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Neuroscience 402 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What is a primary response area?

A

only that specific response/stimulus will activate that brain region

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2
Q

What is a secondary/tertiary area?

A

mainly responsive to one type of stimulus but susceptible to other stimuli

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3
Q

How can brain activity be measured?

A

EEG, electrode arrays, fMRI, patch clamp, dye with microscope, tetrods

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4
Q

What is a tetrod?

A

A way to measure brain activity; can use 2-4 arrays to get single cell resolution/spiking cand measure synaptic communication

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5
Q

What are the two differing views on fundamental organization in the brain?

A

Cajal and Kuffler believed that neurons communicate through chemicals passing through synapses. Golgi and Eccles believed that communication occurred through physical connection and electrical current.

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6
Q

What is a Golgi stain? and where was the first imaged taken?

A

Golgi stain is used to stain 1% of cells but you get complete staining allowing for a closer look at details of cells. In the dentate gyrus of the temporal lobe

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7
Q

How did the fundamental organization controversy get answered?

A

Eccles used electrical recordings to determine that an action potential at one neuron caused an inverse in the other indicating a chemical response. Another method developed at the time was electron microscope

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8
Q

What is the Neuron Doctrine?

A

The neuron is the fundamental anatomical, physiological, genetic, and biochemical unit of the nervous system

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9
Q

What are the four types of neurons?

A
  1. unipolar (one axon in one direction with dendrites branching off axon)
  2. bipolar (one axon in one direction and dendrites in the other)
  3. pseudo-unipolar (axon with dendrites and a soma that branches off the axon)
  4. multipolar cells-
    a. motor neuron of SC (dendrites on soma and axon in one direction)
    b. pyramidal cells of HC (multiple dendrite branch points)
    c. purkinje cell of cerebellum (tree of dendrites)
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10
Q

What are the 3 modes of firing in cortical pyramidal cells?

A
  1. regular
  2. burst
  3. cerebellar Purkinje cell
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11
Q

What are the 3 modes of firing in thalamic relay cell?

A
  1. Transfer mode
  2. burst
  3. medial habenular cell
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12
Q

What are place cells?

A

neurons in the hippocampus that fire when an animal visits specific region of an environment

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13
Q

What are affect or afferent signals?

A

internal and external environment send through sensory ganglia and nerves to the central nervous system

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14
Q

What are effect or efferent signals?

A

signals sent from the central nervous system through the peripheral (autonomic or somatic) nervous system to effector organs such as skeletal muscles and smooth muscles

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15
Q

How does the brain form from an embryo

A

Begins as tube from an invagination from skin that expands overtime forming the telencephalon, diencephalon, mesencephalon, and rhombicencephalon

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16
Q

What are the seven parts of the nervous system?

A

SC, medulla/pons, cerebellum, midbrain, diencephalon, cerebrum

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17
Q

What is parasagital?

A

either way from the midline

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18
Q

What is topography?

A

Representative image of amount of connectivity with the brain a certain region of the body has

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19
Q

What is Broca’s area?

A

Area at the border of the frontal lobe with temporal lobe where a stroke will cause motor problems (i.e. can’t form words)

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20
Q

What is Wernicke’s area?

A

Area bordering parietal, temporal, and occipital lobe where a lesion can cause problems with language appreciation and generation

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21
Q

What are the 4 parts of the SC?

A
  1. cervical
  2. thoracic
  3. lumbar
  4. sacral
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22
Q

Why is gray matter gray?

A

because there is no myelin

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23
Q

What are cortical lesions?

A

Lesions that cause deficits on the opposite side for sensory and motor

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24
Q

What are cerebellum lesions?

A

Lesions that cause deficits on the same side because output to the thalamus crosses the midline and cortex signals cross sides again

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25
Q

What are the 3 functions of the brain stem?

A
  1. receive sensory info from head and moves head
  2. transmit info from cord to higher levels and back
  3. regulate levels of arousal
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26
Q

How could mike the chicken survive without a head?

A

Mike survived because he still had the brain stem which allowed for basic functions such as breathing to occur and the brain stem contain their own sensory nuclei

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27
Q

What happens at the pyramids of medulla?

A

The dorsal column and cortical spinal tract cross

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28
Q

What do glial cells do at synapses?

A

involved in maintaining synapse

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29
Q

Explain Otto Loewi’s demonstration of chemical transmission

A

Using frog hearts in two separate connected bins of fluid, Loewi stimulated the vagus nerve of heart 1 with an electrical stimulator and measured conductance of the second heart. This experiment showed the first demonstration of chemical synapse

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30
Q

What are the results of Loewi’s experiment?

A

Stimulation of heart 1 save a slower heartbeat but the fluid from the first heart on the second heart had a delayed but similar result

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31
Q

Are there electrical synapses in the CNS?

A

yes there are some although more in invertebrates then mammals

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32
Q

How many different transmitters would you need to build a nervous system?

A

At least 2 different transmitters- one that is excitatory and one that is inhibitory OR 1 neurotransmitter with different synapses

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33
Q

What are the 6 classes of neurotransmitters?

A
  1. acetylcholine (seen in Loewi’s experiment)
  2. biogenic amines (DA, 5-HT, NE, E, and histamine)
  3. Amino acids (glutamate, GABA and glycine)
  4. neuropeptides (protein like)
  5. purine (ATP and adenosine)
  6. gases (NO, CO)
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34
Q

Do neurotransmitters vary in size?

A

yes; Ach is a small molecule. Carnosin is a small peptide, insulin is a large peptide

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35
Q

What are the 5 criteria for determining if a compound is an endogenous transmitter for a specific synapse?

A
  1. synthesized in the neuron
  2. present in the presynaptic terminal and released in amounts sufficient to produce an action potential
  3. exogenous administration mimics action of the endogenously released transmitter exactly
  4. mechanism exists for terminating the action (Ach is unique)
  5. when specific antagonists are administered they produce the same actions on the exogenously administered compound as on the neurally released transmitter
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36
Q

Of the three synapses, sympathetic, parasympathetic and motor, which synapses directly on target organ?

A

motor and it uses Ach

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37
Q

Of the three synapses, sympathetic, parasympathetic and motor, which postganglionic synapse uses norepinephrin?

A

sympathetic which uses Ach for pre to postganglionic but norepinephrine for transmission to target (heart, blood vessels and sweat glands (exception))

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38
Q

What is the difference between sensory and autonomic ganglia?

A

sensory has no synapses or interruptions seen in autonomic

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39
Q

What type of neurons are sensory neurons?

A

they are pseudounipolar as in they project to both periphery and spinal cord

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40
Q

What are the 5 steps in the natural history of neurotransmitters?

A
  1. synthesis
  2. storage
  3. release
  4. postsynaptic action
  5. inactivation
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41
Q

How is acetylcholine made?

A

choline and acetyl undergo a reaction with the choline acetyltransferase enzyme

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42
Q

Which synapses use acetylcholine?

A

transmitter between:
1. postganglionic parasympathetic and effector organ
2. preganglionic and postganglionic parasympathetic neurons
3. motor neurons and skeletal muscle
4. preganglionic and postganglionic sympathetic neurons
5. certain neurons in the CNS

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43
Q

Which receptors do only endogenous acetylcholine act on?

A

nicotinic (ionotropic-excite) and muscarinic (metabotropic-excite and inhibit)

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44
Q

How is cholinergic transmission terminated?

A

rapid catabolism of Ach via enzyme acetylcholinesterase which is found in high concentrations in the synapse

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45
Q

How do the inhibitors, sarin, parathion, and tacrine, differ in binding to AChE enzyme?

A

how tightly they bind

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46
Q

Model of cholinergic synapse

A
  1. ACh is made from choline and acetyl-CoA by choline acetyltransferase
  2. ACh enters vesicle by vesicular ACh transporter
  3. released into synapse where it is broken down by AChE
  4. choline is transported back into the axon terminal to make more ACh
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47
Q

What is a catecol?

A

a benzene ring with two adjacent hydroxyl groups

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48
Q

What are the three types of catecholamines?

A

dopamine, epinephrine, norepinephrine

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49
Q

How are all the catecholamines made?

A

L-tyrosine is made into L-Dopa by TH
L-Dopa is made into dopamine by L-Aromatic AA decarboxylase
dopamine is made into norepinephrine by DOPA beta hydroxylase
epinephrine is made into epinephrine by phenylethanolamine n-methyltransferase

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50
Q

What does DOPA stand for?

A

dihydroxyphenylalanine

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51
Q

What is the rate limiting step for catecholamine synthesis?

A

TH (tyrosine hydroxylase)

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52
Q

Where did Carlsson determine that dopamine functions as a neurotransmitter in its own right?

A

straitum- substantia nigra in the nigrostriatal tract

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53
Q

What disease is caused by decreases in nigral neuronal cell bodies?

A

PD due to depletion of dopamine in the substantia nigra and striatum

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54
Q

Carlsson used reserpine to deplete catecholamines but what did he use to restore?

A

L-DOPA

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55
Q

Dopaminergic pathways in the CNS

A

made in substantia nigra and ventral tegmental area and spreads into the mesocortical pathway, nigrostriatal pathway, tuberoinfundibular pathway and mesolimbic pathway

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56
Q

Why do some neurons express dopamine, norepinephrine, or epinephrine?

A

neuron specific expression of the genes required to make the 3 biosynthetic enzymes

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57
Q

What enzymes are expressed in dopaminergic, noradrenergic and adrenergic neurons?

A

DA- TH and I-AAAD
NE- TH, I-AAAD, DBH
E- TH, I-AAAD, DBH, PNMT

58
Q

Noradrenergic system of the CNS

A

originates in the locus coeruleus and spreads all over the brain and down the spinal cord

59
Q

How is NE inactivated?

A

it is inactivated by reuptake where degradation occurs intracellularly

60
Q

Serotonin biosynthesis

A

L-tyrptophan forms 5-hydroxy-L-tryptophan by tryptophan hydroxylase
5HTP forms serotonin (5-hydroxytrptamine 5-HT) by aromatic L-amino acid decarboxylase

61
Q

Serotonin pathways

A

originate in the raphe nuclei and spreads to the whole brain and spinal cord

62
Q

Histamine biosynthesis

A

histidine is made into histamine by histidine decarboxylase

63
Q

Where is the amino acid transmitter, glutamate, stored?

A

it is kept in vesicles to keep is separate from cytoplasmic glutamate that is used in protein synthesis

64
Q

What are the major inhibitory and excitatory amino acid transmitters?

A

glutamate is excitatory and GABA and glycine are inhibitory

65
Q

What percent of inhibitory synapses use Glycine in the spinal cord?

A

50%

66
Q

Where does neuropeptide synthesis occurs?

A

neuropeptides are synthesized in the neuronal cell body based on mRNA from larger peptide molecules that are processed to smaller molecules by peptidases and transported to nerve terminals

67
Q

How are amino acid transmitters terminated?

A

reuptake

68
Q

How are neuropeptide transmitters terminated?

A

diffusion from synaptic cleft

69
Q

How is nitric oxide synthesized?

A

L-arginine with NOS and O2 is made into NO and L-citrulline

70
Q

NO transmission

A

glutamate is stored in vesicles and released into the cleft from the presynaptic synapse
glutamate binds to NMDA receptors allowing Ca2+ in
Ca2+ acts with calmodulin on NO synthase that breaks down arginine to NO
the NO is released and uptaken into the presynaptic cell

71
Q

What are the 3 different methods for neurotransmitter inactivation? and examples?

A
  1. reuptake and recycled or transported to glial cells (5-HT)
  2. enzymes inactivate (ACh)
  3. diffusion out of cleft or into blood (LHRH)
72
Q

What is cotransmission?

A

the release of more than one neurotransmitter from a single nerve terminal

73
Q

What is a neuromodulator?

A

doesn’t carry excitation or inhibition from one neuron to another but instead alters either the cellular or synaptic properties of certain neurons so that neurotransmission between them is changed

74
Q

What type of gating is ionotropic and metabotropic receptors?

A

ionotropic- direct; fast; mediate behavior
metabotropic- indirect; slow; modulate behavior

75
Q

Example of what occurs at an excitatory synapse

A

glutamate is released from the presynaptic terminal and acts on the postsynaptic terminal to allow Na+ (or Ca2+) influx and depolarization

76
Q

Example of what occurs at an inhibitory synapse

A

GABA is released from the presynaptic terminal and acts on the postsynaptic terminal to allow Cl- (or K+ efflux) influx and hyperpolarization

77
Q

How are neuropsychiatric disorders formed?

A

an imbalance between excitation and inhibitory transmission

78
Q

What are the 3 types of ionotropic receptors?

A
  1. Ach, GABA, and glycine receptor channels (4 TM as pentamers)
  2. glutamate receptor channels (3 TM as 4 subunit)
  3. ATP receptor channels (2 TM as trimer)
79
Q

What are AMPA and NMDA receptors?

A

they mediate majority of receptors; gated by glutamate; permeable to Na+ and K+; excitatory

80
Q

Pharmacological inhibitors for AMPA and NMDA

A

AMPA- CNQX, NBQX, DNQX
NMDA- D-APV

81
Q

How do NMDA receptors work?

A

Calcium permeable- to initiate Ca-CaMKII for long term potentiation
Mg2+ ion blocks current until depolarization occurs
AMPA receptor activates and causes membrane depolarization and Mg2+ leaves
Binds glutamate and glycine together to activate channel
DO NOT CONTRIBUTE TO HYPERPOLARIZATION
coincidence detectors

82
Q

Glutamate excitotoxicity

A

high levels on intracellular Ca2+

83
Q

Which is faster AMPA or NMDA?

A

AMPA

84
Q

What function is the postsynaptic density?

A

tethered AMPA and NMDA receptors

85
Q

Difference between GABAa and GABAb?

A

GABAa is ionotropic and fast and GABAb is metabotropic and slow

86
Q

Which GABA receptor is an important drug target?

A

GABAa

87
Q

What is DREADDS?

A

a designere drug that will activate a modified receptor that can be expressed in any region of interest

88
Q

Where are GABAb receptors located? and effects?

A

pre- and postsynaptic
Ca2+ channel effects are presynaptic
K+ channel effects are postsynaptic

89
Q

Who discovered cAMP?

A

Sutherland

90
Q

How is cAMP increased or produced in response to hormones?

A

Hormones/neurotransmitters bind to GPCR and activate G proteins by GEF which act on adenylyl cyclase to produce cAMP

inactivate G protein by GAP

91
Q

How does cAMP activate downstream effectors?

A

cAMP activates PKA: 4 cAMPs bind to R causing a conformational change that decreases affinity for C causing its release to amplify signalling (can be constitutively active in R subunit is degradation during long activation)

92
Q

How is Ca2+ released by Gq?

A

neurotransmitter binds to GPCR and activates Gq which acts on PLC. PLC cleaves PI(4,5)P2 into DAG and IP3. IP3 goes to IP3 receptor on ER membrane and opens the channel releasing Ca2+ into the cytoplasm

93
Q

How are Ca2+ stores in the ER returned to normal after activation event?

A

Less Ca2+ causes the IP3 receptor (ICRAC) STIM1 subunit to move to cluster in one spot to make contact with surface receptor Orai1. extracellular Ca2+ comes in the ER lumen to maintain homeostasis

94
Q

How is Ca2+ concentration regulated?

A

ligand gated channels (ACh and NMDA)
voltage gated Ca2+ channels
circulation system
crosstalk between ER and mitochondria

95
Q

How neuronal Ca2+ signaling leads to diverse and specific changes in cell function?

A

Ca2+ binding proteins, channels and enzymes
Calmodulin
CaBPs– EF hand has the Ca2+ binding domain proteins

96
Q

What are techniques to study Ca2+ signaling?

A
  1. organic calcium indicator dyes
  2. GECIs: single polypeptide chain of a fluorescent protein and a Ca2+ binding motif (FRET or single wavelength)
97
Q

What are basic signaling properties?

A

surface to nucleus signals
convergence and divergence from receptor to G protein or G protein to effector
synergy and differential regulation
balance
crosstalk

98
Q

What are the 3 types of potentials in the nervous system?

A
  1. receptor potential: membrane potential response in a sensory neuron by sensory stimulus (mechanosensitive channels)
  2. synaptic potential: membrane potential response elicited in a postsynaptic cell resulting from synaptic input from a presynaptic cell (ligand gated channels)
  3. action potential: regenerative membrane potential response elicited in excitable cells, either spontaneously or in response to an input (voltage gated channels)
99
Q

Explain how information is encoded by electrical signals is processed by neural circuits in the stretch reflex cycle.

A
  1. muscle spindle stretches inducing a graded receptor potential that turns into an action potential that is conducted to a sensory neuron
  2. the sensory neuron releases transmitter to the motor neuron as a graded synaptic input resulting in an action potential and release of transmitter to the muscle
  3. muscle takes the graded synaptic potential and through an action potential contracts
100
Q

What are determinants of intrinsic electrical properties of excitable cells?

A

plasma membrane
active ion transporters
ion channels

101
Q

How does the membrane serve as the basis for electrical and chemical driving force that influence passive ion movement through channels?

A

electrical: permits separation of charge between external and internal solutions
chemical: permits establishment of differences in chemical composition

102
Q

How does the membrane serve as the source of an electric field inside the membrane?

A

the membrane is like a capacitor, it can store charge, and accumulate charges on surface which generates electric field

103
Q

What is Vm and how does it move ions through the membrane?

A

It is the work required to move a monovalent cation from the external to internal solution; equivalent to the change in energy of the ion inside compared to outside. Electric forces cause ions to move from higher to lower energy and undergo energy change

104
Q

What accounts for differences between internal and external concentrations of other ions, e.g. Cl- and Ca2+?

A

Active transport

105
Q

Which ions flow out of the membrane and which flow into the cell due to the established concentration gradient?

A

Na+/Cl-: move in
K+/Ca2+: move out

106
Q

What are the equilibrium potentials for Na+, K+, Ca2+, and Cl-?

A

Na+: 67
K+: -98
Ca2+:129
Cl-:-90

107
Q

How do transporters and channels contribute to signaling?

A

Active export maintains low intracellular solute concentration creating driving force passive influx through gated channels
Active import maintains high intracellular solute concentration creating a driving force for passive efflux

108
Q

What does the driving force depend on?

A

differences in ion concentration and differences in electrical potential across plasma membrane

109
Q

Which transporter is responsible for maintaining the driving force for Na+ influx and K+ efflux through voltage gated ion channels?

A

Na/K ATPase

110
Q

What are two functional properties of ion channels?

A

permeation and gating

111
Q

What are determinants of ion permeation through channels?

A

ion size
relative energy of dehydration of ion in solution vs within pore
strength of ion binding to intra-pore ion binding sites

112
Q

What is the probability of channel opening?

A

The probability that a channel will open at a set stimulus. The probability increases as more stimulus is present.

113
Q

Macroscopic current

A

summation of a large number of single channel currents recorded by repetitive testing of a single channel

114
Q

Fick’s 1st law of diffusion

A

solute flux is proportional to the change in concentration with respect to position at that time (Jdiff=-D(dc(x,t)/dx))

115
Q

How does the electric field effect ion movement through a pore? (Ohm’s law)

A

drift velocity of ion depends on the magnitude of the electric field and ion mobility and constitutes a current (i=zFJelectro)

116
Q

Nernst-Planck equation

A

explains electrodiffusion using Jdiff and Jelectro (i=zFJtotal=-RT[(dc/dx)+(xFc/RT)(dV/dx)])

117
Q

Interpretation of Nernst potential case 1: c1=c2
-Vm=0
-Vm>0
-Vm<0

A

-Vm=0: total flux is 0, Ek is 0 and (Vm-Ek) is 0
-Vm>0: net current flows from side one (+) to side 2 (-) (Vm-Ek) is increased
-Vm<0: net current flows from side 2 (+) to side 1 (-) (Vm-Ek) is decreased

118
Q

Interpretation of Nernst potential case 1: c1>c2
-Vm=0
-Vm=Veq
-Vm<Veq

A

-Vm=0: net current flows from side 1 to side 2 with Ek and (Vm-Ek) increased
-Vm=Veq: net current is zero with Vm decreasing and Ek increasing
-Vm<Veq: net current flows from side 1 (-) to side 2 (+) with decreased Vm and (Vm-Ek) and increased Ek

119
Q

At what voltage is the current carried by a given ion through a channel equal to 0?

A

when Vm=Veq

120
Q

At what voltage is the total current through a channel equal to 0?

A

channel selective for 1 ion then Vrev
channel permeable to multiple ions then Vrev depends on concentrations and permeation properties

121
Q

What are the main determinants of Vrev?

A

equilibrium potential for permeant ion which depends on ratios of external and internal concentrations
fractional conductance of the channel to the permeant ions

122
Q

GHK theory

A

gives the transmembrane current of an ion species expected at a given membrane potential for a given concentration of the ion on either side of the membrane

123
Q

What is the relationship between ionic, unitary, macroscopic and total membrane currents?

A

ionic-> unitary-> macroscopic-> total membrane current
each step up is sum of the previous

124
Q

How is the resting potential determined?

A

a weighted average of the reversal potentials for the various channel types, each reflecting ion selectivity properties of the respective channels with weighting factors representing the fractional conductances imparted to the membrane by each channel population

125
Q

Membrane potential dynamics

A

Vm is proportional to membrane charge where current flow across PM affects charge
Vm=(Q(t)/Cm)

126
Q

What are three functional properties of excitable cells?

A
  1. resting potential
  2. passive responses
  3. active responses
127
Q

What would you predict for the size of the steady state voltage change produced by current injection if the number of leak channels is doubled?

A

A larger hyperpolarization

128
Q

Role of Na and K channels in AP generation?

A

Na channels are fast activators and inward current
K channels are slow activators and outward current

129
Q

What are the 3 things to notice for voltage gated K+ channels?

A
  1. outward current (Vm>Vk)
  2. slow activation and maintained activity
  3. slow current increase and maintained during pulse
130
Q

What are the 3 things to notice for voltage gated Na+ channels?

A
  1. inward current (Vm<Vna)
  2. fast activation and there is inactivation
  3. fast current increase and transient
131
Q

How does myelin help with signal propagation?

A

acts as a cable to send the electrical signal along the axon at a faster rate then an unmyelinated axon

132
Q

The 3 features that define synapses on EM

A

PSD
vesicles at presynaptic side
2 sides need to have parallel membranes

133
Q

Why is there a latency during IPSPs?

A

the second step in signaling is the slowest step causing latency in postsynaptic response– opening of voltage gated Ca2+ channels

134
Q

IPSP definition

A

postsynaptic response that decreases probability of spike fire

135
Q

EPSP definition

A

postsynaptic response that increases probability of spike fire

136
Q

Why does each pulse create a bigger facilitation during short-term plasticity?

A

Ca2+ influx is the same but the repetitive spikes cause an increase in internal Ca2+ concentration since it is not being used up fast enough

137
Q

What are the 3 reasons for depression to occur during short-term plasticity?

A
  1. desensitize post synaptic receptors
  2. run out of vesicles that are prepped and ready to leave the presynaptic side
  3. negative feedback system that turns off signaling in the presynaptic side (has a higher affinity for the transmitter then receptors on the postsynaptic side)
138
Q

Hebbian synaptic plasticity

A

coincidence detection- some growth or metabolic change takes place to increase efficiency

139
Q

What is the trigger for change in amplitude during long-term plasticity?

A

presence of NMDA receptor that causes Ca2+ influx

140
Q

How do NMDA receptors activate?

A

AMPA responds first and depolarizes the membrane. The change in charge causes electro repulsion of Mg2+ from inside NMDA thereby unblocking the receptor and allowing Ca2+ influx

141
Q

How does initiation in presynaptic influence the postsynaptic side during long term plasticity?

A

NMDA opens and causes AMPA to move from “garage” to the NMDA receptors. AMPA receptor silence

Neuroscience 402 (2 decks)

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