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Neuro Biology > Unit 2 > Flashcards

Unit 2 Flashcards

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1
Q

What are the ways to see the structure of the brain?

A
  • MRI
    -CAT/CT
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2
Q

What does MRI stand for?

A

magnetic resonance imaging

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3
Q

What are the advantages to an MRI?

A
  • no x-rays or radioactive material
  • provides detailed view of the brain in different dimensions
  • shows the structure of the brain
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4
Q

What are the disadvantages to the MRI?

A

-expensive
-gross anatomy only

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5
Q

What does a CAT scan stand for?

A
  • computerized axial tompography
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6
Q

What are the ways to measure the functional brain?

A
  • PET Scan
    -FMRI
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7
Q

What does PET stand for?

A
  • positional emission tomography
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8
Q

What are the advantages to an FMRI?

A
  • non-invasive
    -detects changes in blood flow
    (brain consumes the most O2 and glucose)
  • provides both anatomical and functional view of the brain
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9
Q

What are the disadvantages to the FMRI?

A

-blood flow is an indirect measure of neural activity
-large scale only
-heavy reliance on algorithms to standardize and produce data

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10
Q

What is a conectome?

A

a comprehensive map of neural connections

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11
Q

What are the levels of analysis for the connectome?

A

-microscale
-mesoscale
-macroscale

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12
Q

What does a microscale show?

A
  • neurons immediate vicinity
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13
Q

What does the mesoscale show?

A

single neuron projections and circuit

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14
Q

What does the macroscale show?

A

connections between 1 brain region to another brain region

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15
Q

What scale is the serial electron microscopy on?

A
  • microscale- shows neurons immediate vicinity
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16
Q

What is serial electron microscopy?

A
  • only technique that can probe at the nanometer scale to elucidate a synaptic cleft
  • done by sectioning tissue into thin slices and image
  • aligns consecutive images to create 3-D volumes of individuals
  • used to be done manually
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17
Q

What scale is trans-synaptic tracing on?

A
  • mesoscale
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18
Q

What is trans-synaptic tracing?

A
  • a strategy to determine local and long-distance connections between individual neurons
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19
Q

What are the two types of trans-synaptic tracing?

A
  • anterograde
    -retrograde
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20
Q

What is anterograde trans-synaptic tracing?

A
  • starter cell to post synaptic neurons
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21
Q

What is retrograde trans-synaptic tracing?

A
  • starter cell to pre-synaptic neurons
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22
Q

What is rabies viral trans-synaptic tracing?

A
  • adapted from natural phenomenon
  • retrograde tracer
  • adapted to survive and spread in CNS
  • transmission restricted to connected neurons (circuit info)
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23
Q

What scale is clarity on?

A

macroscale

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24
Q

What is clarity?

A

-allows visualization of deep structures without sectioning the brain
- Light-absorbing lipids are replaced with H20 soluble gel that turns the brain transparent
- neurons are labeled with flourescent molecules
(employs transgenic mice)

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25
Q

What’s the problem with connectome imaging?

A

all these techniques involve dead brains

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26
Q

What is the human connectome project?

A
  • construct a map of the structural and functional; neural connections across individuals in vivo
  • can see where genes are
  • can help map how everything connects
  • mapping is 1 cubic cm at a time
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27
Q

What does ipsilateral mean?

A

same side

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28
Q

What does contralateral mean?

A

different sides

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29
Q

How is the peripheral nervous system divided?

A

autonomic and somatic

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30
Q

What is the autonomic peripheral nervous system?

A
  • controls self-regulated action of internal organs and glands
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31
Q

What is the somatic peripheral nervous system?

A

controls voluntary movements of skeletal muscles

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32
Q

What makes up the nervous system?

A

-meninges
-brainstem
-cerebral cortex
-ventricular system
-corpus callosum
-cerebellum
- spinal cord

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33
Q

What makes up the meninges?

A

-dura mater
-subdural space
-arachnoid membrane
-subarachnoid space
- pia matter

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34
Q

What is dura matter?

A

-thick tough inflexible covering

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35
Q

What is the subdural space?

A

-doesn’t exist under normal conditions but present in pressure disorders

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36
Q

What is the arachnoid membrane?

A
  • resembles a spider web, holds layers close together
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37
Q

What is the subarachnoid space?

A

filled with CSF close to blood vessles

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38
Q

What is pia matter?

A

-adheres to surface of the brain

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39
Q

What is the ventricular system?

A

-contains CSF
- moves ions and nutrients
- no nerves or ganglion

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40
Q

What is in the cerebral cortex?

A

-sulcus
- fissure
-gyrus

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41
Q

What is the sulcus and an example of one?

A

-grooves
-increases area
-central sulcus
-valleys

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42
Q

What is a fissure and an example of one?

A
  • a really deep sulcus
    -increases area
    -lateral fissure
    -valleys
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43
Q

What is a gyrus and an example of one?

A

-ridges
-hills
-increases area
-precentral and postcentral gyrus

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44
Q

What are the types of cerebral cortex?

A
  • molecular layer (surface)
    -external granular layer
    -external pyramidal layer
    -internal granular layer
    -internal pyramidal layer
    -multiform layer
    -all different sizes and densities depending on which part you’re looking at
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45
Q

What are Brodmann’s areas?

A

-distinguished 50 zones of cerebral cortex based on differences in cell

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46
Q

What do broadmann’s areas depends on?

A

-cytoarchitecture which depends on the type, size, density, and lamination (layer size) of the cell
- done using nissal stain

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47
Q

What is the nucleus?

A
  • cluster of neuronal cell bodies with roughly similar functions and connections
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48
Q

What is the cortex?

A
  • sheet-like arrangement (layers) of neuronal cell bodies
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49
Q

What is a tract?

A
  • bundle of axons with same origin and destination
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50
Q

What is a commissure?

A
  • a collection of axons that cross the midline
    -largest is corpus callosum
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51
Q

What is the corpus callosum?

A
  • beneath cortex
    -connects left and right cerebral hemispheres
  • largest white matter structure in brain
  • has colossal commissure
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52
Q

What is the colossal commissure?

A
  • collection of axons crossing the midline
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53
Q

What is the cerebellum?

A

-part of CNS
- bilaterally symmetric (symmetrical off midline)
-coordinates precision, accuracy, timing of movements

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54
Q

What is the brainstem?

A

-part of the cns
-controls fundamentals of life
-contains midbrain, pons, medulla

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55
Q

What is the midbrain?

A
  • involved in vision, hearing, eye movement, body movement
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56
Q

What is the pons?

A
  • involved in motor control and sensory analysis
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57
Q

What is the medulla?

A

-maintains vital functions like heart rate and heart rate)

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58
Q

What are the parts of the spinal cord?

A
  • cervical
    -thoracic
  • lumbar
    -sacral
    (can turkeys leave scars)
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59
Q

What is a simple circuit?

A
  • signal from the cerebrum initiates this
    -underlies knee-jerk reaction
    -organized by dorsal and ventral horns
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60
Q

What are dorsal horns in charge of?

A

sensory circuits

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61
Q

What are ventral horns a part of?

A
  • motor circuits
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62
Q

What are sensory/afferent signals?

A
  • neurons send signals from teh senses, skin, muscles, internal organs to CNS
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63
Q

What are motor/ efferent signals?

A

neurons transmit commands from the CNS to muscles, glands, organs

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64
Q

How is the PNS organized?

A
  • autonomic and somatic
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65
Q

What is the autonomic PNS?

A
  • controls self-regulated action of internal organs and glands
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66
Q

What is the somatic PNS?

A
  • controls voluntary movements of skeletal muscle
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67
Q

What are the parts of the PNS?

A
  • nerves and ganglion
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68
Q

What are nerves?

A
  • bundles of axons in the PNS
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69
Q

What are cranial nerves?

A

-part of PNS
-nerves go to both sides
- damage can effect one side and not the other

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70
Q

What are ganglions?

A

cluster of neuronal cell bodies in PNS

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71
Q

What is plasticity?

A

-adaptability of an organism to change in its environment/ ability to alter the neural connections of the brain as a result of experience in the process of learning

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72
Q

When was the term plasticity used?

A
  • first used in the biological sense by R owen in 1850s
  • “Animals in a state of nature is required to show their degree of plasticity
    -wasn’t used to reference to the nervous system until the early 1950s
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73
Q

What is neural plasticity?

A

the ability of the NS to change in structure and or function

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74
Q

What is synaptic plasticity?

A
  • neural plasticity that occurs at the synapse
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75
Q

What are specific examples of synaptic plasticity?

A
  • synaptic depression at the neuromuscular junction
  • presynaptic facilitation in aplysia gill withdrawal reflex
  • long term potentiation (LTP) in the hippocampus
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76
Q

Describe changes at synapses?

A

-long or short time
-can be presynaptic or postsynaptic
- structural (spines) or electrical (stronger synapse)

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77
Q

What does synaptic plasticity allow for?

A
  • changes in behavior, not just at the synaptic level, but at the behavioral level too
    -experience changes in brain function
  • can enhance memories and change NT receptors
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78
Q

How does feedback at synapses work?

A
  • through NT autoreceptors located on the presynaptic terminal
  • autoreceptors are not always on same cell, just same type of cell
    -respond to NT released by presynaptic terminal
  • located on presynaptic membrane
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79
Q

What kind of synapse does synaptic feedback happen on?

A
  • typically ligand-gated metabotropic receptors
  • ligands can be ionotropic or metabotropic
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80
Q

What kind of feedback happens at synapses?

A
  • negative feedback to decrease NT released by the presynaptic terminal
  • positive feedback but that’s rare
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81
Q

What are examples of NT feedback at synapses?

A
  • dopamine
    -serotonin
    -norepinephrine (noradrenaline)
    -glutamate neurons
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82
Q

How does noradrenaline synaptic feedback work?

A
  1. presynaptic neuron releases NT (noradrenaline) into the synaptic cleft
  2. transmitter acts on receptors of the postsynaptic neuron, but also on autoreceptors typically inhibits further release of NT
  3. Activation of these autoreceptors typically inhibits further release of NT
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83
Q

How does synaptic plasticity occur through NT receptors on glial cells?

A

-glial cells are uniquely placed to mediate synaptic plasticity

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84
Q

How does synaptic plasticity occur through retrograde signals like endocannabinoids?

A

-originates from the postsynaptic terminal and goes back
- several types of messengers
-presynaptic neuron is usually GABAergic or glutamatergic
-may include anandamide and 2AG
- usually act on CB1 receptor to reduce (turn down) the opening of presynaptic v-gated Ca2+ channels
- mechanism for synaptic plasticity is NT receptors on glial cells

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85
Q

What type of receptors are endocannabinoids?

A

metabotropic

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86
Q

Are endocannabinoids autoreceptotrs?

A

no, this is a signal released by the post-synaptic neuron

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87
Q

Describe synaptic depression at neuromuscular junction?

A
  • some patterns of stimulation of presynaptic motor neuron result in a decrease in the size of EPSPs recorded in the muscle fiber (details vary by species and muscle)
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88
Q

How does synaptic depression at the Neuromuscular junction occur?

A
  • a pattern of NT release detected by Mach receptors in Schwann cells leading to feedback into the terminal to cause less NT release for Each AP
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89
Q

Why is a reduction in synaptic activity important?

A
  • a reduction in synaptic activity is important to minimize synaptic fatigue and rundown of NT
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90
Q

What can synaptic depression at the neuromuscular junction be blocked by?

A
  • preventing Ca increases within the perisynaptic glia
  • treating with Adenosine A1 receptor antagonist
  • treating with mACH antagonist
  • NOT by treating with nACHR antagonist
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91
Q

Where does the glial withdrawal reflex occur?

A
  • in aplysia
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92
Q

What is the glial withdrawal reflex?

A
  • learns to keep gills closed in the presence of stimulus
  • learned response
    -more time creates a stronger response
  • underlined by a simple monosynaptic circuit
  • results in a stronger reaction by the muscles but the actual change is occurring at the sensory to the MN synapse, not the neuromuscular junction
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93
Q

What is a neural circuit?

A
  • functional entity of interconnected neurons to accomplish some sort of task
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94
Q

What does the glial withdrawal reflex depend on?

A
  • a neuromodulator
  • depends on input from sensation modulatory interneuron L29 which forms a synapse onto the terminal of the sensory neuron
  • results in a stronger reaction by the muscles but the actual change is occurring at the sensory to the MN synapse, not the neuromuscular junction
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95
Q

What is presynaptic facilitation?

A
  • cellular/ synaptic mechanism that underlies sensitization of the gill withdrawal reflex (behavioral change
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96
Q

What does presynaptic facilitation with the gill withdrawal reflex cause?

A
  • causes a decrease in K+ conductance in the sensory neuron terminal (fewer K channels open) it then stimulates synaptic growth
  • longer refractory period
  • less K+ efflux
  • slower falling fase, less/ no undershoot, broader/ taller AP
  • more depolarization of the terminal membrane
  • could even build another synapse
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97
Q

What is the hippocampus necessary for?

A
  • learning, particularly spatial and short-term memory
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98
Q

What is LTP?

A
  • lasting potentiation of the EPSP
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99
Q

How can LTP be induced?

A

-strong depolarization of input one
- exact parameters vary depending on brain region
- there is input specificity
-NMDA can be essential

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100
Q

What inputs are unique to the hippocampus?

A
  • CA3 inputs to CA1 neurons
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101
Q

What does a strong depolarization for LTP require?

A
  • Postsynaptic CA1 neuron at the same time as pre-synaptic activity
  • synapses not active, when the postsynaptic neuron is strongly depolarized, will not experience LTP (example of input specificity) (hebbian plasticity)
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102
Q

How do NMDA receptors be responsible for LTP

A
  • ligand-gated by glutamate and voltage-gated y depolarization
  • only allow CA2+ in when it is bound by glutamate, the membrane is strongly depolarized, and glycine is present
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103
Q

what are the additional mechanisms underlying LTP?

A
  • increased effectiveness of AMPA receptors
  • increased number of AMPA receptors in the postsynaptic membrane
  • in some cases an increase in NT release and an increase in synaptic number
  • must be communication between postsynaptic terminal to presynaptic terminal
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104
Q

How does retrograde signaling induce plasticity via endocannabinoids?

A

-retrograde messenger is endocannabinoids
-cannabinoid receptors are metabotropic
- presynaptic and postsynaptic neurons are usually gababergic or glutamatergic
- can vary by sex
- usually act on CB1 receptor to reduce the opening of presynaptic v-gated Ca channels

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105
Q

Are endocannabinoids an example of autoreceptors?

A

no, this is a signal released by the postsynaptic neuron

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106
Q

What form of receptors are cannabinoids?

A

metabotropic

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107
Q

How do endocannabinoids vary by sex?

A
  • AEA is only in female hippocampus
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108
Q

What are examples of endocannabinoids?

A
  • anandamide, AEA, 2-AG
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109
Q

How long can LTP last?

A
  • over a year
  • very long time
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110
Q

How can LTP be mediated by structural changes?

A
  • more spines can grow
  • sex and cocaine affect nucleus accumbens core medium spine density
  • spine density is sexually dimorphic (females have enhanced response if they try but are less likely to try)
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111
Q

What is the effect of cocaine on spine density?

A
  • increased density in all genders
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112
Q

What are the methods of synaptic plasticity?

A
  • LTP and depression
  • morphological changes in dendrite. axon structure, including spines
  • genetic (changes in gene expression)
  • molecular/ neurochemical (chemical phosphorylation)
  • synaptic connections (new synapses, get rid of synapses, synaptic rearrangement)
  • intrinsic properties (changes in excitability)
  • neurogensis and neural recruitment
  • structural plasticity
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113
Q

What is plasticity history?

A
  • adult neural plasticity wasn’t widely accepted until 1970s
    -1793: malacrane est. training a dog increased amt of cerebellar folding
    -1890: william james proposed brain and its function aren’t fixed
  • 1894: ramon y cajal said adult brain is fixed but mental exercise leads to more dendrites
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114
Q

Why did it take so long for neural plasticity to be accepted?

A
  • neuron doctrine isnt formed until 1890s
  • synapse wasnt coined until 1897 (can’t name what you don’t know)
  • 19th centruy evidence showed brain had less individual variation in size than other organs and is less effected by body weight changes
  • thought adult brian was anatomially fixed bc they couldn’t see microscopic vidence
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115
Q

What was the plasticity paradigm shitf?

A

-early 1960s altman and DAS reported neurogenesis in rat hippocampus (canaries too later)
- LTP observed by Lomo in 1966
- 1963: Hubel and wisel discover ocular deprivation changes number of cortical neurons responding to light
-1961: rosenzweign said total ACHE activity higher in trained rats given harder problems and alll groups easier than rats given no training

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116
Q

What is structural plasticity?

A
  • brain’s ability to change its neuronal connections an anatomy
  • usually on microlevel (spines, dendrite shape, synapse, sometimes new neurons)
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117
Q

How do some insects have macrochanges like metamorphisis?

A
  • incorporates new neurons into CNS at highly divergent rates depending on species, brain region and developmental stage
  • often studies effect of various internal or external stimuli on brains anatomical recognition
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118
Q

What is the cortex?

A
  • outer layered layer of the brain
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119
Q

What does the nissil stain do?

A
  • shows cell bodies and ribosomes of neurons
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120
Q

What does the golgi stain do?

A

shows dendrites and axons of a random subset of neurons

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121
Q

What is neurogenesis?

A
  • process by which new neurons are formed in the brain via neural stem cells
  • crucial when an embryo is developing, but continues in certain brain regions throughout life
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122
Q

How does neurogenesis happen in adults?

A
  1. proliferation: new cells generated from stem cells
  2. survival of a portion of these new cells and their migration toward target areas
  3. terminal differentiaion into a neuronal or glial phenotype
  4. recruitment into the existing neuronal circuit
    - forms new synapses
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123
Q

What is neural recriuitment?

A
  • incorporation of new neurons into existing neural circuits and brain regions
  • happens in fetal and infant brains
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124
Q

What are the rat experiments?

A
  • altman and das in 1965
  • thymidine H3 labeled granule cells in rat hippocampus
  • used theymadine to show the amount of cell proliferation and neurogenesis
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125
Q

What is thymidine commonly used in?

A
  • cell proliferation assays
  • incorporatied into dividing cells proportionally to the amount of cell proliferation
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126
Q

Who completed the songbird experiments?

A
  • fernado nottebohn
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127
Q

What are the songbird’s experiements?

A

-paper is a brain for all seasons
- seasonal changes in song stereotype in canaries
- og song and then song falls apart and then a new modified song is created
- the final conclusion is that the rate of neurogenesis seems to dramatically differ between environment, brain regions, species, human being substantially lower than some other species

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128
Q

What is the evidence of the songbird experiment?

A
  • same technique as rats, but adults and longer time period after thymidine injection
  • direct link to behavior
  • clear evidence to hormone modulation
  • clear and careful differentiation of neurons, glia, and ventricular cell
  • electron microscopy and electrophysiology
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129
Q

How can adult brains undergo neurogenesis?

A
  • stem cells means its possible to trigger neurogenesis and neural recruitment
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130
Q

What are the cab driver experiments?

A
  • tested cab drivers since they have to navigate without maps
  • showed an increase in spatial learning
  • higher gray matter volume
  • not enough proof because correlation doesn’t equal causation
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131
Q

What makes neurons more lilkely to survive?

A
  • in the adult hippocampus they are more likely to survive if they are used
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132
Q

What are the misc. examples of neural plasticity?

A
  • nursing rats have smaller somatostatin from ventral side
  • neurons process smaller portions of skin meaning that precision and resolution are increased
  • cats with cut whiskers adapt
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133
Q

What is hemifeild neglect:?

A
  • unilateral attention deficit of right side of the brain
  • contralateral damage
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134
Q

What kind of damage does hemifeild neglect create?

A
  • contralateral
  • damage to right side displays on left
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135
Q

What causes hemifield neglect?

A
  • damage to righ parietal cortex
  • after a stroke you can regain some function
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136
Q

What is the hemingeild italy experiement?

A
  • patients were asked to imagine they were standing in different places and what they could see
  • shows this is a problem with perception, not sensation
  • since they were asked to recall it showed they had an internal field that couldn’t imagine the stuff on the left
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137
Q

What is sensation?

A
  • processing of info through senses
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138
Q

What is perception?

A
  • conscious experience of sensory info
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139
Q

What are the general principles of sensory systems?

A
  • have specialized receptor cells
  • has sensory transduction and sensory coding
  • has receptive field and response properties
  • The thalamus is a relay/ processing station
  • thalamus is main part of every sense except olfaction
  • primary sensory cortex
  • has orderly representation (like brain maps)
  • association cortex and higher-order processing
  • has parallel processing
  • descending regulation
    -adaptation
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140
Q

How is the blind spot of the eye created?

A

– optic nerve is where axons and blood vessels go to and from the retina and the rest of the CNS creating it

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141
Q

What are photoreceptors?

A
  • initial light receptors
142
Q

Why is the retina a layered structure?

A
  • light has to go thorugh several layers of cells before reaching photoreceptors
143
Q

What is the adaptation to having photoreceptors in the back of the eye?

A
  • very fragile so having them deeper protects them
  • helps to stabilize them
  • helps with faster transduction to optic nerve
144
Q

what is the retina made of?

A

rods and cones

145
Q

What are rods?

A

-structures with high sensitivity and low acuity
- processes black and white and dim light
-has rhodopsin
-usually used at night

146
Q

What are cones?

A
  • low sensitivity and high acuity
  • bright, light, color vision
  • 3 types of cones because of three types of opsin
147
Q

What is the difference between normal vision and color blindness ?

A
  • normal vision is trichromatic
    -red/green colorblindness is dichromatic
  • red/green can have loss of red or green cones
148
Q

What are the three types of opsin and their sensitivities?

A
  • blue cone: peak sensitivity: 430
  • green cone: peak sensitivity: 530
  • red cone peak sensitivity:560
149
Q

What are the parts of rods and cones?

A
  • synaptic terminal that releases glutamate and no axon
  • inner segments
  • outer segment
150
Q

What does the inner segments of rods and cones include?

A
  • nucleus
  • normal cell components
151
Q

What does the outer segment of the rods and cones include?

A

-has photoreceptors specialized for phototransduction
- cone also has membranous disks containing photopigment

152
Q

Where are rods and cones imbedded?

A
  • pointy/comb end
153
Q

What happens when photoreceptors see light

A

THEY HYPERPOLARIZE

154
Q

What is the cycle of photoreceptors in the dark?

A
  1. cGMP keeps Na+ chanels open
  2. inward Na+ current in outer segment (dark current)
  3. RMP is -30 - -40mV
155
Q

What is the cycle of photoreceptors in the light?

A
  1. cGMP levels decrease
  2. fewer Na+ channels open
  3. hyperpolarization
  4. graded decrease in NT release
156
Q

What happens to photoreceptors in the light and the dark?

A
  • no AP just graded potentials
  • NT release is like any other neuron, depolarization= release
157
Q

How does phototransduction happen in the dark?

A

-dark Na+ channels open mostly in outer segment is kept open by cGMP
- also K_ channels open mostly in the inner segment
- need more NaK+ pumps than typical to maintain ion gradients in comparison to the rest of the brain

158
Q

How does phototransduction happen in the light?

A
  1. photon absorbed by photopigment (rhodopsin in rods, three different opsins)
  2. causes change in conformation
  3. activates an intracellular messenger called transducin (g-protein)
  4. transducin activates a phosphodiesterase (PDE)
  5. PDE hydrolyzes cGMP reducing its concentration
  6. decreased cGMP levels result in the closing of Na channels
  7. loss of Na current results in hyperpolarization (toward ek of -70)
  8. hyperpolarization leads to less Ca influx leading to less glutamate released
159
Q

How is phototransduction turned off?

A
  • when light goes away
    1. transducin inactivates itself and also gets inactivated by arrestin
    2. Calcium based mechanisms are in place to re-open the Na channels even if light elvels don’t change
  • part of this is light adaptation
    -returns Vm to -35mv or so ( in part Ca through Na channels inhibits cGMP synthesis enxyme guantyl cyclase
160
Q

What are the types of neurons in the retina?

A
  • photoreceptors
    -interneurons
    -horizontal
    -bipolar
    -amacrine cells
  • retinal ganglion cells
161
Q

What is the basic neuronal circuit?

A
  • photoreceptors to bipolar cells to retinal ganglion cells to the thalamus via the optic nerve
162
Q

What is the visual field of one eye?

A
  • each visual point corresponds to a point of the retina
    -each photoreceptor in the retina has a receptive field
  • both eyes see almost all of the visual field not split into two halves
  • visual space maps onto the retina in an orderly manner
163
Q

What is the receptive field?

A
  • a portion of visual field within which a stimulus causes a change in activity
164
Q

What is the fixation point?

A
  • where we are looking which corresponds to the fovea
    -where we direct light when we are focusing
165
Q

What is the fovea?

A
  • related to the fixation point
    -layers are pushed to one side to allow a more direct path for light to get to the photoreceptors (less scattering of light
    -strong direct line for information
    -minimal light scattering
166
Q

What is the photorecepter RGC ratio in the fovea?

A

1:1

167
Q

Are there rods in the fovea?

A

no

168
Q

Are there blood vessels in the fovea?

A

no

169
Q

Do bipolar cells have a receptive field?

A

yes

170
Q

Does the fovea have a receptive field?

A

yes

171
Q

Do bipolar cells have an AP?

A

no

172
Q

What is the direct pathway?

A
  • info carried directly from photoreceptors to RGCs
  • not necessarily 1:1
173
Q

What is the indirect pathway?

A

-receive info indirectly from photoreceptors vis horizontal cells

174
Q

What do the indirect and direct pathways have in common?

A
  • usually have opposite effects on the bipolar cells
  • create a center-surround field organization for bipolar cells
175
Q

What are the two types of bipolar cells?

A
  • on center and off center
  • creats on center and off center RGCs
176
Q

What is the direct on center pathway cell cycle?

A
  1. light onto the center of the receptive field hyperpolarizes the photoreceptors
  2. photoreceptors release less glutamate (NT)
  3. less glutamate binds to mgluR6 then mgluR6 deactivation gate opens and then CGMP-gated Na+ channels which result in depolarization
    - glu is inhibitory
177
Q

How is the action of the NT determined?

A
  • by what receptors are present on the postysynaptic terminal
178
Q

What is the indirect pathway of an on center cell?

A
  1. light onto the surround of the receptive field hyperpolarizes the photo pathway
  2. photoreceptors release less glutamate (NT)
  3. horizontal cell is then hyperpolarized
  4. horizontal cell forms inhibitory gaba synapse on the center photoreceptor this hyperpolarizing the horizontal cell causing less gaba release at inhibitory synapse, depolarizing center photoreceptor
  5. the center photoreceptor then releases more glutamate
    6.since the synapse onto the bipolar cell is inhibitory, this hyperpolarizes the bipolar cell
    -horizontal- gaba
179
Q

Where do bipolar cells transmit info to?

A

RGCs

180
Q

What would the strongest stimulus on a RCG be?

A
  • a tiny dot of light or donut shape, but the visual field doesn’t work like this
  • actual strongest stimuli are those that have edges, contrast between a light area and a dark area
  • an edge in the right place is the best stimulus
181
Q

Do RCGS have center surround receptive cells?

A

yes

182
Q

How do bipolar cells create a a response?

A
  • bipolar cells form excitatory glutamatergic synaps on RCG, then the RGC express AMPA, NMDA, kainate receptors
    -RCGS make AP to get a signal to thalamus
183
Q

What are the types of RGCs?

A

-m-type
-p-type

184
Q

Describe p-type RCGs

A

-smaller cells
-smaller receptive field
-slower AP conduction
-slower adapting
-sensitive to light wavelentghs (cones have to go through light wavelengths)
- discerns stimulus forms and fine details - high resolution visual
-cells are sustained

185
Q

Describe M-type RCGS?

A
  • stimulus movement
    -low resolution vision
  • big
  • info from rods
  • causes a transient response
186
Q

Can M-type and P-type cells generate AP?

A

no

187
Q

Where do RCG axons project to through the optic nerve?

A
  • Lateral geniculate nucleus of thalmus (primary visual pathway
  • midbrain (superior colliculus)
  • hypothalamus (circadian clock)
188
Q

How do RCG axons go to the LGN, midbrain, and hypothalamus?

A
  • the optic nerve
189
Q

What does the lateral geniculate nucleus allow us to do?

A

percieve information

190
Q

What does the midbrain do?

A

maps that link points in space

191
Q

What part of the brain is sensitive to blue light waves?

A

the hypothalamus which controls circadian rhythm

192
Q

What is the primary visual pathway?

A

photoreceptors send dignals to bipolars which go to RGCs which then goes to the GLN in the thalamus, the primary visual cortex, the secondary visual cortex and then other associaiton cortexes

193
Q

Where is the thalamus located?

A

part of the diancephalon region

194
Q

Where do retinal inputs go?

A

the lateral geniculate nucleus of the thalamus

195
Q

Does information from the parts ot the RGCs mix?

A

no
(P and M are kept seperate)

196
Q

What type of cells are LGNs?

A

mononucleic

197
Q

How is info from the LGN organized, segregated, and processed?

A

parallel

198
Q

Wat is the primary visual pathway made of?

A

-rgc axons

199
Q

What RGC axons are part of the primary visual pathway?

A
  • eye
    -optic nerve
    -optic chiasm
  • stalk of pituitary gland
    -optic tract
    -brain stem
200
Q

What does the optic nerve do?

A

connects eye to optic nerve

201
Q

What does the optic chiasm do?

A

connects to optic tract

202
Q

Can Lateral RCGS cross the midline of the visual hemifields?

A

-no
- sends info to ipsilateral thalmus
-stays on the same side

203
Q

What are the visual hemifields?

A

-right and left vision fields with fixation point in the middle

204
Q

Do medial RCGs cross midline?

A
  • sends info to contralateral thalamus
  • criss crosses
205
Q

What part of the visual field is only seen by one eye?

A
  • only the peripheral edges, most is binocular
206
Q

Where does info from the right visual field go?

A

left cortex

207
Q

Where does info from the left visual field go?

A

the right cortex

208
Q

What broadmans area is the primary visual cortex?

A

17

209
Q

Where do outputs from the primary visual cortex go?

A
  • mapped back to LGN
  • if you modify the map you modify perception
    -signals will go up and down the map for more processing
210
Q

How many layers does the primary visual cortex have and describe the layers?

A
  • 6
  • neocortex
  • layers are striated
  • right eye input and left eye inputs are seperate in layer four because they are in the LGN
211
Q

What is the primary visual cortex?

A
  • part of the primary visual pathway
212
Q

How are the layers of the primary visual cortex monocular?

A

one eye at a time in mapped in layers but binocular overall

213
Q

What are ocular dominance columns?

A
  • across layers, cells within a column respond more strongly to 1 eye or the other
214
Q

What is orientation selectivity?

A
  • many neurons in primary visual cortex show a preference for bars of light of a particular orientation
  • response properties tend to get more complex as we progress from neurons in periphery to neurons in primary then the secondary association cortex
215
Q

What is the dorsal processing streams?

A
  • into parietal association cortex
  • critical for processing object potion
    -portions arranged in direction of motion columns
216
Q

How is the dorsal ventral processing stream organized?

A
  • direction of motion columns
217
Q

What is the dorsal processing stream critical for?

A

object motion

218
Q

What is the ventral parallel processing stream?

A
  • into temporal association cortex
  • few direction ion selective cells
219
Q

What is the ventral parallel processing critical for?

A

-object recognition including shape, color, and force perception

220
Q

What do the cells in Layer 4 of the primary visual cortex like?

A
  • bars of light of a particular orientation
221
Q

What is the oval of excitation with bordering regions of inhibition in the primary visual cortex?

A
  • kind of like on-off RCGS
  • much of this info comes from M-type RCGs
  • on a graph it peaks is what it prefers
    -has to do with orientation selectivity
222
Q

What is direction selectivity?

A

the response properties of some cortical neurons include a preference for movement in a particular direction (magnocellular stream)
- specific for one column of light moving in one direction

223
Q

How is directon sensitivity formed?

A

direction cells with adjacent fields synapse on a single simple cortical cell

224
Q

How is the somatosensory system divided?

A
  • 2 subsystems distinct in function and anatomy also different sensory receptor cells and pathways to cerebral cortex
  • mechanical and tactile
225
Q

What is the mechanical stimuli of the somatosensory system?

A

tough presssure vibration and joint position

226
Q

What is the tactile stimuli of the somatosensory system?

A
  • light, touch, vibration, and joint position
227
Q

What is proprioception?

A
  • position of body in space
228
Q

What is the somatosensory system made of?

A
  • specialized cells (somatosensory receptor neurons)
  • not proteins
229
Q

What do somatosensory receptor neurons do?

A

convert stimuli to the language of the nervous system

230
Q

What is sensory transduction?

A

-transduces mechanical signals to electrical signals

231
Q

What does sensory transduction depend on?

A
  • stimulus, quantity/ size, strength, frequency of AP
    (more Ap= stronger signal)
    -stimulus location (sensory receptor and cortex location)
  • stimulus quality and native type (sensory receptor and CNS neuron properties)
232
Q

What are the three functional categories of somatosensation?

A
  • mechanoreceptors
  • nocireceptors
    -thermoreceptors
233
Q

What are mechanoreceptors?

A

-touch, proprioceptive and tactile, a wide variety of specialized strucutres

234
Q

What are proprioception organs

A
  • muscle spindle, golgi tendon orgon, joint receptors
235
Q

How are the tactile mechanoreceptors different?

A
  • each tactile mechanoreceptor has a different response property and receptive field on the skin
  • every sensory neuron has different response properties
  • most sensory neurons have a receptive field
    -type of stimulus that excites them
  • axon diameter
  • threshold
  • adaptation
236
Q

What are response properties?

A

describes the stimulus to which a sensory neuron responds (what, where, etc)

237
Q

What is the somatosensory receptive field?

A
  • tactile somatosensory the receptive field is the area on the skin within which the appropriate stimulus will cause a depolarization of the neuron
238
Q

Why do somatosensory organs vary in their receptive fields?

A
  • if they didn’t we wouldn’t be able to distinguish a touch on the face from a touch on the hand
239
Q

What are nocireceptors?

A
  • pain, all free nerve endings
240
Q

What are thermoreceptors?

A
  • heat/cold and all free nerve endings
241
Q

What is phasic adaptation?

A

fast adaptation

242
Q

What is tonic adaptation?

A

slow adaptation

243
Q

Where does adaptation of somatosensory neurons occur?

A

-pacinion corpsucles

244
Q

What are pacinion corpsucles?

A
  • specialized structure around nerve endings that are responsible for adaptations because it contains somatosensory ion channels that detect membane stretching
245
Q

What are the three types of ion channels that happen iwth somatosensory adaptations?

A
  • some are sensitive to lipid stretching
  • some open when a cytoskeletal protein is moved
    -some open when a extracellular protein is moved
246
Q

What does a high threshold mean for somatosensory receptors?

A

high= less sensitive

247
Q

What does a low threshold mean for somatosensory receptors?

A
  • more sensitive
248
Q

What does axon diameter do to somatosensory cells?

A
  • changes conduction velocity, some types of info reach CNS quicker and then more later
249
Q

What is the size of a primary sensory receptor axon?

A

varies in size and in myelination

250
Q

What type of azons to pain and temperature have?

A
  • slower but there are two types of pain receptors because we have different types of pain
251
Q

What kind of axon whould a chronic, lasting, throbbing pain have?

A

-unmyelinated because it lasts longer

252
Q

What kind of axon would a sharp pain have?

A

myelinated

253
Q

What is two point discrimination?

A
  • ability to discern that two nearby objects touching the skin are truly two distinct points, not just one
  • describes a particular aspect of perception of touch, not general sensitivity to touch, acuity in terms of the location of touch
  • ACUITY NOT SENSITIVITY
254
Q

How is two point discrimination measured?

A
  • minimal interstimulus distance required to perceive 2 simultaneous stimuli as distinct
255
Q

What is the 2 point discrimination distance for fingertips?

A

2mm apart

256
Q

What is the 2 point discrimination distance for the forehead?

A

17mm apart

257
Q

What is the 2 point discrimination distance for the back?

A

40 mm apart

258
Q

What is the 2 point discrimination distance for the calf?

A

45 mm apart

259
Q

What factors affect 2 point descrimination?

A

receptor density
receptive field size (plasticity because more receptors can be added or subtracted)

260
Q

What is one segment of the spinal cord segment of the somatosensory pathway made of?

A

bipolar neurons

261
Q

What are the names for the peripheral somatosensory neurons?

A
  • primary
    -first order
  • sensory
    -afferent
262
Q

Are cell bodies ganglion or dorsal?

A
  • ganglion
  • the peripheral branch of the axon is a spinal nerve and the central branch of the axon is a dorsal root
263
Q

How are spinal cord segments defined?

A

doorsal and ventral roots

264
Q

What is the order of the spinal cord segments?

A

-cervical
-thoracic
-lumbar
-sacral

265
Q

How many cervical spine segments are there?

A

8

266
Q

How many thoracic spine segments are there?

A

12

267
Q

How many lumbar spine segments are there?

A

5

268
Q

How many sacral spine segments are there?

A

5

269
Q

What are dermatomes?

A

-territory innervated by a given spinal nerve
-reveals the segmental organization of our bodies

270
Q

What is the anterior head portion of our body mediated by?

A
  • cranial nerves which extend from brainstem, not spinal cord
271
Q

Is the dorsal column-medial lemnisical pathway contralateral or ipsilateral?

A

ipsilateral

271
Q

What is the dorsal column-medial lemnisical pathway?

A

-a mechanosensory pathway
-primary sensory afferents involved in mechanosynchronization make both local synapses and rostral projections

272
Q

Where do local synapses involved in spinal reflex go?

A
  • local synapses involved in spinal reflexes and rostral projections run in the ipsilateral dorsal column of the spinal cord and medulla
273
Q

Where do excitatory synapss on 2nd order turn contralateral?

A
  • medulla
    -this crossover is different then pain and temp
274
Q

Where do pain and temperature cross over signals?

A
  • crosses over in the spinal cord and ignores medulla
275
Q

Describe first order afferent signals?

A
  • cell bodies are in dorsal root ganglion
  • project to ipsilateral second degree afferent
276
Q

Describe 2nd order afferent signals?

A
  • cell bodies are in the spinal cord
    -project to contralateral thalamus
277
Q

Why do we care about where crossing over occurs?

A
  • because of spinal cord damage
278
Q

What is the difference between the mechanosensory and pain and temp pathways?

A

-its a matter of where the secondary sensory neuron has its cell body

279
Q

How are the mechanosensory and pain/temp pathways the same?

A

info in both pathways end up in contralateral to thalamus and then cerebral cortex

280
Q

Where is the cell body in the mechanosensory pathway?

A

medulla

281
Q

Where is the cell body for pain and temp pathway?

A

spinal cord

282
Q

where is the thalamus?

A

part of diancephalon

283
Q

Where does sensory info go?

A

-almost all sensory info passes through the thalamus and continues to the cerebral cortex in the thalamocortical projections

284
Q

Where do somatosensory secondary afferents synapse?

A
  • 2 regions of the thalamus
    -ventral posterior nucleus and intralaminar nuclei
285
Q

Where is the primary somatosensory cortex?

A
  • in the postcentral gyrus
    -part of the cerebral cortex that first receives sensory info
    -each sensory modality goes to a different region of the cerebral cortex?
286
Q

Does the primary somatosensory cortex have broadman’s areas?

A

yes

287
Q

What is a somatotopic map?

A

-simmilar to orderly representation of the visual field and retina in the primary visual cortex
somatosensory version of a cortical map

288
Q

Is the somatosensory map ipsilateral or contralateral of the body?

A

contralateral

289
Q

What is the somatotopic map of the visual cortex?

A

-retinotopic map

290
Q

What are cortical maps?

A
  • representational of the body, where the senses are perceived in the cerebral cortex
    -orderly (fingers are all near each other
291
Q

How is the somatosensory cortex organized?

A

-columnar
- like the visual cortex
- neurons within a column process info from the same region of the body

292
Q

Where do thalamocortic projections synapse onto neurons?

A
  • layer 4 of the primary sensory cortex (like the primary visual cortex)
293
Q

Does the somatosensory map only apply to humans?

A

no

294
Q

How does phantom limb syndrome work?

A

-there is a perception of pain even though the limb is gone
-doesn’t matter how this perception arises
- perception may get mixed so tough on the face could be perceived on the phantom limbs because of the somatotopic map

295
Q

Does phantom limb syndrome happen because of sensation or perception?

A

-perception causes pain
- sensation is gone when limb is lost

296
Q

What can people with phantom limb syndrome feel?

A
  • proprioception, nocireception, touch
297
Q

How can you treat phantom limb syndrome?

A
  • mirrorbox treatment
298
Q

How many somatosensory maps are there?

A

many maps for many different sensory cortices

299
Q

How are response properties of S1 neurons different than sensory receptors?

A

-response properties of S1 neurons tend to be more complex
- ex. some prefer movement while some prefer movement in a particular direction
- more cells in S1

300
Q

What does s1 stand for?

A

primary somatosensory

301
Q

What does s2 stand for?

A

secondary somatosensory

302
Q

Where are S1 signals sent and why?

A

-s1 signals are projected to s2 signals
- this continues the processing of sensory info including the association of it with other sensory modalities and motor and emotional processes

303
Q

Are there more ascending or descending projections in the somatosensory system?

A
  • descending
304
Q

What are descending projections?

A

-projections sent down from the brain to the motr output

305
Q

How are descending projections sent?

A

-sent using projections from the cortex to the thalamus, brainstem and spinal cord

306
Q

What is an example of a descending projection?

A

pain

307
Q

How is pain a descending projection?

A
  • endogenous pain system involves neurons in the PAG which express opioid at every level
    -also manufactures endogenous opioids
308
Q

What does PAG stand for?

A

periaqueductal gray

309
Q

What does opioids being expressed at every level of pain projection do?

A
  • affects tolerance, addiction and resistance
310
Q

What are endogenous opioids?

A

-neuropeptides
- endorphins
- intrinsic pain management

311
Q

What are tastants?

A
  • chemicals in food that are detected by taste buds which consist of special sensory cells
312
Q

What are odorants?

A

-airborne odor molecules
- nose version of tastants

313
Q

How do odorants work?

A
  • stimulate receptor proteins found on the cilia at the tips of sensory signals
314
Q

How do we taste the flavor of food?

A

-taste and smell messages converge

315
Q

What are the types of taste receptors on the tongue?

A
  • papillae
  • taste buds
    -taste receptor cells
  • basal cells and gustatory afferent axons
316
Q

What are papillae and what do they contain?

A

-papillae are the little taste-sensitive bumps on the tongue
- contain between 1-100s of taste buds

317
Q

What do taste buds contain?

A
  • between 50-150 taste receptor cells
  • basal cells
    -gustatory and afferent axons
318
Q

Is the tongue map real?

A

no. taste perception is intermixed with sensations coming from all regions of the tongue

319
Q

Why do people think the tongue map is real?

A

different parts of the tongue are more sensitive to certain flavors

320
Q

Why are different parts of the tongue more sensitive to flavors than other flavors?

A
  • different tastants will trigger depolarization and sometimes an AP in the taste cell
  • the particular transudtion method will vary in each taste cell and that’s what gives them more or less chemical specificity
  • most taste buds are sensitive to one basic taste
321
Q

When are you able to perceive a taste?

A

when the taste receptor cells reach threshold of an AP

322
Q

How many basic tastes are there?

A

-number is under debate
- we know there is sweet, sour, umami (protein), and maybe CO2

323
Q

What does synsepalum dulcificum?

A
  • causes sour foods to taste sweet by having miraculin (a glycoprotein) that binds and activates sweet taste preceptors at a low pH
324
Q

Where is the gustatory nucleus?

A

in the medulla

325
Q

How do gustatory afferents make it to the gustatory nucleus?

A

travel through at least three of the cranial nerves

326
Q

IS the central taste pathway contralateral or ipsilateral?

A

primary ipsilateral unlike vision

327
Q

Are taste info and tongue somatosensation the same thing?

A

no. two different processes

328
Q

How is the central taste pathway organized?

A

-we don’t know yet

329
Q

What is ageusis?

A

-loss of taste preception via a lesion of cortex or thalamus

330
Q

What is anosmia?

A

loss of olfaction

331
Q

What is broca’s aphasia?

A
  • impaired language production not due to impaired motor control
332
Q

What is wernickes aphasia?

A

impaired language comprehension despite normal auditory function

333
Q

What is asterognosia?

A
  • inability to recognize objects by feeling despite a normal senese of touch
    -can be limited ot the contralateral hand?
334
Q

What is hemifeild neglect?

A

-can’t see left half of visual field even though there is no visual damage

335
Q

What is prospagnosia?

A

-inability to recognize faces (faceblindness)

336
Q

What type of sensation is olfaction?

A

-chemical sensation

336
Q

How does olfaction occur?

A
  • odorants in mucus bind directly to (or can be shuttled via odorant binding proteins) to one of many receptor molecules located in the membranes of cilia
  • this then activates odorant-specific g-protein triggering an intracellular signaling pathway that causes membrane depolarization
337
Q

What is population coding?

A
  • different patterns of receptor cells respond to each odorant, the overall pattern of many cells provides specificity for each particular cell
  • similar to taste
338
Q

What does orderly representation in the olfactory bulb come from?

A

glomeruli

339
Q

What are glomeruli?

A
  • spherical structures inside of which around 25,000 primary olfactory axons converge
340
Q

How are glomeruli organized?

A
  • by odorant being etected
  • cortex organization is less clear
341
Q

What is the central olfactory pathways?

A

-usually thalamus to orbitofrontal neocortex
-unusual: direct projection to pyriform cortex (temporal lobe, in parahippocampal cortex) which plays a role in odor identification
- amygdala for social functions
entohinal cortex for memory

342
Q

What is the sensory receptor for autidory and vestibular systems?

A

hair cells

343
Q

Where are auditory system receptors?

A
  • in specialized organs that contain fluid like the chchlea
344
Q

How do auditory system receptors send signals?

A
  • movement causes waves in that fluid which causes movement of stereocilia on hair cells
  • movement in one direction causes depolarization and movement in the other direction causes hyperpolarization
    -K+ flows in which is why there is an unusually high amount of surrounding fluid
345
Q

What is the primary difference for auditory systems vs the other systems?

A

-auditory has more processing before cortex
- multiple regions process
- heavy descending projections

346
Q

How is the auditory info organized?

A
  • into tonotopic map
347
Q

How is context conveyed to the auditory system?

A

neuromodulators

348
Q

What is the association cortex?

A
  • most of cerebral cortex
  • expanded the most during the evolution of primates
  • has the highest levels of processing, so the most complex disorders

Neuro Biology (4 decks)

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