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Clinical Neuroscience Final > Clinical Neuroscience Final > Flashcards

Clinical Neuroscience Final Flashcards

1
Q

Which lobe of the brain is considered to be most closely associated with touch or pain sensation?

a. Temporal lobe
b. Frontal lobe
c. Occipital lobe
d. Parietal lobe

A

d. Parietal lobe

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2
Q

Which type of neuronal recording uses electrodes especially for finite position recording?

a. Invasive EEG
b. Multiple Unit Recording
c. Extracellular Unit Recording
d. Intracellular Unit Recording

A

a. Invasive EEG

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3
Q

Which deep brain structure is most responsible for emotional processing (e.g. stress or reward function)?

a. hypothalamus
b. amygdala
c. pituitary gland
d. hippocampus

A

b. amygdala

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4
Q

Which method is NOT considered an intracellular electrophysiology method?

a. patch clamping
b. sharp electrode
c. voltage clamping
d. multi-unit electrode array

A

d. multi-unit electrode array

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5
Q

Which is NOT considered a main division of the spinal cord?

a. cervical
b. sacral
c. ribcage
d. lumbar
e. thoracic

A

c. ribcage

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6
Q

Which of the following ions has a lower extracellular concentration compared to intracellular concentration in the mammalian neuron?

a. calcium (Ca2+)
b. potassium (K+)
c. chloride (Cl-)
d. sodium (Na+)

A

b. potassium (K+)

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7
Q

Which of the following is not true regarding an EPSP?

a. is a local depolarization of the postsynaptic membrane

b. stands for “excitatory postsynaptic potential”

c. brings the neuron away from the threshold potential

d. is induced by influx of positively charged ions

A

c. brings the neuron away from the threshold potential

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8
Q

In reference to the GHK equation, which of the following ions has the highest relative Pm across the membrane of a neuron at rest?

a. sodium ion
b. potassium ion
c. chloride ion
d. calcium ion

A

b. potassium ion

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9
Q

Which of the following is NOT correct in regards to neuropeptide synthesis, storage, release, or inactivation?

a. Pro-peptides are packaged in the Golgi apparatus

b. storage occurs in dense-core vesicles

c. post-synaptic effects can be excitatory or inhibitory

d. neuropeptide release occurs close to the target site

e. removal from the synapse involves enzymatic degradation via peptidases

A

d. neuropeptide release occurs close to the target site

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10
Q

Which of the following is NOT classified as a possible component for signal transduction?

a. G-protein-coupled receptor
b. enzyme-linked receptor
c. intracellular receptor
d. channel-linked (ligand-gated) receptor
e. ALL of the above are involved in signal transduction

A

e. ALL of the above are involved in signal transduction

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11
Q

Arrange the following components of chemical signaling in the CORRECT order.

receptor
effector molecule
signal
response

A

signal
receptor
effector molecule
response

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12
Q

Which of the following is NOT a key activator protein associated with nuclear signaling?

a. c-fos
b. cAMP response element binding (CREB) protein
c. nuclear receptors
d. all of the above are key activator proteins

A

d. all of the above are key activator proteins

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13
Q

Which of the following is NOT correct regarding activation/inactivation of kinases in signal transduction?

a. increase in second messenger concentration activates a kinase

b. kinases catalyze the phosphorylation of amino acids

c. kinases are held inactive by regulatory regions

d. kinases facilitate the removal of phosphate groups from target proteins

A

d. kinases facilitate the removal of phosphate groups from target proteins

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14
Q

Whereas most forms of short-term plasticity occur over a timescale of milliseconds to seconds, which of the following can occur over a timescale of seconds to minutes?

a. facilitation
b. augmentation
c. potentiation
d. depression

A

c. potentiation

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15
Q

Which of the following is NOT a location that is important for mediating proprioception?

a. muscle spindles
b. golgi tendon organ
c. joint receptors
d. all of the above are specialized mechanoreceptors for proprioception

A

d. all of the above are specialized mechanoreceptors for proprioception

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16
Q

Which of the following asserts that non-painful input can prevent pain sensations from traveling to the CNS (e.g. rubbing the site of injury)?

a. Gate Control Theory
b. The Dorsal Column-Medial Lemniscal System
c. Central Pain Theory
d. Peripheral Sensitization
e. The Anterolateral System

A

a. Gate Control Theory

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17
Q

Which of the following is NOT classified as a spinal reflex?

a. stretch reflex
b. all of the above are spinal reflexes
c. golgi tendon reflex
d. flexion reflex

A

b. all of the above are spinal reflexes

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18
Q

Which of the following has an important role in the bilateral control of “anti-gravity” extensor muscles?

a. corticobulbar tract
b. reticulospinal tract
c. vestibulospinal tract
d. corticospinal tract

A

c. vestibulospinal tract

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19
Q

Of the following, which TWO areas are important for the modulation of movement by regulating activity of upper motor neuronal circuits?

basal ganglia
cerebellum
motor cortex
brain stem
spinal cord

A

basal ganglia
cerebellum

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20
Q

true or false: nondeclarative memory is also referred to as “procedural” memory

A

true

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21
Q

true or false: long-term memory can last for an entire lifetime

A

true

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22
Q

true or false: priming cues are an example of declarative memory

A

false

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23
Q

which of the following is an example of negative reinforcement?

a. driving the speed limit after you just received a speeding ticket

b. leaving your house earlier so that you can make it to class

c. moving your car in response to someone honking their car horn

d. driving the speed limit to get a perfect score on your driving test

A

c. moving your car in response to someone honking their car horn

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24
Q

In the example of classical conditioning presented in class, which of the following is the conditioned stimulus?

a. saliva
b. dog food
c. whistle
d. the dog

A

c. whistle

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25
Q

Which of the following is NOT true about autism spectrum disorder (ASD)?

a. autism affects all ethnic and socioeconomic groups

b. boys are four times more likely to be diagnosed compared to girls

c. the measles, mumps, and rubella (MMR) vaccine increases the likelihood of ASD

d. ASD affects how a person acts and interacts with others, communicates, and learns

A

c. the measles, mumps, and rubella (MMR) vaccine increases the likelihood of ASD

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26
Q

Which of the following is not a likely cause or risk factor for ADHD?

a. alcohol or tobacco use during pregnancy

b. brain injury

c. genetics

d. low birth weight

e. lack of vitamin B1 (thiamine)

A

e. lack of vitamin B1 (thiamine)

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27
Q

Which of the following criterion for Major Depressive Disorder (MDD) is required for a DMS diagnosis?

a. diminished interest or pleasure in activities most of the day

b. diminished ability to think/concentrate

c. fatigue or loss of energy

d. significant weight change

A

a. diminished interest or pleasure in activities most of the day

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28
Q

Reduction of which of the following neurotransmitters is NOT consistent with the Monoamine Hypothesis of depression?

a. acetylcholine
b. norepinephrine
c. dopamine
d. serotonin

A

a. acetylcholine

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29
Q

true or false: chronic stress can be MALADAPTIVE, whereas acute stress can be ADAPTIVE.

A

true

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30
Q

Which of the following mechanisms makes Lithium an effective medication for the treatment of bipolar disorder?

a. enhances apoptotic processes through activation of the glycogen synthase kinase 3 enzyme

b. decreases brain-derived neurotrophic factor (BDNF).

c. reduces inhibitory (GABA) neurotransmission

d. reduces excitatory (DA and glutamate) neurotransmission

A

d. reduces excitatory (DA and glutamate) transmission

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31
Q

Which of the following are possible mediators of Anxiety Disorders?

a. behavioral genetics
b. endocrine changes
c. corticolimbic circuit dysfunction
d. only A and C.
e. all of the above

A

e. all of the above

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32
Q

Which of the following is NOT a category of anxiety disorders?

a. phobias
b. post-traumatic stress disorder
c. obsessive-compulsive disorder
d. panic disorders
e. all of the above are classified as anxiety disorders

A

e. all of the above are classified as anxiety disorders

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33
Q

Select which physiological changes (3 CORRECT ANSWERS IN TOTAL) are most often associated with emotions.

a. tinnitus (i.e. ringing in the ears)

b. change in heart rate

c. hyper-excitability of muscles

d. gut motility

e. change in skin temperature

A

b. change in heart rate
d. gut motility
e. change in skin temeprature

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34
Q

Which of the following is/are effect(s) of Kluver-Bucy Syndrome? (SELECT ONLY 1 ANSWER)

a. Inappropriate Tameness
b. Hyperorality
c. Hypersexuality
d. Answers A and B only
e. all of the above

A

e. all of the above

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35
Q

Which of the following individuals is the current Director if the National Institute on Drug Abuse

a. Nora Volkow, Ph.D.
b. Phineas Gage, Ph.D.
c. Brenda Milner, Ph.D.
d. Santiago Ramón y Cajal, Ph.D.
e. George Koob, Ph.D.

A

a. Nora Volkow, Ph.D.

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36
Q

Which of the following does NOT directly influence the subjective “reward value”?

a. reward amount
b. individual resting state
c. reward type
d. reward probability
e. individual satiety state

A

b. individual resting state

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37
Q

How many genes are expressed exclusively in the nervous system?

A

6000 genes

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38
Q

How many genes are expressing all cell and tissue types?

A

8000 genes

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39
Q

What allows for increased diversity?

A

splice variants

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40
Q

Camillo Golgi

A
  • reticular theory
  • staining technique with silver salts
  • Golgi apparatus
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41
Q

Santiago Ramón y Cajal

A
  • neuron doctrine
  • described micro-organization of the nervous system
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42
Q

Charles Sherrington

A
  • neuron doctrine
  • studied the transfer of electrical signals
  • coined the term “synapse”
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43
Q

What is the rough ER known for?

A

synthesis of proteins

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44
Q

What is the smooth ER known for?

A

synthesis of lipids

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45
Q

What is the Golgi Apparatus known for?

A

packages proteins

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46
Q

What is the mitochondria known for?

A

produce energy via oxidative phosphorylation

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47
Q

How many neurons are in the human brain?

A

90 billion

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48
Q

What is the most common neuronal classification?

A

multipolar

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49
Q

what is intra-neuronal communication?

A

the action potential travels down the length of the axon away from the nerve terminal

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50
Q

what is the inter-neuronal communication?

A

the presynaptic nerve terminal comes in close apposition to another postsynaptic neuron, releasing transmitter in the the synapse

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51
Q

What are the functions of glial cells?

A

-support
nutrition
maintain ionic (K+, NT) concentrations
tight junction of the BBB
-insulation via myelination
-scavenge debris
-axonal guidance

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52
Q

which macroglia are in the CNS?

A

oligodendrocytes

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53
Q

which macroglia are in the PNS?

A

Schwann cells

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54
Q

What do astrocytes do?

A

structural support, nutritional supply, maintain ionic balance

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55
Q

what do microglia do?

A

scavenge debris, immune response

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56
Q

What are glial stem cells

A

self-renewing, multipotent cells located next to the ventricles

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57
Q

what are ependymal cells

A

line the ventricular system of the CNS

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58
Q

what do radial glia do

A

guide neuronal migration and pathway formation

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59
Q

what is the role of the frontal lobe?

A

personality characteristics, decision-making, movement

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60
Q

what is the role of the parietal lobe?

A

spatial awareness, pain sensation, touch

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61
Q

what is the role of the occipital lobe?

A

vision

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62
Q

what is the role of the temporal lobe?

A

short-term memory, speech, smell

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63
Q

what is the role of the hypothalamus?

A

homeostatic processes, temperature, hunger, thirst

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64
Q

what is the role of the pituitary gland?

A

hormone (anterior: ACTH, FHS, GH, LH; posterior: oxytocin, ADH)

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65
Q

what is the role of the amygdala?

A

emotion, stress, reward

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66
Q

what is the role of the hippocampus?

A

learning, memory

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67
Q

what is the role of the pineal gland?

A

melatonin

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68
Q

What are the names of the 3 meninges?

A

dura mater, arachnoid mater, pia mater

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69
Q

describe the dura mater

A

(tough mother)
thick, tough, inextensible; is innervated and has vasculature

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70
Q

describe the arachnoid mater

A

resembles a web’ forms subarachnoid space with CSF; no vasculature/inntervation

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71
Q

describe the pia mater

A

(tender mother)
thin, tightly adheres; follows brain contours; highly vascularized

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72
Q

What is the purpose of the spinal cord?

A

-control body mvmts and function, report sensory info to the brain, manage reflexes (i.e. involuntary mvmts)

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73
Q

is the dorsal or ventral horn known for sensory?

A

dorsal

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74
Q

is dorsal column ascending, descending, or both

A

ascending

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75
Q

name the types of intracellular recording

A

patch clamping, sharp microelectrode, voltage clamping, current clamping

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76
Q

name the types of extracellular recording

A

single unit recording, multi-unit electrode array

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77
Q

what is an action potential?

A

Changes in resting membrane potential in relation to K+ concentration

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78
Q

who developed the action potential?

A

Hodgkin and Katz

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79
Q

describe intracellular unit recording

A

***inside a neuron
an intracellular

microelectrode records the membrane potential from one neuron as it fires

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80
Q

describe a multiple-unit recording

A

***measure rate of firing/action potentials; larger electrode picks up potentials form many nearby neurons

a small electrode records the action potentials of many nearby neurons. these are added up and plotted.

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81
Q

describe extracellular unit recording

A

**near a neuron

an extracellular microelectrode records the electrical disturbances that is created each time an adjacent neuron fires

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82
Q

describe an invasive EEG recording

A

***finite position recording

a large implanted electrode picks up general changes in electrical brain activity

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83
Q

what is GCamp3

A

calcium indicator

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84
Q

describe calcium imaging

A

optically measure calcium
*** in vivo, freely moving objects

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85
Q

describe fiber photometry

A

detect bulk activity changes in neuronal populations

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86
Q

describe miniscope

A

visualize neuronal activity at single-cell level

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87
Q

what is immunohistochemistry

A

antibody-based detection of an antigen in tissues

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88
Q

what is immunocytochemistry

A

antibody-based detection of an antigen in cells

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89
Q

what is immunofluorescence

A

detection method, during which antibody binding to an antigen is visualized using a fluorophore

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90
Q

what is in situ hybridization

A

a means of identifying where mRNAs are present in fixed tissue samples

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91
Q

what is heavy metal staining

A

electron microscopy to visual subcellular structures

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92
Q

what are the three bacterial opsins used for single-component optogenetics

A

bacteriorhodopsin, halorhodopsin, channelrhodopsin

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93
Q

describe optogenetics

A

genetic and optical methods to activate or inhibit neuronal events

transmembrane ion conductance

tool for mapping functional activity

microbial opsin genes and microbiral rhodopsin proteins

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94
Q

are neurons strong or poor conductors of electricity?

A

poor!

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95
Q

what is electrochemical equilibrium?

A

when there is no net flux of ions; a balance between the electrical and chemical gradients

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96
Q

what is the Nernst equation

A

used to calculate the equilibrium potential for a single ion based on its concentration difference across the membrane

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97
Q

what is learning

A

process through which new info is acquired by the nervous system (i.e. cellular and molecular plasticity of neuronal connections)

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98
Q

what is memory

A

recovered experiences that can be brought into consciousness and/or manifest as changes in behavior

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99
Q

who developed forgetting?

A

Hermann Ebbinghaus

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100
Q

what is the forgetting curve?

A

decline of memory retention in time; “strength” of memory

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101
Q

what is the spacing effect?

A

encoding of info via spaced repetition vs massed presentation

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102
Q

what is declarative memory?

A

material that is available to consciousness and can be expressed by language

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103
Q

what is nondeclarative (procedural) memory

A

material NOT available to consciousness, at least not in any detail

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104
Q

describe immediate/sensory memory

A

ability to hold onto ongoing experience for approximately one second

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105
Q

describe short-term/working memory

A

ability to hold & manipulate info for seconds to minutes while it is being used to achieve a particular goal or process

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106
Q

describe long-term memory

A

retaining info in a more permanent form of storage for days, week, or even a lifetime

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107
Q
A
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108
Q

what is consolidation

A

the process by which info is transferred into LTM at the cellular level

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109
Q

describe synaptic/cellular consolidation

A

rapid biochemical/morphological changes to the neuronal network supporting new memory

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110
Q

describe systems consolidation

A

gradual reorganization of hippocampal-dependent memory across a cortical network

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111
Q

what is BF Skinner known for?

A

behaviorism
- operant conditioning
- schedules of reinforcement

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112
Q

describe positive punishment

A

***punishment
-adding something unpleasant like time out

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113
Q

describe negative punishment

A

removing something valued or desired
-penalty

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114
Q

describe positive reinforcement

A

adding something valuable or desirable
- gold star

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115
Q

describe negative reinforcement

A

avoiding something unpleasant
-taking advil before wax to avoid pain

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116
Q

what is priming

A

Change in the processing of a stimulus due to a previous encounter with the same or related stimulus with/without conscious awareness of the original encounter

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117
Q

Who tested the subject that was unable to forget?

A

Alexander Luria

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118
Q

Describe patient H.M.

A

suffered from epilepsy, so had his medial temporal lobes and bilateral hippocampus removed
-induced anterograde amnesia
**preserved semantic memory, and procedural memory, but has poor long-term memory and had temporally-graded retrograde amnesia

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119
Q

what is amnesia

A

loss of memories. may be transient, meaning for a short time.

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120
Q

what are the causes of amnesia?

A

normal aging, brain injury, alcohol or substance abuse

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121
Q

what is amnesia a sign of?

A

alzheimers, Lew body dementia, Creutzfeldt-Jakob disease

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122
Q

what is semantic priming?

A

improved processing of a stimulus after exposure to one that has a related meaning

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123
Q

what is subliminal priming?

A

stimuli use to influence a person’s cognitive processing without that person being aware of the prompts

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124
Q

what is repetition priming?

A

a stimulus and response are paired repeatedly; experience

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125
Q

what is perceptual priming?

A

based on the form of the stimulus and is enhanced by the match between the early and later stimuli

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126
Q

what are symptoms

A

manifestation of disease apparent to the patient themselves
–subjective

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127
Q

what are signs?

A

manifestation of disease that is perceptible to the physician
–objective

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128
Q

what is cerebral localization?

A

precise science of predicting which regions of the brain are damaged or malfunctioning

based on careful examination of a patient’s signs and symptoms

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129
Q

do all neurodegenerative diseases lead to disability and death?

A

yes

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130
Q

motor disorders of basal ganglia

A

parkinsons and huntingtons

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131
Q

motor disorders of cerebellar ataxias

A

creutzfeld-Jakob disease

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132
Q

what are the 3 principle features of alzheimer’s disease?

A

neurofibrillary tangles
AB plagues
loss of neurons

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133
Q

where does alzheimers cause the most changes in the brain?

A

neocortex
limbic system

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134
Q

what is the most common form of dementia?

A

alzheimer’s

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135
Q

what does schizophrenia mean?

A

splitting of the mind

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136
Q

when is schizophrenia diagnosed?

A

after the first episode of psychosis

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137
Q

what are positive symptoms of schizophrenia?

A

overt symptoms that should not be present
-hallucinations
-delusions
-disorganized thoughts
-movement disorder

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138
Q

what are negative symptoms of schizophrenia?

A

lack of characteristics that should be present
-reduced speech
-lack of emotional and facial expression
-diminished ability to begin or sustain activities
-less pleasure
-social withdrawal

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139
Q

what are cognitive deficits of schizophrenia?

A

difficulties with following aspects of cognition can make it hard to live a normal life or earn a living
-memory
-attention
-planning
-decision making

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140
Q

what is Alogia?

A

reduced speech

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141
Q

what is affective flattening?

A

lack of emotional and facial expression

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142
Q

what is avolition

A

diminished ability to begin or sustain acitivites

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143
Q

what is anhedonia

A

decreased ability to find pleasure in everyday

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144
Q

what is asociality

A

social withdrawal

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145
Q

How to diagnose schizophrenia?

A

2+ symptoms for at least one month
1. delusions
3. hallucinations
3. disorganized speech

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146
Q

what is the original dopamine hypothesis for schizophrenia?

A

hyperactive dopamine transmission results in schizophrenic symptoms

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147
Q

How does inhalation change drug pharmacokinetics?

A

-similar peaks effects by inhalation vs injection
-achieved at a lower overall plasma level after inhalation
-achieved on rising phase (much quicker)
-plasma levels decline more rapidly after inhalation
-recipe for more frequent re-dosing, potentially binging

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148
Q

what are some criteria for SUD in DMS5

A

defense against increasing workload, tolerance, continued drug taking with aversive stimuli or alternate reinforcers

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149
Q

where are the endocannabinoid receptors in addiction-related circuitry?

A

CeNA, VTA, Nuc.Accum

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150
Q

What are the physiological changes associated with emotions?

A

-heart rate
-blood flow
-skin temp
-sweating
-piloerection
-pupil size
-gut motility

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151
Q

What are symptoms of Kluver-Bucy syndrome

A

-inappropriate tameness
-hyperorality
-hypersexuality

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152
Q

what are the components of limbic system

A

-cingulate gyrus
-hippocampus
-amygdala
-hypothalamus
-thalamus

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153
Q

what does the corticolimbic circuit do?

A

recognizes danger and organizes adaptive behavioral responses

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154
Q

what does the corticostriatal circuit do?

A

involved in reward learning and goal-oriented behavior

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155
Q

what is the function of cingulate gyrus

A

-regulates emotion and pain
-conscious response to unpleasant experiences
-negative learning

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156
Q

what is the function of hippocampus

A

memory formation

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157
Q

what is the function of amygdala

A

fight-or-flight
fear and other complex emotions
regulates emotional responses
emotional memory

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158
Q

what is the function of hypothalamus

A

regulates autonomic functions
fighting, fleeing, feeding, fornicating

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159
Q

what is the function of the thalamus

A

sensory info
alertness/awareness

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160
Q

What neurotransmitters are involved in psychosis?

A

dopamine, glutamate, GABA

161
Q

what are chemogenetics?

A

designer receptor exclusively activated by designer drugs

162
Q

what is CRISPR/Cas9?

A

clustered regularly interspaced short palindromic repeats

163
Q

what is GWAS?

A

genome wide association studies
-data collections
-genotyping
-quality control
-imputation
-association testing
-meta-analysis
-replication
-post-GWAS analysis

164
Q

PET scan

A

use of radioactive tracers

165
Q

what are the advantages of fMRI?

A

good spatial resolution
shows activity in the brain based on bloodflow

166
Q

what are the disadvantages of fMRI?

A

poor temporal resolution
time-consuming
subjects cant move

167
Q

What are the advantages of MEG scan?

A

noninvasive
great spatial resolution of cortical regions
good temporal resolution

168
Q

what are the disadvantages of MEG?

A

very expensive
time consuming

169
Q

what are the advantages of EEG?

A

good temp res
cost effective
animal subjects

170
Q

what are the disadvantages of EEG?

A

poor spatial red
limited to cortical activity

171
Q

What are Event-related potentials?

A

time-locked to sensory, motor, or cognitive events
summed activity of post synaptic potentials

172
Q

What is transcranial magnetic stimulation?

A

brief, strong magnetic field that alters. neural activity
activate/deactivate brain regions

173
Q

What is transcranial magnetic stimulation used for?

A

treatment-resistant depression
anxiety
Parkinson’s disease

174
Q

How do contrast x-rays work and what’re they used for?

A

inject something that absorbs x-rays differently than tissue

medical purposes

175
Q

How do ct scans work and what’re they used for?

A

x-rays of the brain from multiple angles

primarily medical settings

176
Q

How do pet scans work and what’re they used for?

A

radiolabel for a substance (usually glucose) of interest and scan brain for that radioactivity

brain activity

177
Q

How does an mri work and what’re they used for?

A

magnetic and radio waves to map location of water, fat, tissues

brain structure

178
Q

How do fMRIs work and what’re they used for?

A

alignment of hydrogen molecules BOLD signal: blood oxygen level dependent

brain activity

179
Q

How do MEG scans work and what’re they used for?

A

changes in magnetic fields on the scalp shows underlying neural activity

neuronal activity

180
Q

what is a neuron’s resting membrane potential?

A

-70mV

181
Q

which ion is most concentrated intracellulary?

A

potassium

182
Q

which ions are commonly concentrated extracellularly?

A

sodium, chloride, calcium

183
Q

What is the function of NA/K pump (ATPase)

A

to keep membrane “battery” charged
maintains appropriate ionic concentrations

184
Q

what is the rule about Na And K?

A

3 Na+ out 2K+ in
ATP is required against concentration gradients

185
Q

what would cooling do to membrane potentials?

A

mildly deprolarize

186
Q

what would heating do to membrane potentials?

A

mildly hyperpolarize

187
Q

What is the Goldman-Hodgkin-Katz equation used for?

A

when the membrane is simultaneously permeable to several ions

188
Q

What is an EPSP

A

a local depolarization of the postsynaptic membrane

brings the neuron closer to the threshold potential

can be induced by influx of positively charged ions

189
Q

What is an IPSP

A

a local hyperpolarization of the postsynaptic membrane

brings the neuron away from the threshold potential

can be induced by influx of negatively charged ions

190
Q

at rest, the neuronal membrane is selectively permeable to ___?

A

K+

191
Q

what is an action potential?

A

an electrical signal generation by nerve cells and arises from changes in membrane permeability to specific ions

a rapid, brief reversal of membrane potential

result of voltage and time-dependent changes in membrane permeability

192
Q

What is excitotoxicity

A

changes in glutamate homeostasis during psychostimulant addiction

193
Q

what is the voltage clamp method used for?

A

to determine the membrane conductance for Na and K

time and voltage dependent

194
Q

what is saltatory conduction?

A

depolarization occurs only on bare axon between myelin segments and not along the entire axon surface

195
Q

what is an example of a myelination disorder?

A

multiple sclerosis

196
Q

what are some examples of ion channels disorders?

A

epilepsy
febrile seizures
migraine
cerebral ataxia

197
Q

what is multiple sclerosis?

A

a disabling disease of the nervous system resulting from a disruption neural communication

198
Q

what causes MS?

A

autoimmune disease

“bystander effect” of response to clearing a viral infection of oligodendrocytes

199
Q

what are ways to improve neuronal signalling?

A

increase diameter of axon

myelin

200
Q

where are voltage-gates Na+ channels localized?

A

nodes of ranvier

201
Q

what are examples of neurotoxins?

A

tetrodotoxin
alpha toxin
beta toxin

202
Q

describe alpha toxin

A

derived from scorpions

slow inactivation of Na+ channels, reducing APs

paralysis and arrhythmia

203
Q

describe beta toxins

A

derived from scorpions

negative shift of the voltage dependence of Na+ channel

fast contraction paralysis

204
Q

describe tetrodotoxin

A

potent blocker of voltage-gated Na+ channels

205
Q

what is SCN9A?

A

sodium voltage-gated channel

responsible for making NaV1.7 on nociceptors

a molecular gatekeeper of pain detection at peripheral nociceptors

206
Q

what is episodic ataxia type 1?

A

single gene mutation: KCNA1

autosomal dominant

loss of function mutation

207
Q

what are symptoms of episodic ataxia type 1?

A

brief attacks of incoordination, dominated by gait ataxia

neuromyotonia

myokymia

208
Q

severe myoclonic epilepsy of infancy

A

Na+ channel mutations

209
Q

benign familial neonatal convulsion

A

K+ channel mutations

210
Q

childhood absence epilepsy

A

Ca2+ channel mutations

211
Q

what is the most common type of synapse?

A

axodendritic

212
Q

What key experiment was done to support idea of chemical synapses?

A

Otto Loewi

stimulation of the Vagus nerve attached to a donor’s heart caused the heart to slow. A solution from donor’s heart was allowed to flow to a secondary recipient heart, slowing that heart rate as well.

***vagusstoff now known as acetylcholine

213
Q

How are neurotransmitters stopped?

A

diffusion
removal by glial cells
enzyme degradation
reuptake into presynaptic terminal

214
Q

what are the two primary NT release modes?

A

full fusion and kiss and run

215
Q

what is full fusion?

A

terminal and vesicle membranes fully merge and flatten

requires full exocytosis

216
Q

what is kiss-and-run

A

vesicle content exits through a fusion pore

quickly disconnects after NT release

217
Q

what is myasthenic syndrome

A

synapse disorder

abnormal transmission at NMJ leading to weakness and fatigability of skeletal muscles

218
Q

what is botulism?

A

synapse disorder

caused by a clostridium botulinum toxin, can impair NT release at skeletal and smooth muscles leading to flaccid paralysis

219
Q

what is tetanus?

A

synapse disorder

caused by clostridium tetani toxin, can impair inhibitory control of primary motor neurons leading to spastic paralysis

220
Q

what is alpha-latrotoxin?

A

synapse disorder

from black widow spider venom induces exhaustive release of neurotransmitters from vertebrate nerve terminals

221
Q

what presynaptic proteins are used in mobilization?

A

synapsins
CaMKII

222
Q

what presynaptic proteins are used in fusion?

A

synaptotagmins
SNAREs

223
Q

describe ligand-gated ion channels

A

direct, fast transmission

224
Q

describe g protein-coupled receptors

A

indirect, slow activation, long-last effects
impacts intracellular biochemistry

225
Q

how is vesicle mobilization done?

A

vesicles held in a reserve pool by synapsin

CaMK-II phosphorylates synapsin to release vesicles

226
Q

what presynaptic proteins are used in endocytosis

A

NSF & SNAP
Clathrin

227
Q

what presynaptic proteins are used in docking/priming

A

SnaRe proteins
–syntaxin, SNAP-25
synaptobrevin

228
Q

what is the rate-limiting step in vesicular release?

A

docking/priming

229
Q

how to small molecules and peptides differ in synthesis?

A

SM: enzymatic, in final form, in nerve terminal
peptide: propeptide, in soma, axonal transport to NT

230
Q

how to small molecules and peptides differ in storage?

A

sm: small, clear-core vesicles; vesicle recycling
peptide: large, dense-core vesicles; no vesicle recycling

231
Q

how to small molecules and peptides differ in release?

A

sm: close to target site
peptide: target often distant

232
Q

how to small molecules and peptides differ in inactivation?

A

sm: reuptake, enzymatic degradation
peptide: enzymatic degradation

233
Q

how to small molecules and peptides differ in synthesis location?

A

sm: cytosol of presynaptic terminal
peptide: rough ER and golgi

234
Q

how to small molecules and peptides differ in speed of action?

A

sm: fast
peptide: slow

235
Q

what is the rate-limiting step in ACh synthesis?

A

choline uptake
ChAT

236
Q

what are Sarin, VX, insecticides

A

irreversible AChE inhibitors

237
Q

what are Aricept and Exelon?

A

reversible AChE inhibitors

238
Q

what modulators block nACh?

A

a-bungarotoxin (snake)
alpha-conotoxin (snail)

239
Q

what modulators stimulate nACh?

A

betal nut and nicotine

240
Q

What is myasthenia gravis?

A

chronic autoimmune disorder affecting voluntary muscles of the body

antibodies destroy ACh

241
Q

what is oxycodone?

A

potent opioid analgesic

schedule II controlled substance

m and k opioid receptor

242
Q

what is fentanyl?

A

potent opioid analgesic

schedule II

243
Q

what are examples of exogenous cannabinoids?

A

CBD
THC

244
Q

who discovered cannabis sativa?

A

Carl Linnaeus

245
Q

who discovered cannabis indica

A

jean-baptiste lamarck

246
Q

what drug schedule is cannabis?

A

schedule I

247
Q

what is psilocybin?

A

a naturally occurring psychedelic compound found in magic shrooms

treatment for major depression and anxiety

248
Q

what are some effector proteins?

A

adenylyl cyclase and phospholipase c

249
Q

what are some second messengers

A

cAMP, diacylglycerol, IP3

250
Q

what are some late effectors?

A

protein kinase A, protein kinase C, Ca2+ release

251
Q

what is a kinase?

A

an enzyme that adds phosphate groups to other molecules

252
Q

what is phosphatase?

A

an enzyme that removes phosphate groups to other molecules

253
Q

what are the steps of activation/inactivation of G proteins?

A
  1. inactive–> GDP bound
  2. exchange GDP for GTP
  3. active–> GTP bound
  4. hydrolyze GTP into GDP
254
Q

what are the Ca2+ binding proteins

A

calbindin and calmodulin

255
Q

what are 3 key activator proteins?

A

CREB
nuclear receptors
c-fos

256
Q

What is the rate limiting step for catecholamine synthesis?

A

TH

257
Q

who coined the phrase “cells that wire together fire together”

A

Donald Hebb

258
Q

what is Hebb’s organization of behavior?

A

the 1st comprehensive theory of how complex psychological phenomena might be produced by brain activity

259
Q

what are sensitization and habituation?

A

changes in behavior

260
Q

describe synaptic facilitation

A

increase calcium due to quick AP succession
increase vesicle release
10s of milliseconds
synaptotagmin 7

261
Q

describe synaptic augmentation

A

increase calcium-induced fusion
enhance SNARE protein –Munc-13
increase vesicle release
few seconds

262
Q

describe synaptic potentiation

A

increase calcium-induced fusion
protein kinases
increase vesicle release
10 sec to minutes

263
Q

describe synaptic depression

A

depletion of vesicles due to high release rate
decrease vesicle release
100s of milliseconds

264
Q

describe long-term sensitization

A
  1. PKA phosphorylates CREB
  2. pCREB activates tf’s
  3. ubiquitin hydrolase
265
Q

what type of signaling is used to convey sensation to brain

A

afferent signalling

266
Q

sensory receptors are ____

A

organs!

267
Q

describe receptor potentials

A

–pasive, electrotonic
–are NOT all-or-none responses
–can sum
–may trigger APs

268
Q

proprioception receptor type

A

muscle spindle
1a, II
large diameter

269
Q

touch receptor type

A

merkel, meissner, pacinian, riffini
A beta
6-12 micro m diamter

270
Q

pain, temp receptor type

A

free nerve endings
a delta
1-5 micro m diameter

271
Q

slow adapting

A

merkel and ruffini

272
Q

fast adapting

A

meissner and pacinian

273
Q

small receptive field

A

merkel
meissner

274
Q

large receptive field

A

pacinian
ruffini

275
Q

meissner corpsucle

A

movement of across the skin

276
Q

merkels disc

A

shape and texture

277
Q

pacinian corpuscle

A

detect vibration through objects

278
Q

riffini endings

A

stretch of skin

279
Q

Piezo 1 and Piezo 2

A

mechanosensitive ion channels
proprioception

ardem patapoutian

280
Q

what is responsible for mechanosensory system

A

dorsal column/ medial lemniscal system

281
Q

what is responsible for pain and temp

A

anterolateral system

282
Q

Ia muscle fibers

A

large myelinated sensory axons, rapidly adapt; respond to changes in muscle length
myelinated

283
Q

II muscle fibers

A

sustained responses to constant muscle lengths; provides sense of muscle position when still
myelinated

284
Q

1b muscle fibers

A

golgi tendon organ
myelinated

285
Q

describe dissociated sensory loss

A

unilateral spinal cord injury results in loss of sensation on the ipsilateral side and pain symptoms on the contralateral side

286
Q

allodynia

A

non-painful becomes painful

287
Q

hyperalgesia

A

increased pain in response to painful stimuli

288
Q

inflammatory pain

A

increases pain sensitivity due to inflammation associated tissue damage

289
Q

neuropathic pain

A

chronic pain that persists in the absence of an ongoing pain stimuli, likely caused by damage to nervous system

290
Q

type I A delta

A

low threshold for mechanical and chemical stimulation

291
Q

type II A delta

A

low heat threshold

292
Q

what brain structures are responsible for short term memory storage

A

hippocampus

293
Q

what brain structures are responsible for long term storage

A

cerebral cortex
wernicke’s area
temporal cortex (memories of objects and faces)

294
Q

the hippocampus is important for establishing ______ memories

A

declarative!

295
Q

what type of amnesia is caused by damage to hippocampus

A

anterograde amnesia

296
Q

what brain structures are responsible for non-declarative long-term storage

A

basal ganglia
cerebellum
premotor cortex

297
Q

what brain structure helps build habit?

A

caudate

298
Q

how is wernicke-korsakoff syndrome caused?

A

lack of vitamin B1
–chronic alcohol abuse
–gastric or colon cancers
–kidney dialysis
–AIDS

299
Q

pathophysiology of Wernicke-korsakoff syndrome

A

-volume loss
-loss of Purkinje cells in superior cerebellar vermis
–decreased GABA and aspartate

300
Q

what is Autism Spectrum Disorder

A

a neurodevelopmental disorder that begins early in childhood and lasts throughout a person’s life

301
Q

what is the function of the NEGR1 gene?

A

modulates synapse formation in hippocampal neurons

302
Q

what is the function of the PTBP2 gene?

A

alternative-splicing programs

303
Q

what is the function of the CADPS gene?

A

exocytosis of neurotransmitters

304
Q

what is the function of the KCNIN2 gene?

A

voltage-independent Ca2+-activated K+ channel; modulate neuronal excitability

305
Q

what is the function of KMT2E gene?

A

chromatin regulation, control of cell-cycle progression, and maintaining genomic stability

306
Q

what is the function of MACROD2 gene?

A

expressed in lung and brain, nuclear enzyme that binds mon-ADP-ribosylated proteins

307
Q

what is WNT2 secreted growth factor responsible for?

A

neuronal migration, axon guidance, and dendrite branching

308
Q

what is BDNF responsible for?

A

neurogenesis, axodendritic growth, neuronal/synaptic differentiation

309
Q

what is reelin responsible for?

A

neuronal migration, cortical patterning, and brain development

310
Q

what is psychosis

A

conditions that affect the mind, where there has been some loss of contact with reality

311
Q

tonic-clonic seizure

A

“grand-mal”

loss of consciousness, stiffening of body then jerking of limbs

312
Q

absence seizure

A

“petit mal”

staring fit

313
Q

tonic seizure

A

“drop attack”

abrupt fall, either with stiffening or loss of muscle tone

314
Q

myoclonic

A

sudden muscle jerks

315
Q

focal (partial) seizures

A

with or without loss of awareness, or with impaired awareness

316
Q

what is the monoamine hypothesis of depression?

A

reduced levels of monoamine disorders (NE, 5-HT, DA) underlie depression

317
Q

what is often used to treat bipolar disorder?

A

lithium

318
Q

lithium mechanism for treatment of bipolar

A

reduces dopamine and glutamate, increasing GABA

increased BDNF

319
Q

which brain structure integrates info from amygdala to hippocampus

A

BNST

320
Q

neurons in _______ release ________ in response to threat

A

LC
NE

321
Q

increasing NE is _______

A

anxiogenic

322
Q

decreasing NE is _______

A

anxiolytic

323
Q

Prazosin

A

alpha1 AR antagonist
increase peripheral vasodilation
reduces sleep disturbances in PTSD

324
Q

endocrine changes in PTSD

A

decreased cortisol
increased CRH

325
Q

cingulate gyrus function

A

involved in prediction of negative consequences and avoidance

326
Q

what brain structures are the major sources of DA

A

SNc
VTA

327
Q

tonic mode of DA transmission

A

steady, baseline level of DA in downstream neural structures and vital for normal circuit function

328
Q

phasic mode of DA transmission

A

sharp increase or decrease in firing rates, causing large changes in DA concentration in downstream structures

329
Q

describe the mesocorticolimbic system

A

VTA –> Nucleus accumbens –> amygdala

learning, motivation, reward, memory, mvmt

330
Q

describe the nigrostriatal pathway

A

SNc –> caudate nucleus –> putamen

learning, motivation, reward, memory, mvmt

331
Q

reward value is influenced by

A
  1. reward type
  2. reward amount
  3. reward probability
  4. individual’s satiety state
332
Q

TRPV1

A

found in A delta and C fibers

detects noxious heat and confers sensitivtiy to capsaicin

333
Q

what modulates TRPV1 receptor activity?

A

Ca2+

334
Q

ASIC

A

potent proton sensors located in the PNS and CNS to detect extracellular acidification in the periphery and brain

335
Q

SCN9A

A

voltage-gated Na+ channel

c fibers

volume knob on pain

336
Q

Brown-Séquard syndrome

A

dissociated sensory loss

ipsilateral loss of discriminative touch
contralateral loss of pain/temp sense

337
Q

what is cognitive wanting

A

goal-oriented and based typically on declarative memories and on cognitive expectations of ant-outcome relations, and less tied to mesolimbic dopamine-related systems

338
Q

substance use disorders are diseased characterized by disturbances in what 3 major circuits?

A

basal ganglia
extended amygdala
prefrontal cortex

339
Q

what brain structures are involved with binge/intoxication?

A

basal ganglia

340
Q

what brain structures are involved with withdrawal/negative?

A

extended amygdala and habenula

341
Q

what brain structures are involved with preoccupation/anticipation?

A

PFC, insula, allocortex

342
Q

neurobiological mechanisms of the withdrawal/negative affect stage

A

–increases in receptor responsivity to drugs
–decreases in GABAergic and increases in NMDA glutamatergic transmission in the nucleus accumben
–HPS axis and brain stress system mediated by CRF are dysregulated

343
Q

______ potentiates the escalation of oxycodone self-administration

A

intermittent abstinence

344
Q

_______ to oxycodone self-administration attenuates escalation under LgA

A

daily access

345
Q

_______ attenuates escalation of oxycodone self-administration under LgA

A

KOR antagonism

346
Q

in preoccupation/anticipation stage, what does the overactive glutamatergic and CRF systems mediate?

A

craving-like responses

347
Q

what are the 4 neural centers for mvmt

A
  1. local circuit neurons
  2. descending systems
  3. cerebellum
  4. basal ganglia
348
Q

what is the serial organization in the motor system

A

cortex –> brainstem –> spinal cord

349
Q

extrafusal muscle fibers are innervated by what?

A

alpha motor neurons

350
Q

intrafusal muscle fibers are innvervated by what?

A

gamma motor neurons

351
Q

what maintains spindle sensitivity when muscle shortens

A

gamma motor neurons

352
Q

slow motor unit categories

A

type I

contract slowly with relatively small force (posture)

small “red” muscle fibers, rich in myoglobin, mitochondrial, and capillary beds

resistant to fatigue

353
Q

fast fatigue-resistant motor unit categories

A

in between properties and intermediate size

slower than FF, but sustain lower than S

use both oxidative phosphorylation and glycolysis

354
Q

fast fatigable motor unit category

A

Brief extension, large force

larger, pale, muscle fibers, less mitochondria

355
Q

describe muscle spindles

A

detect muscle length

arranged in parallel

356
Q

describe golgi tendon organ

A

detect muscle tension

arranged in series

357
Q

phasic stretch reflex

A

–simple, monosynaptic reflex
elicited by muscle stretch

activates la afferents

358
Q

flexion reflex

A

–complex, polysynaptic and often coordinates withdrawal of whole limbs

often occurs with extension of the opposite limb

359
Q

golgi tendon reflex

A

innervated by ib sensory organs

in series w muscle fibers

360
Q

central pattern generators

A

can control timing and coordination, as well as adjust in response to changes

361
Q

what does the medial divison of motor tract control

A

***from brainstem

primarily posture, balance, and orienting mechanisms

362
Q

what does the lateral division of motor tract control?

A

voluntary, skilled mvmts of the distal extremities

363
Q

vestibular nuclear complex

A

body posture and position; feedback concerning postural instability

364
Q

reticular formation

A

body posture & position; autonomic and stereotypical behaviors

365
Q

superior colliculus

A

orienting of the head and eyes; muscles of the neck

366
Q

red nucleus

A

control arms/forearms in non-human mammals

367
Q

latVST

A

bilateral control of “anti-gravity extensor muscles

368
Q

LMN and LC neurons medial VH bilateral

A

control bilateral axial and proximal limb muscle

involved in feedforward postural control

369
Q

primary motor cortex

A

firing rates code the force of contraction and direction of mvmt

370
Q

premotor cortex

A

planning and programming of mvmt

lateral premotor areas driven by external cues, medial driven by internal cues

371
Q

PFC

A

integration and evaluation of multimodal sensory inputs

motivation to elicit behavior

372
Q

cortical pyramidal neurons in primary motor cortex

A

corticobulbar, to the brainstem

corticospinal to spinal cord

373
Q

betz cells in primary motor cortex

A

about 5%

fine control of the hand/fingers

374
Q

red nucleus

A

controls the limbs
cerebellum training

375
Q

reticular formation

A

control the trunk

376
Q

pons

A

provides cerebellum with info about the motor plan

377
Q

cranial nerve nuclei

A

control muscles of the face, jaw, throat, and eyes

378
Q

ALS

A

affects both UMN and LMN

379
Q

PLS

A

only affect UMN

380
Q

PMA

A

LMN

381
Q

SMA

A

LMN disease, related to defects in SMN1 gene

  1. Wernig-Hoffmann disease: evident by 6 months of age
  2. 6-18 months of age; can sit but not stand/walk independently
  3. Kugelberg-Welander disease: 2-17 years of age
382
Q

areflexia

A

loss of reflexes

383
Q

symptoms of LMN

A

paralysis, paresis, areflexia, fibrillations, fasciculations, muscle atrophy

384
Q

symptoms UMN

A

babinksi sign and clonus

fine voluntary mvmts impaired

385
Q

who discovered als?

A

jean martin charcot

386
Q

basal ganglia function

A

voluntary mvmt
motor planning
initiation of mvmt
nondeclarative learning
motivation

387
Q

corticostriatal projections

A

–excitatory
–synapse onto medium spiny neurons
–topographically organized

388
Q

Parkinson’s Disease

A

hypokinetic disorder

symptoms:
–tremor
–stiffness/rigidity
–slowness of mvmt
–impaired balance and coordination

389
Q

Huntington’s Disease

A

hyperkinetic disorder

related to atrophy of caudate and putamen

result of a mutation in the HTT gene

390
Q

Creutzfeld-Jakob disease

A

symptoms:
–cerebellar ataxia
–myoclonic jerks and seizures
–dementia
–fatal

spongiform degeneration
–caused by a prion (protein that can trigger normal proteins in the brain to fold abnormally)

391
Q

cerebellar ataxia

A

lack of muscle control/coordination of voluntary mvmt

symptoms:
–brain degen
–substances
–stroke/tumor
–cerebral palsy
–genetic factors
–infections

392
Q

purkinje cells

A

GABAergic neuron inhibiting neurons in the deep cerebellar nuclei

393
Q

granule cells

A

glutamatergic cells that excite Purkinje cells via axonal branches called “parallel fibers”

394
Q

basket cells

A

GABAergic interneuron that inhibit Purkinje cells

395
Q

climbing fibers

A

axons from the olivary nucleus of the medulla oblongata that use glutamate to excite Purkinje cells and neurons in the cerebellar nuclei

396
Q

mossy fibers

A

other axons that enter the cerebellum, excitatory granule cells and neurons in the cerebella nuclei

397
Q

superior peduncle

A

major efferent pathway
tracts from the deep nuclei of cerebellum to contralateral cortex

398
Q

middle peduncle

A

major afferent pathway
tracks from the contralateral cortex

399
Q

inferior peduncle

A

afferent and efferent pathways
afferent tracts carrying ipsilateral proprioceptive info from the spinal cord
efferent tracks form purkinje cell axons

Clinical Neuroscience Final (2 decks)

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