrum)
  3. Ossicles
  4. Oval window
  5. Fluid in cochlea
  6. Auditory sensory neuron
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90
Q

What occurs in the middle ear?

A

pressure through ossicles is amplified, allowing footplate to move like a piston, causing fluid movement in cochlea

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91
Q

auditory receptor cells (hair cells)

A

receptor cells that are activated by sounds; located on the organ of Corti, which sits on the basilar membrane; have stereocilia (hair-like structure)

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92
Q

2 types of hair cells

A
  1. Outer hair cells (OHC)
  2. Inner hair cells (IHC)
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93
Q

endolymph

A

liquid in the cochlea that has high [K+] and low [Na+]

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94
Q

perilymph

A

liquid in the cochlea that has low [K+] and high [Na+]

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95
Q

What happens in the inner ear?

A
  1. Oval window in middle ear acts like a piston, causing vibrations in cochlear fluid
  2. Vibrations in cochlear fluid lead to vibration of the basilar membrane
  3. When basilar membrane vibrates, stereocilia on hair cells on organ of corti are bent
  4. Bending of hair cell stereocilia causes sound to be converted into a neural signal (receptor potential)
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96
Q

What causes receptor potential of hair cells?

A

the bending of stereocilia; when bent in a certain direction, tension in tip link increases, opening the channel and allowing for K+ flow

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97
Q

What occurs at the normal state of tip link in hair cells?

A

stereocilia are not bent, but K+ channels are partially open, allowing for some K+ flow

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98
Q

hair cell transduction cascade

A
  1. Stereocilia bends and tip link is stretched (increased tension)
  2. Mechanically-gated K+ channels open, and K+ enters the cell
  3. Hair cells depolarize
  4. Ca2+ flows into the cell and releases glutamate
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99
Q

What neurotransmitter is released by hair cells?

A

glutamate

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100
Q

What is unique about hair cell transduction and K+?

A

K+ flows from outside the cell into the cell, as endolymph has high [K+] concentration

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101
Q

OHC vs. IHC

A
  1. Ratio of OHC/IHC is 3:1
  2. 1 IHC feeds ~10 spiral ganglion cells
  3. IHCs contribute to 95% of output to spiral ganglion cells
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102
Q

inner hair cells (IHC)

A

less prevalent than OHC (1:3), but contribute to 95% of output to spiral ganglion cells; a single IHC feeds about 10 spiral ganglion cells

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103
Q

outer hair cells (OHC)

A

more prevalent than IHC (3:1), but only contribute to 5% of output ot spiral ganglion cells; OHCs amplify basilar membrane deflections (cochlear amplifier) by compression of motor proteins called prestin, which shortens hair cells

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104
Q

prestin

A

motor protein in OHCs that is compressed in response to OHC depolarization, shortening hair cells and amplifying basilar membrane defelctions; causes stereocilia of IHC to bend more

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105
Q

cochlear amplifier loop mechanism

A

process of OHCs amplifying basilar membrane deflections, making vibrations more impactful and thereby causing IHCs to bend more

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106
Q

central auditory pathway

A
  1. Spiral ganglion
  2. Ventral cochlear nucleus
  3. Superior olive
  4. Inferior colliculus
  5. MGN
  6. Auditory cortex

Steps 1-2: input from one ear only
Steps 3-6: input from both ears

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107
Q

What is the most common cause of deafness and how can it be treated?

A

hair cell damage or loss is the most common cause (auditory nerve often remains intact), cochlear implants common treatment

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108
Q

characteristic frequency

A

frequency at which a neuron is most responsive

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109
Q

structural properties of basilar membrane base and apex

A

base is narrow and stiff (high frequency encoding), while the apex is wide and floppy (low frequency encoding)

110
Q

auditory system tonotopy

A

the systematic organization within an auditory structure based on sound frequency; represented by:
1. High frequency at basilar membrane base, low frequency at basilar membrane apex
2. There is also a tonotopic map in primary auditory cortex

111
Q

phase locking

A

the consistent firing of a cell at the same phase of a sound wave; occurs with sound waves up to ~5 kHz (low frequency)

112
Q

Can high-frequency sound elicit phase-locked response in neurons?

A

No, phase locking does not occur with sound waves >5 kHz; sound frequency is encoded by tonotopy at high frequencies

113
Q

mechanisms for encoding sound frequency

A
  1. Low frequency (20-200 Hz) - phase locking
  2. Intermediate frequency (200-5,000 Hz) - tonotopy + phase locking
  3. High frequency (5,000-20,000 Hz) - tonotopy
114
Q

mechanisms for encoding sound intensity

A
  1. Firing rate of auditory nerve; more bending of stereocilia, more NT release, more firing
  2. Number of active neurons in auditory nerve
115
Q

complete sound detection cascade

A
  1. Pinna and ITD/IID localize sound and funnel it into auditory canal
  2. Tympanic membrane converts sound waves into vibrations
  3. Ossicles in the middle ear amplify pressure, causing the oval window to fire like a piston
  4. Cochlear fluid moves the basilar membrane, compressing hair cells on the organ of corti
  5. OHCs amplify basilar membrane deflections, causing IHC stereocilia to bend more
  6. Bending of stereocilia causes K+ channels to open, and K+ from the endolymph flows into the cell, depolarizing it
  7. Ca2+ flows into the presynaptic terminal, releasing glutamate to spiral ganglion cells (95% of this output done by IHCs, which synapse ~10 SGCs)
  8. Action potential propogates through auditory nerve, then lateral lemniscus to the auditory cortex
116
Q

How is sound localized in the horizontal plane (duplex theory)?

A
  1. Interaural Time Delay (ITD) (low frequency sounds) - difference in time for sound to reach each ear
  2. Interaural Intensity Difference (IID) (high frequency sounds) - sound at one ear less intense because of head’s sound shadow
117
Q

Interaural Time Delay (ITD)

A

the superior olive has binaurual neurons (it receives input from both cochlear nuclei), allowing it to detect the delay between sound reaching the first and second ear; works for frequencies between 20-2,000 Hz

118
Q

Interaural Intensity Difference (IID)

A

the head forms a sound shadow, partially blocking sound waves, and using this shadow, the nueron can use intensity to localize sounds; works for frequencies between 2,000-20,000 Hz

119
Q

How is sound localized in the vertical plane?

A

the pinna reflects sounds; delays between direct path and reflected path changes as the sound source moves vertically

120
Q

Do muscles pull or push?

A

muscles pull, not push; purely contraction

121
Q

lower motor neurons in spinal cord

A

muscle contraction is primarily dictated by innervation by lower motor neurons in the spinal cord

122
Q

neuromuscular junction (NMJ)

A

chemical synapse between motor neuron axon and muscle fiber

123
Q

myofibril

A

composed of stacked sarcomeres; multiple myofibrils form a muscle fiber, and multiple muscle fibers form muscle

124
Q

What are the thin filaments of the sarcomere?

A

actin

125
Q

What are the thick filaments of the sarcomere?

A

myosin

126
Q

sliding-filament model of muscle contraction

A
  1. Ca2+ binds to troponin, allowing myosin heads to bind to actin
  2. Myosin heads pivot, causing filaments to slide and muscle to contract
127
Q

structure of skeletal muscle`

A
  1. Muscle is a bundle of muscle fibers
  2. Muscle fiber is a bundle of myofibrils
  3. Myofibrils are composed of sarcomeres
  4. Sarcomeres are composed of actin and myosin filaments
128
Q

complete muscle contraction cascade (excitation-contraction cycle)

A
  1. Action potential causes lower motor neurons in the ventral horn of the spinal cord to release ACh across NMJ
  2. ACh receptor activates, Na+ enters the cell and causes depolarization (large EPSP)
  3. Action potential in postsynaptic terminal (muscle) propagates into T tubules
  4. Sarcoplasmic reticulum releases Ca2+
  5. Ca2+ binds troponin, allowing myosin to bind actin
  6. Myosin heads pivot, causing filaments to slide
  7. EPSPs end, sarcolemma return to resting potential and Ca2+ reuptake occurs by sarcoplasmic reticulum
129
Q

motor unit

A

one motor neuron and all the muscle fibers it innervates

130
Q

How many muscle fibers can one motor neuron innervate?

A

one motor neuron can innervate multiple muscle fibers

131
Q

How many motor neurons can innervate a single muscle fiber?

A

one muscle fiber is innervated by a single motor neuron

132
Q

3 types of motor units

A
  1. Fast fatigable - huge amount of force, but tire quickly and must rest
  2. Fast fatigue-resistant - sizable force that tires slowly
  3. Slow - small force that tires very slowly
133
Q

motor neuron pool

A

all the alpha motor neurons that innervate a single muscle

134
Q

What causes sustained muscle contraction?

A

increased firing rate of alpha motor neurons

135
Q

2 ways muscle force is controlled

A
  1. Firing rate of motor units
  2. Recruitment of motor units - size principle - small motor units recruited first, allowing for fine activity
136
Q

Where in the spinal cord are lower motor neurons located?

A

ventral horn

137
Q

2 types of lower motor neurons

A
  1. Alpha motor neurons - control muscle in an on/off manner; synapse to normal muscle fibers
  2. Gamma motor neurons - allow for fine-tuning (modulate force generation); synapse to modified muscle fibers (intrafusal fibers)
138
Q

proprioception

A

“body sense” which informs us of how our body is positioned and moving in space

139
Q

muscle spindles

A

propioreceptors that are innervated by Ia axons to provide sensory feedback to muscle; AKA stretch receptors

140
Q

stretch reflex

A

tendency of a muscle to pull back when pulled (e.g., knee-jerk reflex); feedback loops where discharge rate of sensory axons is related to muscle length; monosynaptic

141
Q

stretch reflex cascade

A
  1. Force stretches muscle spindle
  2. Ia axon rapidly fires action potential to alpha motor neuron, causing muscle to “pull back” (e.g., knee-jerk reflex)
142
Q

What do gamma motor neurons innervate?

A

the two poles of intrafusal fibers inside muscle spindle

143
Q

gamma motor neuron loop

A
  1. Gamma motor neuron
  2. Intrafusal muscle fiber
  3. Ia afferent axon
  4. Alpha motor neurons
  5. Extrafusal muscle fiber
144
Q

How does the activation of motor neurons affect Ia activity?

A
  1. Activation of alpha motor neuron (no/less spindle stretching) -> decrease Ia activity
  2. Activation of gamma motor neuron (spindle stretching) -> increase Ia activity
145
Q

“on air” spindles

A

gamma motor neurons keep spindle “on air”

146
Q

Golgi tendon

A

connects muscle to bone and monitors muscle tension via Ib axons; additional proprioceptive input

147
Q

sensory feedback on muscle tension cascade

A
  1. Muscle contracts
  2. Increased tension of tendon
  3. Ib axons fire
148
Q

anatomical arrangement of proprioceptors

A
  1. Muscle spindles in parallel with fibers -> muscle length proprioception
  2. Golgi tendons in series with fibers -> muscle tension proprioception
149
Q

reciprocal inhibition of flexors and extensors

A

contraction of one muscle set causes relaxation of antagonist muscle (e.g., bicep/tricep); inhibitory input from interneurons

150
Q

flexor withdrawal reflex

A

reflex arc used to withdraw limb from adverse stimulus; poly-synaptic, excitatory input from interneurons that activates flexor muscles on the same side of body

151
Q

crossed-extensor reflex

A

activation of extensor muscles and inhibition of flexors on opposite side of body

152
Q

flexor withdrawal reflex vs. crossed-extensor reflex

A

flexor withdrawal reflex activates flexor muscles and inhibits extensor muscles on the same leg, while the crossed-extensor reflex activates extensor muscles and inhibits flexor muscles on opposite side

153
Q

rhythmic activity in a spinal interneuron cycle

A
  1. Glu binds NMDA receptor, causing depolarization
  2. Ca2+-activated K+ channels open, causing K+ to leave and hyperpolarize the membrane
  3. Glu binds NMDA again, restarting cycle
154
Q

reciprocal inhibition and rhythmic pattern

A

Both A and B want to fire but…
1. A fires, inhibiting B
2. A gets “tired” and stops firing
3. B starts to fire, inhibiting A
4. Cycle continues, generating a rhythmic pattern

155
Q

central pattern generator

A

circuits that give rise to rhythmic motor activity (e.g., reciprocal inhibition)

156
Q

What is the largest sensory organ?

A

skin

157
Q

What is the stimulus for touch?

A

pressure on the skin

158
Q

What receptors detect touch?

A

mechanoreceptors - convert mechanical force to neural signals

159
Q

2 types of skin

A
  1. Hairy skin - hairy
  2. Glaborous skin - hairless
160
Q

What somatic sensory receptor is in the epidermis?

A

Merkel’s disks

161
Q

What somatic sensory receptors are in the dermis?

A
  1. Pacinian corpuscles
  2. Ruffini’s endings
  3. Meissner’s corpuscles
162
Q

receptive field

A

the region of a sensory surface that, when stimulated, changes the membrane potential of a neuron

163
Q

Meissner’s corpuscle

A

somatic sensory receptor located in the dermis that has:
1. Small receptive field
2. Rapid adaptation (transient response at beginning and end of stimulus)

164
Q

Pacinian corpuscle

A

somatic sensory receptor located in the dermis that has:
1. Large receptive field
2. Rapid adaptation (transient response at beginning and end of stimulus)

165
Q

Merkel’s disk

A

somatic sensory receptor located in the epidermis that has:
1. Small receptive field
2. Slow, sustained response during stimulus

166
Q

Ruffini’s ending

A

somatic sensory receptor located in the dermis that has:
1. Large receptive field
2. Slow, sustained response during stimulus

167
Q

corpuscle special ending

A

the corpuscle is a special ending of somatic sensory receptors that allows for rapid adaptation (transient response at beginning and end of stimulus); when removed, adopts slow adaption response profile

168
Q

larger receptive field vs. smaller receptive field

A

larger receptive field allows sensory receptor to detect touch at a lower threshold (more sensitive)

169
Q

two-point discrimination

A

method used to measure spatial resolution of touch sensation

170
Q

How do mechanosensitive ion channels open?

A
  1. Stretching of lipid membrane
  2. Pressure on skin causes extracellular protein to “pull” the channel open (from the outside)
  3. Pressure on skin causes cytoskeleton to “pull” the channel open (from the inside)
171
Q

Piezo 1 and Piezo 2

A

mechanosensitive, non-selective ion channels that open via lipid stretching

172
Q

Technical Tuesday: gene knockout with Cre/LoxP system

A

Cre: site specific recombinase
LoxP: short sequence recognized by Cre

Cre will cut the DNA section between two LoxP sites in the same orientation, removing a gene

173
Q

Piezo 2 and Merkel cells

A

Merkel cells require Piezo 2 to transduce mechanical stimuli into electrical signals

174
Q

primary afferent axons for pain

A

Initial pain: Agamma fiber
Second pain: C fiber

175
Q

primary afferent axons for temperature

A

C fibers

176
Q

primary afferent axons for itch

A

C fibers

177
Q

primary afferent axons for touch

A

Abeta

178
Q

Abeta afferent axons

A

extremely thick (myelinated), innervate mechanoreceptors on skin for detection of touch

179
Q

C afferent axons

A

extremely thin (unmyelinated) and mediate pain, temp, and itch

180
Q

Where in the spinal cord do primary afferent sensory axons project?

A

dorsal horn/columns

181
Q

segmental organization of spinal cord

A

30 spinal segments across four divisions of spinal cord (cerebral, thoracic, lumbar, sacral)

182
Q

dermatomes

A

the area of skin innervated by the right and left dorsal roots of a single spinal segment (one-to-one correspondence between spinal segments and dermatomes)

183
Q

2 different central touch pathways

A
  1. The dorsal column-medial lemniscal pathway - body
  2. Trigeminal touch pathway - face and top of head
184
Q

dorsal column-medial lemniscus pathway

A

touch sensation from body, where one side of the primary somatosensory cortex of the brain is concerned with touch originating from the contralateral (opposite) side of the body

  1. Dorsal root axon (Aalpha, Abeta, Agamma)
  2. Dorsal column
  3. Dorsal column nucleus
  4. Medial lemniscus
  5. Thalamus
  6. Cerebral cortex
185
Q

trigeminal touch pathway

A

touch sensation from face, where one side of the primary somatosensory cortex of the brain is concerned with touch originating from the contralateral (opposite) side of the face

186
Q

somatotopy

A

the topographic organization of somatic sensory pathway; somatic sensory map that helps determine the location of touch sensation

187
Q

What is the stimuli for pain?

A

any stimuli that signal body tissue being damaged or have the potential of causing tissue damage

188
Q

What are the receptors for pain?

A

nociceptors - ion channels

189
Q

3 types of nociceptors

A
  1. Mechanical - pressure
  2. Thermal - temperature
  3. Chemical - histimines, etc.
190
Q

most common type of nociceptors

A

most are polymodal (all 3)

191
Q

How are nociceptors activated?

A
  1. Strong mechanical stimulation, temperature extremes, oxygen deprivation, chemicals
  2. Substances released by damaged cells - proteases, ATP, K+ ion channels, histamines
192
Q

What substances are released from damaged cells that activate nociceptors?

A
  1. Proteases (-> bradykinin)
  2. ATP
  3. K+
  4. Histamine
193
Q

TRPV1

A

thermoreceptor that responds to both hot peppers (capsaicin) and high temperature

194
Q

Transient Receptor Potential (TRP) channels

A

cation channels that can be activated by temp, chemicals, light, etc.

195
Q

TRPM8

A

thermoreceptor that responds to both menthol and cold temperature

196
Q

6 distinct TRP channels in thermoreceptors

A

From coldest to hottest:
1. TRPA1 (cold)
2. TRPM8 (cold)
3. TRPV4
4. TRPV3
5. TRPV1
6. TRPV2

197
Q

2 major ascending pathways of somatic sensation

A
  1. Dorsal column-medial lemniscus pathway
  2. Spinothalamic pathway
198
Q

spinothalamic pathway

A

For pain, temperature, and some touch:
1. Dorsal root axon (Agamma, C)
2. Lateral spinothalamic tract
3. Thalamus
4. Cerebral Cortex

199
Q

connection between frequency, wavelength, and energy

A

higher energy = higher frequency = lower wavelength
lower energy = lower frequency = higher wavelength

200
Q

colors and wavelength

A

gamma radiation and cool colors have low wavelengths (high energy), while radio waves and warm colors have high wavelengths (low energy)

201
Q

retina

A

area where we perceive light

202
Q

fovea

A

thinnest area in the retina; visual center that has cones almost exclusively and is very active during the day

203
Q

What does the cornea do?

A

the cornea refracts (bends) light towards a single point of the retina

204
Q

What does the lens of the eye do?

A

accomodates the cornea by changing shape to provide extra focusing power; allows us to see objects at different distances

205
Q

2 types of photoreceptors

A
  1. Rods
  2. Cones

both are photoreceptors that convert light into neural signals

206
Q

Why are rodes and cones arranged in a disc-like manner?

A

discs provide large membrane surface area for inserting lots of light sensors

207
Q

rods

A

photoreceptors that are more senstive to light and are used for night vision

208
Q

cones

A

photoreceptors that are less sensitive to light and are used for day vision and color vision

209
Q

rhodopsin

A

GPCR light sensor of rods; light causes change in shape of retinal, activating rhodopsin

210
Q

retinal

A

used as a cofactor in opsins, it changes shape in response to light

211
Q

What is the receptor potential of rods?

A
  1. In dark, cells are depolarized
  2. In light, cells hyperpolarize
212
Q

complete LIGHT detection cascade by rods

A
  1. Light causes retinal to change shape, activating rhodopsin
  2. G subunit activates guanylate cyclase (GC)
  3. GC converts GTP to cGMP
  4. Phosphodiesterase (PDE) converts cGMP to GMP
  5. GMP blocks Na+ channel, causing hyperpolarization
  6. Release of glutamate is inhibited
213
Q

complete DARK detection cascade by rods

A
  1. Absence of light meand that rhodopsin is inactive
  2. G subunit activates GC
  3. GC converts GTP to cGMP
  4. PDE is inactive, meaning GMP is NOT produced
  5. cGMP activates cGMP channel, allowing Na+ to flow in and depolarize the cell
  6. Glutamate is released from the cell
214
Q

dark current

A

Na+ ions moving into the cell in dark conditions (absence of PDE), causing depolarization

215
Q

3 types of cones

A
  1. Red (long wavelength)
  2. Green (medium wavelength)
  3. Blue (short wavelength)
216
Q

opsins

A

GPCR light sensors; in rods, only rhodopsin, but in cones, there are 3 opsins

217
Q

3 types of opsins in cones

A
  1. Red cone opsin (L-opsin)
  2. Green cone opsin (M-opsin)
    3 Blue cone opsin (S-opsin)
218
Q

Young-Helmholtz trichromacy theory

A

cones are sensitive to RGB, and when these colors are combined, eyes can tell a difference between million of colors

219
Q

Why can’t rods detect color?

A

rods only have a single opsin - rhodopsin - which cannot detect color; this is why we can’t detect color in the dark when rods dominate

220
Q

scotopic conditions

A

e.g., nighttime lighting; rods contribute to vision (no color info)

221
Q

photopic conditions

A

e.g., daytime lighting; cones contribute to vision

222
Q

mesopic conditions

A

e.g., indoor lighting; both rods and cones contribute to vision

223
Q

dark adaptation

A

conversion from all-cone daytime vision to all-rod nighttime vision; occurs over minutes to an hour

224
Q

factors in dark adaptation

A
  1. Dilation of pupils (lets more light in)
  2. Regeneration of unbleached rhodopsin in rods
  3. Adjustment of functional circuitry

All lead to increased light sensitivty

225
Q

light adaptation

A

conversion from all-rod nighttime vision to all-cone daytime vision; occurs over 5-10 minutes

226
Q

Ca2+ role in light adaptation

A

to prevent complete hyperpolarization of rods, Ca2+ inhibits conversion of GTP to cGMP, bringing Vm to about -35 mV; allows cones to continue responding to light

227
Q

laminar organization of the retina

A

seemingly inside-out layers; light passes through the eye as follows:
1. Ganglion cell layer
2. Inner plexiform layer (synapses)
3. Inner nuclear layer
4. Outer plexiform layer (synapses)
5. Outer nuclear layer
6. Photoreceptors
7. Pigmented epithelium

228
Q

5 types of cells in the retina

A

Vertical pathway:
1. Ganglion cells
2. Bipolar cells
3. Photoreceptor cells
Indirect Pathway:
1. Amacrine cells
2. Horizontal cells

229
Q

What retinal cells fire action potentials and send outputs to the brain?

A

Only ganglion cells; other retinal neurons produce graded changes in membrane potential

230
Q

How does information flow in the retina (2 pathways)?

A
  1. Vertical pathway
  2. Indirect pathway
231
Q

direct (vertical) pathway of info flow in retina

A
  1. Photoreceptors
  2. Bipolar cells
  3. Retinal ganglion cells
232
Q

indirect pathway of info flow in retina

A

retinal processing also influenced by lateral connections
1. Amacrine cells - receive input from bipolar cells and project to ganglion cells, bipolar cells, and other amacrine cells
2. Horizontal cells - receive input from photoreceptors and provide inhibitory feedback signals to other photoreceptors and bipolar cells

233
Q

amacrine cells

A

receive input from bipolar cells and project to ganglion cells, bipolar cells, and other amacrine cells; part of indirect pathway

234
Q

horizontal cells

A

receive input from photoreceptors and provide inhibitory feedback signals to other photoreceptors and bipolar cells; part of indrect pathway

235
Q

retinal receptive field

A

area of retina where light changes neuron’s firing rate

236
Q

center ON/surround OFF receptive fields of retinal ganglion cells

A
  1. Center ON - light only on central photoreceptors increases APs in retinal ganglion cells (firing rate increases in center)
  2. Surround OFF - light only on surround photoreceptors decreases APs in retinal ganglion cells (firing rate diminished in center)
  3. Light on both - slight increase in APs, but really weak (close to baseline)
237
Q

How are receptive fields of RGCs established?

A

ON and OFF bipolar cells and lateral inhibition from horizontal cells
Excitatory synapse between PR and bipolar cells = center OFF
inhibitory synapse between PR and bipolar cells = center ON

Lateral inhibition via horizontal cells yields opposite response

238
Q

OFF bipolar cells

A

have excitatory synapses that preserve the sign of the cone and are therefore hyperpolarized by light (excitatory Glu receptors)

239
Q

ON bipolar cells

A

have inhibitory synapses that reverse the sign of the cone and are therefore depolarized by light (inhibitory Glu receptors)

240
Q

parallel processing in the visual system

A

simultaneous input from two eyes allows us to compare info in the cortex and also determine depth and distance of an object

241
Q

How do we gather info about light and dark?

A

ON-center and OFF-center ganglion cells

242
Q

central visual pathway

A
  1. Photoreceptors in eye
  2. Other retinal neurons
  3. LGN
  4. Visual cortex
243
Q

retinofugal projection: visual pathways from eye to brain

A
  1. Retina
  2. Optic nerve
  3. Optic chiasm
  4. Optic tract
  5. LGN
  6. Optic radiation
  7. Primary visual cortex (V1)
244
Q

Where does decussation of the visual system occur?

A

ganglion cell axons from nasal retina cross in optic chiasm

245
Q

binocular visual field

A

visual field where we use both eyes to see

246
Q

What can you see if you’re blind in left eye only?

A

you can still see some of the left visual field due to overlap

247
Q

What if you’re blind in the left visual field?

A

you have optic tract damage and the entire visual field is “broken;” can only see right visual hemifield (right half of normal vision)

248
Q

What if you’re blind in the peripheral visual fields on both sides?

A

you have optic chiasm damage and can only see in the binocular visual field

249
Q

retinotopy

A

topographic organization of visual pathway in which neighboring cells in the retina send info to neighboring cells in a target brain structure; represented by: position in retina sends info to similar LGN structure to the visual cortex

250
Q

Can LGN neurons respond to light in more than one eye?

A

No, they are monocular:
1. LGN layer 2, 3, 5 from ipsilateral (same side) eye
2. LGN layer 1, 4, 6 from contralateral (other side) eye

251
Q

LGN layer differences

A
  1. 2, 3, 5 from same side eye, and 1, 4, 6 from other side eye
  2. Layers 1 and 2 have larger neurons, while 4-6 have smaller neurons
252
Q

complete organization of different layers (RGC, LGN, V1)

A

P-type retinal ganglion (small) —> Layers 3,4,5,6, all Parvocellular LGN neurons (small) —> IVCbeta of striate cortex
- small center-surround receptive fields with sustained response

M-type retinal ganglion (large) —> Layers 1,2, both Magnocellular LGN neurons (large) —> IVCalpha of striate cortex
- large center-surround receptive fields with transient response

253
Q

Where do most LGN neurons project in the striate cortex

A

layer 4…
1. Magnocellular LGN project to layer IVCalpha
2. Parvocellular LGN project to layer IVCbeta
3. Koniocellular LGN axons synapse in layers 1/3
some LGN neurons project to layer 2/3

254
Q

pyramidal cells of striate cortex

A

have spines and thick apical dendrites; found in layers III, IVC, V, VI

255
Q

spiny stellate cells of striate cortex

A

spine-covered dendrites; found in layer IVC

256
Q

inhibitory neurons of striate cortex

A

lack spines and form local connections; found in all layers

257
Q

Technical Tuesday: anterograde tracing

A

injection of dye to trace from soma to synapse

258
Q

Technical Tuesday: retrograde tracing

A

injection of dye to trace from synapse to soma

259
Q

ocular dominance columns

A

stripes of neurons in the visual cortex of certain mammals (including humans) that respond preferentially to input from one eye or the other; found in layers > IV (IVC, VI, etc.)

260
Q

Where are binocular neurons found?

A

most layer III neurons are binocular (but not layer IV or greater)

261
Q

receptive fields of the striate cortex

A

monocular receptive fields: found in layer IVC; have one receptive field

binocular receptive fields: found in layers before IVC (mainly III); have two receptive fields

262
Q

patterns of intracortical connections within striate cortex

A

some cortical neurons project locally to deeper or shallower layer, establishing “columns” of interacting neurons, but others project sideways (horizontally)

263
Q

orientation selectivity of neurons in striate cortex

A

neuron fires action potentials depending on the orientation of the bar of light in visual field, which is important for the analysis of object shape

264
Q

orientation-selective columns

A

adjacent cortical neurons tend to have similar orientation selectivity, and neighboring cortical cells share identical or similar orientation selectivities (pinwheels)

265
Q

direction selectivity of neurons in striate cortex

A

neuron fires action potentials in direction-dependent response to moving bar of light; important for the analysis of object motion

266
Q

How are receptive fields of cortical cells unique?

A

they are usually oblong instead of circular, making cortical cells orientation-selective - respond best to light with specific orientation

267
Q

How are oblong cortical center-surround fields formed?

A

input from several LGN neurons with adjacent circular fields combined

268
Q

cytochrome oxidase blobs

A

monocular, no direction-selectivity, likely orientation selectivity, but specialized for the analysis of object color

269
Q

What info does the magnocellular pathway process?

A

motion

270
Q

What info does the blob pathway process?

A

color

271
Q

What info does the parvocellular pathway process?

A

shape

272
Q

What is the capability of a cortical module of the striate cortex?

A

each module is capable of analyzing every aspect of a portion of the visual field (direction, color, orientation, light/dark, etc.)

Neurobiology 523 (3 decks)

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