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Systemic Physiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Declarative memory

A

facts, events, places; made possible by hippocampus

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2
Q

Procedural memory

A

aka non-declarative memory, how to do motor actions

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3
Q

Association cortex

A

short term memories from the hippocampus go here after about a month

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4
Q

Cerebrum lobes

A

frontal, parietal, occipital, temporal

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5
Q

Hippocampus

A

temporal lobe structure, found in medial temporal lobe, has connections with other regions of the brain that hold visual and auditory information, crucial for declarative memory, name derived from sea horse’s genus name

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6
Q

Limbic system structures

A

sit above the brainstem and between other cerebral structures, memory and emotion

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7
Q

How to keep a group of neurons active for a longer period of time? Is this excitotoxicity?

A

cell should keep action potential depolarization longer by modifying voltage gated potassium channels so that they are harder to open. Not excitotoxicity because it’s only sustained for a very small amount of time

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8
Q

Short term memory vs long term memory when keeping nerurons active for a longer period of time

A

working memory requires changes in proteins that are already present; long term memory requires the synthesis of new proteins (ie/ long term potentiation)

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9
Q

membrane channels and learning and memory

A

either channels are blocked or channels are opened for a longer period of time

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10
Q

Configural learning system

A

all sense information comes to the hippocampus and then the hippocampus will determine if it will be remembered or not

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11
Q

Entohinal cortex

A

corticol area which receives sensory information, it will then send it to the configural learning center, associated with the hippocampus but not a part of it, has large cell bodies referred to as pyramidal cells

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12
Q

Perforant path

A

axons from the entorhinal cortex that synapse onto the dentate gyrus

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13
Q

Dentate gyrus

A

a part of the hippocampus, looks like a row of teeth or a bite mark, cells are referred to as granule cells due to very small cell bodies

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14
Q

CA1,2,3,4

A

CA stands for Cornu Ammonius, cells curl around like a ram’s horn, other regions of the hippocampus

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15
Q

Mossy fibers

A

axons from the dentate gyrus that will synapse on CA3

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16
Q

Schaffer collaterals

A

axons from CA3 that will synapse with CA1

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17
Q

CA3

A

sends information to septurm and mammillary bodies, primary output region

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18
Q

Mammillary bodies

A

a part of the hypothalamus, associated with the hippocampus, damage to the mammilary body cells and hippocampus can be seen with chronic alcoholism and stroke

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19
Q

CA1

A

communicates with the hippocampus on the other side of the brain

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20
Q

Lomo and Bliss experiment

A

used rabbit brains to stimulate the performant path and measure the activity of cells in the dentate gyrus

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21
Q

Lomo and Bliss experiment results

A

low frequency stimulation will lead to low activity in the dentate gyrus (some action potentials, doesn’t depolarize membrane sufficiently), high frequency stimulation of path leads to high activity in dentate gyrus (many action potentials, leads to threshold for which LTP can occur), high frequency of the path wait for a while (1hr, 2hr, 1wk, 1month) and come back with low frequency leads to high activity in the dentate gyrus

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22
Q

Long term potentiation (LTP)

A

model for change in connection between neurons in the brain, how memories are formed

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23
Q

Which neurons in the brain undergo LTP

A

all of them

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24
Q

Long term depression (LTD)

A

process of forgetiing

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25
Q

Threshold for LTP and action potentials

A

is no the same

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26
Q

Hebb’s law

A

neurons that fire together wire together, neurons that produce action potentials at the same time will increase their strength of connection

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27
Q

Doggie mice

A

discovered in 1992, mice that overexpress NMDA receptors, this illustrates how important NMDA is to LTP

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28
Q

> quanta amount of glutamate released

A

glutamate could still bind to all three of its receptors but it doesn’t mean that enough sodium will enter through AMPA in order to open NMDA, AMPA needs to be open long enough for a depolarization that will open NMDA to allow calcium to enter

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29
Q

Calcium calmodulin complex

A

protein regulated by calcium, it will take the inactive form of calcium calmodulin kinase 2 and activate it, leads to the activation of adenalyl cyclase

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30
Q

CAM Kinase 2

A

will autophosphorylate, enzyme

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31
Q

CAM Kinase 2 and AMPA

A

CAM Kinase 2 will lead to phosphorylation of mechanisms that will insert AMPA receptors into the post synaptic dendrite membrane such that the next time the presynaptic neuron produces an action potential glutamate will bind to more AMPA receptors because the synapse has already been potentiated

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32
Q

Adenalyl cyclase

A

will take ATP and convert it to cAMP

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33
Q

Kreb

A

will be activated by a series of enzyme activations of cAMP, will serve as a transcription factor for a multitude of things and increase expression of them

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34
Q

cAMP

A

cyclic AMP, response element binding protein

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35
Q

BDNF

A

product of Kreb, brain derived neurotrophic factor, produced by the cell and will make its way to the synapse to bind with TrKB in pre and post synaptic neuron, acts in autocrine and paracrine way to increase the size of the synapse

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36
Q

TrKB

A

tyrosine kinase B, increases activity/production of F actin

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37
Q

F Actin

A

main cytostructural protein of a dendrite, will polymerize and increase the surface area of pre and postsynaptic cell

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38
Q

Actin and presynaptic cell

A

increases the surface area so that there’s an increase in the amount of vesicles that can attach to the presynaptic membrane to release more neurotransmitter

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39
Q

Actin and postsynaptic cell

A

increase the surface area to increase the amount of receptors on the dendrite membrane

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40
Q

Protein Kinase C

A

will lower the threshold/sensitivity of calcium channel so that it can easily open; this and the metabolic glutamate transporter will also lead to an increase concentration of calcium

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41
Q

Nitric Oxide synthase

A

activated by calcium to produce nitric oxide which will diffuse into presynaptic cell from the post synaptic dendrite (retrograde)

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42
Q

Presynaptic cell and nitric oxide

A

nitric oxide will increase the activity of VGlut

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43
Q

VGlut

A

vesicular glutamate transport, the channel of the vesicles in the presynaptic cell that glutamate will enter in order to be recycled

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44
Q

VGlut increase activity

A

the quanta amount of glutamate will then increase within the vesicle such that next time the presynaptic cell reaches an action potential more gluatamate will be released

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45
Q

LTP mechanisms with Glutamate

A

Calcium and nitric oxide synthase, Calcium calmogulin complex, CAM Kinase 2, Adenalyl cyclase

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46
Q

Names for end of axon

A

axon terminal, synaptic end knob, synaptic bouton

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47
Q

Why is the end of the axon wider than the rest of the axon

A

there’re a lot of mitochondria due to high need for energy production, there’re a lot of vesicles which contain neurotransmitters

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48
Q

Vesicles

A

made by the golgi apparatus in the neuron cell body and they “walk” down the axons of the neuron with the help of microtubules

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49
Q

Synaptic clef

A

space between neurons, a few nanometers in distance

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50
Q

Presynaptic neuron

A

cell that releases the neurotransmitter

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51
Q

Vesicle docking site

A

proteins that will grab onto vesicles in the high density area

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52
Q

Perforated synapse

A

synapse splits initially due to neurotrophic factor BDNF working through TrKB increasing the size of the synapse by polymerization of F actin and once it reaches a certain size it will split into two axon terminals

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53
Q

Active zone

A

portion of the end of the presynaptic neuron where axons fuse and exocytosis of neurotransmitter occurs

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54
Q

Perforated synapse and AMPA

A

all perforated synapses have AMPA receptors

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55
Q

Chemical tag

A

activity regulated cytoskeletal associated protein attaches to elements like F actin so that BDNF knows which synapse to move to

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56
Q

Hippocampus death and LTP

A

if the hippocampus dies the ability to undergo LTP also goes

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57
Q

How does the hippocampus die

A

it’s usually the first structure to go if there’s any damage to the brain due to how vascularized it is and it shows the most default activity within the brain active even when asleep, diseases like viral encephalitis leads to the hippocampus dying

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58
Q

Long term glucocorticoid exposure

A

cortisol acts in the hippocampus which allows us to remember stressful events better by making LTP easier by increasing calcium levels

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59
Q

Chronic stress

A

is excitotoxia as prolonged increase of calcium levels in the cell cause apoptosis, this is why a symptom of PTSD is memory loss

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60
Q

Glial scar

A

when the cells of the hippocampus die a combination of connection tissue and neuroglial cells will fill in

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61
Q

Aplysia californica

A

marine sea slug about the size of a fist, model system used to study neuroscience

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62
Q

Gill withdrawal reflex

A

contact to the siphon on the dorsal side will lead to the muscles contracting and skin forcefully closing over it, it’s a two neuron circuit consisting of a sensory neuron and a motor neuron

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63
Q

Neurons of the gill withdrawal reflex

A

the sensory neuron will send information from the skin to the motor neuron who will move the skin and muscles to protect the siphon

64
Q

Habituation

A

decrease in responding after continual stimulation

65
Q

Sensitization

A

increase in responding to non-noxious stimulus following a threatening stimulus

66
Q

Aplysia californica experiment

A

done by Eric Kandel; touched the siphon with a nonthreatening stimulus such as touching it with glass rod or a little jet of water and after a while the withdrawal relfex would not happen and habituation would occur. they then delivered a shock to the snail at a random location of the body and then touched the siphon with a non threatening stimulus and the snail responded with the gill reflex

67
Q

Aplysia californica experiment results

A

the shock modified the activity of the sensory neuron through an axoaxonic synapse on the sensory neuron such that anything that activates the sensory neuron associated with the siphon will activate the motor neuron

68
Q

Mechanism of gill withdrawal reflex

A

found by Eric Kandel; the sensory neuron releases glutamate onto the motor neuron and it will be activated causing it to undergo an action potential and contract the muscles.

69
Q

Sensitization of the gill withdrawal reflex mechanism

A

serotonin is being released by the facilitating interneuron onto serotonin receptors of the sensory neuron. after serotonin binds to one receptor PLC will cleave PIP2 to make DAG and PIP3. DAG will activate PKC which will lower the threshold of L type voltage gated calcium channels increasing neurotransmission. PKC will also move vesicles containing glutamate closer to the active zone. Serotonin will also bind to another receptor which will activate adenylyl cyclase to make cAMP which will activate cAMP dependent PKA. PKA will lower the threshold of L type voltage gated calcium channels as well as move vesicles closer to the active zone. PKA will act on the potassium channel to make them stay inside the neuron longer to maintain depolarization longer and open voltage gated calcium channels

70
Q

Serotonin receptor types

A

g protein coupled receptors

71
Q

Sensitization of the neurons leads to

A

next time the sensory neuron is activated by any stimulus it will release glutamate and therefore keep activating the motor neuron leading to the circuit being sensitized

72
Q

Experiment of giving aplysia californica infections of prozac results

A

make sensitization of the circuit easier as fluoxetine prevents reuptake of serotonin leading to serotonin being in the synaptic clef

73
Q

Neurogenesis

A

neurons are born all the time and most of them come from the hippocampus

74
Q

Lateral ventricles

A

are lined by progenitor cells which give rise to amount 1 million new neurons per day and sits next to the hippocampus

75
Q

How new neurons incorporate themselves into circuits

A

reinforcement of circuits, reconnections to the other parts of the brain, neurons are born into a spot if it’s needed there

76
Q

Exercise and hippocampal neurogenesis

A

exercises leads to the increase of neurogenesis due to an increase of cerebral blood flow and increase insulin sensitivity in the brain

77
Q

Cerebral blood flow and hippocampal neurogenesis

A

due to an increase of cerebral blood flow there’s more oxygen and glucose going to the brain

78
Q

Insulin sensitivity and hippocampal neurogenesis

A

it’s easier for brain cells to bring in glucose also limiting the chance of type 2 diabetes

79
Q

Type 2 diabetes and alzheimers

A

there’re many links between the two, type 2 can cause the blood brain barrier weaker such that infections can easily come in and the immune reaction and inflammation could lead to alzehimers, daily brisk walks appear to reduce alzheimer’s incidences

80
Q

Exercise and memory

A

exercise has a lot of protective effects on the brain

81
Q

Post synaptic neuron

A

cell that receives the neurotransmitter

82
Q

Post synaptic density

A

seen via electron microscopy, a high concentration of proteins within the membrane or waiting to be inserted into the membrane

83
Q

Neuron parts

A

cell body, axon, split into collaterals with thousands of axon terminals, thousands of dendritic spines which has branching dendrites

84
Q

Dendrite

A

receiving part of the neuron

85
Q

Synapsis in the body

A

found in neurological but also in meiosis 1 prophase 1 with gene exchange

86
Q

Mechanism of neurotransmitter release

A

action potential reaches axon terminal, voltage gated calcium channels with open in response to about +30mv, calcium will move into the cell and the channel closes, neurotransmitter is diffused into synaptic clef, neurotransmitter binds to receptors located in postsynaptic membrane, neurotransmitters are removed just as soon as it binds, presynaptic neuron will either reuptake or the neurotransmitter will undergo enzymatic degradation by enzymes of postsynaptic neuron

87
Q

Voltage gated calcium channel types and characteristics

A

F,L,N, and T; N are open for a normal amount of time, L is open longer, and T are open for a short amount of time, F are open when cell membrane is hyperpolarized

88
Q

Calcium concentration of neurons

A

there’s 10000x more concentration of calcium outside than inside the cytosol

89
Q

Calcium

A

important second messenger than changes protein conformations, moved out of cytosol by calcium ATPase which is powered by ATP from the mitochondria

90
Q

Synaptotagmin

A

protein within the synaptic vesicle membrane, only found in the presynaptic neuron

91
Q

Synaptotagmin and SNARE

A

synaptotagmin will change conformation due to calcium and interact with SNARE proteins to pull the vesicle open so that the contents are exposed to the extracellular space (exocytosis)

92
Q

Ionotropic

A

receptors that have to be associated with an ion channel, leads to a graded potential

93
Q

Metabotropic

A

receptors that aren’t directly linked to an ion channel, leads to receptor tyrosine kinase or G protein coupled receptors

94
Q

Synaptic delay

A

from the point of release of neurotransmitters in presynaptic cell to the indication of change of membrane potential in the postsynaptic cell takes about 0.2 milliseconds, this is due to the rate of diffusion and binding to the receptors and incorporation of transmitter into postsynaptic neuron

95
Q

Excitatory neurotransmitters

A

increase chance action potential will be produced by postsynaptic cell; does not cause action potential; moves the positive charges towards the axon hillic to increase the likelihood of reaching threshold

96
Q

Inhibitory neurotransmitters

A

decrease the change action potential will be produced by postsynaptic cell; does not prevent action potential; draws positive charges away from the axon hillic decreasing the chance of reaching threshold

97
Q

Monoamine hypothesis of depression

A

there isn’t enough neurotransmission involved with serotonin (5-HT)

98
Q

Serotonin and depression

A

low levels of serotonin transmission leads to depression

99
Q

Risorine

A

drug designed to increase the amount of serotonin in the synaptic clef in both the central and peripheral nervous system to lower blood pressure, it was reported that people wouldn’t feel as sad when taking the drug

100
Q

Serotonin and peripheral nervous system

A

causes vascular smooth muscle to relax decreasing blood pressure

101
Q

Tricyclics

A

three drug classes that treat depression, prevents reuptake of 5HT by inhibiting the transporter protein which would reuptake 5HT increasing the time 5HT was in the synaptic clef and increasing transmission

102
Q

Tricyclics side effect

A

also prevents the reuptake of norepinephrine

103
Q

Norepinephrine

A

created by the locus ceruleus and is transported everywhere in the brain in response to epinephrine, causes corticol arousal and increases alertness

104
Q

Locus ceruleus and sleep cycle

A

the activity of the locus ceruleus decreases as the phases of sleep continue

105
Q

MAO

A

monamine oxidase, found generally in postsynaptic membrane to break down serotonin

106
Q

MAOi

A

monamine oxidase inhibitor, inhibits enzymatic degradation of serotonin by binding to MAO

107
Q

MAOi side effect

A

inhibits the breakdown of norepinephrine leading to more alertness and disturbed sleep cycle

108
Q

Fluoxetine

A

reported to be a selective serotonin reuptake inhibiter (SSR), blocks only serotonin transporters

109
Q

Postsynaptic potentials

A

are graded potentials

110
Q

IPSP

A

inhibitory postsynaptic potential leads to hyperpolarization

111
Q

EPSP

A

excitatory postsynaptic potential leads to depolarization; when EPSP reaches threshold action potential will occur

112
Q

EPSP and IPSP over time

A

the potential of the membrane over time will fluctuate between IPSP and EPSP

113
Q

Quanta

A

the amount of neurotransmitter released by a neuron, under normal circumstances it will be the same amount and the same type of neurotransmitter released by a neuron

114
Q

Amount of receptors on the postsynaptic membrane

A

is always the same leading to the same change of membrane

115
Q

Summation of graded potentials

A

if a neuron fires once and then again but before the first graded potential is over the second graded potential will begin leading to the graded potentials being summed, allowed because the mechanism for graded potentials is a ligand gated ion channel which is dependent on the concentration of the ligand

116
Q

Summation of action potentials

A

cannot happen due to the refractory period which allows for propagation and prevents cytoxicity

117
Q

Temporal summation

A

successive firing of an excitatory neuron causing graded potentials to be summed

118
Q

Spatial summation

A

more than one neuron firing at the same time interacting with different spots on the postsynaptic membrane leading to graded potentials being summed

119
Q

IPSP and EPSP firing together

A

can lead to a lack of net change in the membrane

120
Q

Temporal and spatial summation

A

can lead to reaching threshold and an action potential

121
Q

Axoaxonic synapse

A

synapse between a presynaptic neuron and a facilitating interneuron which will change whether or not the presynaptic neuron will release neurotransmitters

122
Q

Autorecetpros

A

presynaptic neurons have receptors for the neurotransmitter they release so that it is able to detect if it released the neurotransmitter and has a negative feedback response

123
Q

Agonist

A

will bind to a receptor and have the same effect as the normal neurotransmitter

124
Q

Antagonis

A

binds to a receptor but doesn’t activate it, it will bind to the side or sit in the channel to block it

125
Q

Drugs and autoreceptors

A

there’re drugs that will interact with autoreceptors so that the autoreceptor doesn’t tell the neuron that it is releasing the neurotransmitter leading to a break in negative feedback loop

126
Q

Neuromodulator

A

molecule released by a neuron that acts on multiple cells through diffusion

127
Q

Adenosine

A

is a neuromodulator, binds to receptors and shuts down neuroactivity around it, levels of adenosine build up due to higher metabolism of ATP

128
Q

Caffeine

A

antagonist for adenosine receptors, keeps cAMP in neurons by inhibiting phosphodiesterase

129
Q

Acetylcholine

A

exciatatory neurotransmitter, when released by motor neurons onto skeletal muscle cells it will cause skeletal muscle contractions

130
Q

Fostridium tetni

A

tetanus produces a toxin which leads to tetanic paralysis, this suggest that the toxin facilitates the interaction between SNARE and synpatotaged without the need of calcium leading to a high amount of acetylcholine release, effects the masseter causing lock jaw

131
Q

Tetanic paralysis

A

sustained muscle contraction

132
Q

Botulinum toxin

A

causes flaccid paralysis by preventing the release of acetylcholine by locking SNARE proteins leading to them unable to react with synaptotagmin, can be used medicinally for chronic cramping or cosmetically to prevent contraction of muscles leading to less pronounced wrinkles

133
Q

Flaccid paralysis

A

inability to have muscle contractions

134
Q

Black widow spider

A

produces a venom which leads to motor neurons getting rid of all acetylcholine at once so that the stores of acetylcholine are lost, initially causes tetanic paralysis then flaccid paralysis

135
Q

Blow darts

A

have curare on the tips of the darts which is a fast acting antagonist for the acetylcholine receptor causing flaccid paralysis

136
Q

Nicotine

A

agonist for acetylcholine receptors in the central nervous system, leads to increase of alertness

137
Q

Nicotinic acetylcholine receptor

A

controls sodium channel

138
Q

Sarin nerve gas

A

inhibits acetylcholinesterase which breaks down acetylcholine leading to an increased expression of acetylcholine causing tetanic paralysis

139
Q

Myasthenia gravis

A

antibodies are made against acetylcholine receptor leading to flaccid paralysis, almost always starts on the left side of the face, will eventually lead to suffocation due to the diaphragm being effected

140
Q

Glutamate

A

derived from glutamic acid, excitatory neurotransmitter, all vertebraet species use this as a primary excitatory neurotransmitter

141
Q

Glutamate receptor

A

AMPA, NMDA, metabotropic glutamate receptor

142
Q

AMPA

A

ligand gated, ionic tropic, channel for sodium

143
Q

NMDA

A

ligand and voltage gated, there has to be a depolarization of 20-30mv, magnesium sits in the pore of the channel, once it’s released calcium will enter, there have to be enough sodium ions to have entered through AMPA to cause depolarization

144
Q

Metabotropic glutamate receptor

A

G protein coupled receptor, glutamate will bind, then the alpha subunit will activate phospholipase C which will break down a the membrane phospholipid PIP2 into DAG and IP3, DAG will stay in the membrane and activate protein kinase C which will lower the threshold of voltage gated calcium channels making it easier for calcium to enter, IP3 will move to the cell body and act as a ligand for calcium channels in the ER

145
Q

DAG

A

diacylglycerol

146
Q

IP3

A

inositol tris phosphate

147
Q

Dopaminsergic

A

neuron that produces and releases dopamine

148
Q

Dopamine

A

involved in modd, effects learning and memory processes, culprit in parkinsons, reinforces and reward system

149
Q

Ventral tegmental area

A

holds a lot of dopaminergic neurons which will release dopamine on o the nucleus accumbous ending to the reward and reinforcement circuit

150
Q

Olds and Milder

A

operantly conditioned rodents pushed down a bar in order to receive an electrical stimulation of the nucleus accumbous to lead to an action potential mimicking dopamine, the rodents eventually disregarded the need for food, water, and reproduction

151
Q

Opiods

A

resembles dopamine and leads to a sense of euphoria

152
Q

GABA

A

gamma amino butyric acid, released by a facilitating interneuron onto the presynaptic dopaminsergic neuron, primary inhibitory neurotransmitter, opens channels for chloride at the presynaptic neuron which will lower membrane potential and lower the amount of dopamine being released

153
Q

Opioid receptors

A

Delta or Kappa receptors, are on the facilitating interneuron, when an opioid binds it shuts off the neurotransmission of GABA and lead to the presynaptic neuron releasing dopamine in higher amounts due

154
Q

Endorphins

A

natural effect of shutting off GABA release

155
Q

Tolerance and downregulation

A

if the body anticipates something there’s downregulation and inactivation of the receptors which bind to that thing

156
Q

Downregulation of Delta or Kappa receptors

A

leads to the need for taking more of an opioid, the higher concentration of the substance for a fewer amount of receptors

157
Q

How drugs affect neurotransmission

A

increase leakage of neurotransmitter from vesicles in the cytoplasm lead to breakdown, increase transmitter release into the clef (tetanic tetni), block transmitter release (botulinum toxin), inhibit transmitter synthesis (amino acids, proteins which are made), block transmitter reuptake (SSRI, tricyclics), block clef enzymes that metabolize transmitter (MAOi, serin nerve gas), bind to receptors on postsynaptic membrane lead to antagonis to agonist transmitter action (nicotine: agaonist, curare: antagonist), inhibit or stimulate second messanger activity within postsynaptic cell (caffeine with cAMP)

Systemic Physiology (5 decks)

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