Chapter 6 and 7

Question 1

Myasthenia Gravis

Answer 1

Problem with synaptic transmission with acetylcholine

Question 2

Presynaptic terminal

Answer 2

Axon terminal

Question 3

Neurotransmitter

Answer 3

Ligand that gets released from axon terminal

Question 4

Synaptic cleft

Answer 4

Synaptic space

Question 5

Postsynaptice terminal

Answer 5

the membrane of the dendrite or cell body that receives the ligand and allows ligand to open up gates and change polarity.

Question 6

Events at synapse

Answer 6

Action potential reaches the end of the line,
action potential opens voltage gated channels that let calcium in (moves all the vesicles down to the very end of the axon),
vesicles of neurotransmitters fuse with the membrane of the end of axon and open up and let all of neurotransmitters out into the synaptic space,
Neurotransmitters migrate across the synapse and binds to receptor on the membrane channel and cause membrane channel to open and allow ions to flow through,
Once ions enter postsynaptic cell they start the local potential right at the channels (if big enough, it sparks an action potential).
Mechanisms clear the synapse and get it ready for the next signal (enzymes)

Question 7

Axosomatic synapse

Answer 7

from axon to the cell body of the next neuron (increase or decrease the chances that an action potential will be created in the next neuron)

Question 8

Axodendritic synapse

Answer 8

From axon to the dendrite (increase or decrease the chances that an action potential will be created in the next neuron)

Question 9

Axoaxonic synapse

Answer 9

axon of one neuron makes a synapse with the axon of a different neuron- increases or decreases the amount of neurotransmitter that gets released (the NS can adjust how much neurotransmitter gets released)

Question 10

EPSP

Answer 10

excitatory postsynaptic potential- starter signal for something bigger, most often with sodium or calcium going into the cell. Increases likelihood of action potential-facilitation (depolarize)

Question 11

IPSP

Answer 11

Inhibitory postsynaptic potential- small and graded and doesn’t go very far. inhibitory local potential, caused most often be letting chloride go in or potassium go out. Hyperpolarize

Question 12

Presynaptic facilitation

Answer 12

anything that increase the amount of calcium channel opening in the transmitting axon will increase the amount of neurotransmitter that will be released into the synapse. (anti-depressant drugs may do this)

Question 13

Presynaptic Inhibition

Answer 13

Reduces Calcium influx, inhibits neurotransmitter release. (rubbing it to decrease pain) prevent calcium channels from opening (TENS unit)

Question 14

Two Categories of ligands

Answer 14

Neurotransmitters- ligand released into the synaptic cleft. Acts immediately on synaptic receptors, can excite or inhibit (quick and short lived response).
Neuromodulators- released outside of the synapse, can affect many neurons, slower onset and longer lasting, same molecule can be either (it just depends)

Question 15

Directly open ion channels

Answer 15

(fast) part of the membrane channel is directly opened and lets ions in right away when bound to (most often in the synapse and really good for signaling).

Question 16

Indirectly open ion channels

Answer 16

Slow- binds to another protein that indirectly opens the gate (can be inside or outside the synapse). Ligand binds to a receptor which activates the g protein complex inside the cell. g protein floats over and activates (opens) the channel from inside the cell. (butler hears the doorbell) takes longer to occur but the door stays open longer

Question 17

Activate intracellular events

Answer 17

Slow- ligand binds and it goes and flips a switch on an intracellular machine (enzyme) which makes stuff). Ligand binds to g protein receptor again (gets energized by ATP, breaks off and turns on the enzyme from inside the cell which then makes stuff. Second messenger sequence (1st messenger is our neuromodulator (ligand) that binds to g protein. 2nd messenger is the something that is created by the enzyme (makes something that affects cell function somewhere else)

Question 18

Agonist

Answer 18

nontraditional ligands that can enhance the effects of internal ligands. Nicotine- binds and mimic the same type of receptor such as acetylcholine and mimic the effect of natural ligands. can increase effects of acetylcholine. It can also facilitate the release of the neurotransmitter which increases the effects of a ligand.

Question 19

Antagonist

Answer 19

Will diminish the effects of indigenous ligands. will either bind/block receptor or it will diminish how much neurotransmitter gets out of the receptor membrane. Botox- acts at the calcium channel and prevents the calcium channel from opening. prevents the neuron from sending acetylcholine.

Question 20

Acetylcholine

Answer 20

facilitatory/excitatory. it depolarizes when it binds. can be fast action and gets out of the way for the next to come. in the PNF it is fact acting at the neuromuscular junction. is slow acting in the autonomic nervous system and in the CNS (some sort of G protein that is linked to a membrane channel) slow to open but effects last longer)

Question 21

Glutamate

Answer 21

Excitatory (depolarizes) good and bad
good- makes action potentials for the brain to work.
Bad- too much is also toxic for brain cells.
Most prevalent fast acting excitatory neurotransmitter in CNS.
Fast acting (CNS) AMPA receptor
Slow actin (CNS) NMDA receptor.

Question 22

GABA

Answer 22

Amino Acid, Inhibitory (hyperpolarizes) fast acting in the CNS (GABAa receptor), slow acting in the CNS (GABAb receptor). Most prevalent fast acting inhibitory neurotransmitter in CNS.

Question 23

Dopamine

Answer 23

Motor control, plays role in cognition and in behavior (can cause pleasure but can also cause addictive behavior)

Question 24

Norepinephrine

Answer 24

In the NS it increases awareness and attention to sensory information. In the ANS it is part of the sympathetic system (fight or flight)

Question 25

Serotonin

Answer 25

one of our anti-depressant neurotransmitters, affects mood and our perception of pain, adjusts our level of arousal.

Question 26

Histamine

Answer 26

Inflammation neurotransmitter, part of inflammatory process.

Question 27

Interaction effect

Answer 27

how different medications and neurotransmitters interact with eachother.

Question 28

Peptide

Answer 28

Two types
Endogenous opioids- pain relieving, turn down signaling in the pain pathway.
Substance P- the neurotransmitter of the pain pathways can send the signal of pain or enhance the route for the perception of pain. It is overactive in those with chronic pain.

Question 29

Down regulate

Answer 29

reduces chances of action potential or signal in this pathway. Internalizing- pulling receptors down inside the cell so that the receptors cannot be activated and opened.
Inactivate- leave the receptors there but lock the gate so it no longer opens.

Question 30

Up regulate

Answer 30

increases the odd of an action potential. Externalize- take receptor that is floating inside the cell and stick it up into the membrane.
Activate- to unlock the gate and allow to open so that ions can flow through the channel into the cell.

Question 31

SSRI (selective serotonin reuptake inhibitor)

Answer 31

anti-depressant drug that turns off the vacuum cleaner letting serotonin float around the synapse longer which increases the likelihood that it will have an effect.

Question 32

Habituation

Answer 32

Decrease in response to a repeated, benign stimulus.

Question 33

Short term habituation

Answer 33

turns down the signaling in a specific pathway. there are billions of neurons and tons of connections and ties into presynaptic connection. Neurons make presynaptic connections that are more presynaptic inhibition or less presynaptic facilitation, both reduce the amount of neurotransmitter that spills out into the synapse. cognitive and emotional state in rest of brain can influence cell signaling in the rest of the brain.

Question 34

Long term habituation

Answer 34

Post synaptic membrane can take receptors away (down regulate- bring receptor sites into the cell which is an adaptation due to it being a structural element change.

Question 35

Long Term Potentiation (LTP)

Answer 35

to make it easier for synaptic signaling. (us trying to commit something to memory everyday with learning) turning up the strength of synaptic connections

Question 36

LTP- Converting from silent synapses

Answer 36

Convert silent synapse into an active one.

Question 37

Silent synapse

Answer 37

closeness of presynaptic membrane and postsynaptic membrane but no signaling- a physical synapse but no signaling

Question 38

AMPA (receptors)

Answer 38

fast acting, but buried in the cell, why there is no signaling. Responsive to glutamate (let in sodium for action potentials)

Question 39

NMDA

Answer 39

Responsive to glutamate but off to the side of the neuron. It is a G protein mediated opening of the gate. Slow acting, stays open for a long time (lets in calcium, not for action potentials but for remodeling the cell) bringing AMPA receptors to cell surface.

Question 40

NMDA and calcium

Answer 40

neuron releases glutamate trying to make an action but the receptors aren’t therem we keep trying and the NMDA opens and stays open for a long time and lets calcium in. calcium does 2 things to promote learning in postsynaptic membrane.

1) it tells the AMPA receptors to get up in the membrane (pathway is now active and the action is much better (cell remodeling)
2) helps the effort of the task go down. calcium breaks the postsynaptic membrane into spines so the cell depolarizes at multiple different spines and creates an action potential at each spine (spatial summation) greater outcome and makes action easier/makes more connections (learning)

Question 41

Importance of astrocytes

Answer 41

They can store and release calcium and glutamate

Question 42

LTD- Long term depression

Answer 42

Down regulating (takin receptors out of the cell membrane)- stimulate with benign stimulus so that it remodels the membrane and pathways. Turning down the strength of synaptic connections. When stimulus is repeated the NS realizes it doesn’t need as many receptors and so it takes away channels at the cell membrane (structural change)

Question 43

Penumbra

Answer 43

shadow of death in the brain- around the cells that have died. a number of cells that are without oxygen and sugar and have fallen asleep, could die next.

Question 44

excitotoxicity

Answer 44

process that could kill the cells in the penumbra. when a cell gets killed it spreads its guts that have a lot of glutamate in them. When it spills to the surrounding cells it opens NMDA channels in all the cells which lets in too much calcium and kills the effected cells. The calcium turns on glycolysis and acids itself to death, too much calcium lets in protease which eats cells/[proteins. Protein enzymes are turned on inappropriately and bring too many oxygen free radicals that are poisonous. too much calcium going into the cell brings a lot of fluid with it causing the cell to swell up and can burst=solute

Question 45

Axonal injury

Answer 45

Damage to point of death at a node of ranvier, the axon lesion (has been squeezed to death and 3 things happen distal to point of death)

1) axon distal to point of death will degenerate
2) Myelin from point distal will also degenerate
3) the muscle will atrophy because it is no longer innervated/connected

proximal piece that has survived can regrow.

Question 46

Wallerian degeneration

Answer 46

distal degeneration of axon and myelin distal to injury.

Question 47

Collateral Sprouting

Answer 47

extra sprouts that innervate what has lost its nerve supply. One neuron on left dies completely, surviving neuron on left senses there is a missing connection and sends out a collateral branch to reconnect tissue to nerve supply.

Question 48

Regenerative sprouting

Answer 48

the surviving proximal axon can regenerate itself. The distal axon dies and the axon body regenerates and connects itself to a tissue. At the rate of about one inch per month.

Question 49

Damage in CNS

Answer 49

functional regeneration does not occur. excitotoxicity occurs more often in CNS than in the PNS

Question 50

Cellular recovery from injury

Answer 50

recovery of synaptic effectiveness- area of neuroinflammation shuts off synaptic transmission to another axon. A piece of the skull is taken out so brain is able to swell out during inflammation so the brain can stay alive (also given meds that reduce fluid in body and NS), Once edema/ inflammation goes down, the brain is able to wake neurons back up and return to function.

Question 51

Denervation hypersensitivity

Answer 51

Upstream neuron is damaged by stroke or trauma looses connection with another axon. this creates a hypersensitive membrane that is searching for input.

Problem: all receptors may become triggered by neurotransmitter that is floated from another synapse. NS is trying to get the signal back

Question 52

Synaptic Hypereffectiveness

Answer 52

Axon upstream has 3 terminal branches to another axon. two vesicles are at each end of axon terminal. Damage has taken away two terminal branches and the surviving axon branch was made stronger by the body by putting 4 vesicles in the axons terminal hoping to flood synapse with more ligand to make up for the decrease in number of connections.

Question 53

Unmasking silent synapses

Answer 53

What patients come to therapy for. Many silent synapses in our brain and our job is to wake them up within the contexts of meaningful function. Increases dendritic spines that emerge to increase the odds of an action potential.

Question 54

Functional reorganization of the cerebral cortex

Answer 54

Map of KC with blocked bridge example

Question 55

Squirrel monkey brain study

Answer 55

whatever part of the body that moved after electrical stimulation shows the part of the body that an area of the brain has the strongest connection with. showed what areas were activated with a task of eating. gave the monkey a stroke and made it eat with the affected side. Saw the brain remap and areas of the brain were repurposed to focus on digits and wrist motion because that is what was needed for function of task. ABA design proved the findings. returned to eating preference of the monkey and brain reverted back to initial mapping. Used CIMT again and the brain remapped again to the same findings post stroke CIMT.