Chapter 4 - Electrical & Chemical Signalling Between Neurons Flashcards

1
Q

epilepsy

A

accounts of epileptice seizures throughout human history - often attributed to mystical or demonic forces now attributed to misfiring of electrical signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

galviani - 18th century - view on electrical stimulation and behaviour

A

reflexive responses of disscted frog legs to electrical impulses - figured that must have an impulse at some point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hans berger

A

inventor of the first EEG
waves differ through stages of sleep
electrical activity in the brain forms different wave patterns
confirmation of evolvement of electricity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

microelectrodes

A
  1. measure a neuron’s electrical activity
  2. deliver an electrical current to a single neuron
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how can it be easier to measure neuronal activity

A

since human neurons are very small - it is easier to look at bigger neurons - the giant axon of the squid which is visible to the human eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cations

A

positively charged ions - sodium and potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

anions

A

negatively charged ions - chloride, A- (negatively charged proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

two gradients that control the movement of ions

A

concentration gradient
voltage gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

concentration gradient

A

movement of ions to a space where there are fewer of them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

voltage gradient

A

opposites attract - movement of ions to a space where they are attracted to based on there charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

movement of chloride ions being impacted by both gradients

A

chloride in one side of the cup
concentration gradient causes it to move to the other side but voltage gradient does not allow a lot to go outside but outside is more negative and inside is more positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

resting potential

A

-70mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

rmp

A

a store of negative energy inside the neuron membrane relative to the outside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

internal potential at rmp

A

lots of negative proteins
lots of pottasium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

K+ characterstics

A

eflux of this controls hyperpolarization
easy to get in and out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

external potential at RMP

A

lots of sodium
lots of calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cl- ion characteristics

A

harder to move in and out
influx of these might cause hyperpolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

sodium potassium pump

A

3 NA out
2 K in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Na+ characteristics

A

causes depolarization by influx
controlled by voltage gated channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

inhibitory signals

A

hyperpolarization - reduce the chance that an action potential will be created

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

excitory signals

A

depolarizatin - increase the chance of the action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how an action potential is created

A

when the membrane recieves enough stimulation - voltage gated sodium channels and sidum flows in (depolarization)
pottasium gates open adn potassium goes out (repolarization)
sodium channels inactivate pottasium keeps flowing out (hyperpolarization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

rules of action potential

A
  1. one direction
  2. length of axon
  3. all or none law
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

relative refratory period

A

During relative refractory, voltage-gated potassium channels are open, allowing positively charged potassium ions to leave the cell. Some voltage-gated sodium channels begin to recover from inactivation and may be opened again.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
absolute refractory vs relative refractory
During absolute refractory, the neuron cannot fire another action potential. Relative refractory occurs after absolute refractory. During relative refractory, it is possible for the neuron to produce another action potential, but it requires a much greater stimulus to reach the threshold.
26
myelin in CNS
oligodendrocyte
27
myelin in the PNS
shwaan cells
28
myelin colour
white - white matter
29
nodes of ranvier
gaps in myelin - where the sodium and potassium channels are
30
purpose of myelin
signal goes faster - does not recieve resistance at every point - more efficent
31
saltatory conduction
signal doesn't react at every point
32
which disease attacks myelin
MS
33
2 types of interneuron signals
EPSP + IPSP - inhibitory and excitory
34
temporal summation
Temporal summation involves a single presynaptic neuron rapid-firing signals to a single postsynaptic neuron's synapse. Because the signals are received in rapid succession, they compound into a greater signal.
35
spatial summation
Spatial summation involves multiple presynaptic neurons simultaneously sending signals to a single neuron.
36
where are signals summed
axon hillock
37
postsynaptic potentials can be...
graded - vary in strength
38
what affects the influence of the dendrites
it's location in relation to the axon hillock - closer = more influence
39
hair cells + AP
displacement of hair cells opens up mechanically gated sodium channels in the sensory neuron which causes action potential and causes voltage sensitive pottasiuma dn sodium channels to open
40
anisthetic
prevent's action potentials
41
which cells have a lot of dendrites
cerebellum - purkinje cells
42
deep brain simulation
electrodes implanted deep in the brain stimulate a targeted area with a low voltage electrical current to facilitate behaviour - parkinsons, epilepsy, and other brain disorders
43
deep brain stimulation in parkinson's
cell die in substantia nigra - in the mid brain - stimulation in this area
44
hypothesis of the otto loewi
stimulated the vagus nerve of a frog heart in water - slow beating connected fluid transfer also slowed the heartbeat - evidence of chemical neurotransmitter
45
1st neurotransmitter
acetylecholine
46
criteria for identifying neurotransmitters
1. chemical must be synthesized or present in neuron - created inside or produced onsite 2. when released chemical must produce response in target cell 3. same receptor action must be obtained when chemical is experimentally placed on target 4.there must be a mechanism for removal after chemical's work is done
47
microtubule
transport structure that acrries substances to the axon terminal
48
mitchondrion
organelle that provides the cell with energy
49
synaptic vesicle
round granule that contains neurotransmitter
50
storage granule
large compartment that holds synaptic vesicles
51
synaptic cleft
small space seprating presynapti c termicnal and postsynaptic dendritic spine
52
presynaptic membrane
encloses membrane that transmit chemical messages
53
postsynaptic membrane
contains receptor molecules that recieve chemical messages
54
postsynaptic receptor
site to which a neurotransmitter molecule binds
55
electrical synapses are
gap junctions - fast but inflexible can't amplify or diminish signal
56
neurotransmitter release
action potential reaches terminal opens calcium channels calcium binds to protein forming a complex complex binds to vesicles - releasing some from filaments or exocytosis
57
steps of neurotransmission
synthesis release receptor action inactivation
58
synthesis
some neurotransmitters are trandported from the cell nucelus and others are made from building blocks imported into the terminal and are packaged into vesicles
59
release
in response to an action potential the transmitter is released across the membrane by exocytosis
60
receptor action
the transmitter crosses the synaptic cleft and binds to a receptor
61
inactivation
the transmitter is either taken back into the terminal or inactivated in the synaptic cleft
62
5 types of inactivation
diffusion enzyme degradation reuptake astrocyte uptake autoreception
63
diffusion - inactivation
float away - maybe picked up by other cells
64
enzyme degradation
neurotransmitter will be broken down by enzymes
65
reuptake
taken back up into presynaptic cell
66
astrocyte uptake
taken back up by astrocyte and used again at some point
67
autoreception
might engage the neurotransmitter on presynaptic cell - used as feedback mechanism
68
neurotransmitter activated receptors
act as binding sites for specific neurotransmitters
69
two types of receptors
ionotropic + metbotropic
70
ionotropic receptor
simple fast lets ions in depolarixe or hyperpolarize
71
metabotropic receptor
involved and delayed g protein + 2nd messenger first messenger is metabotropic receptor second messenger is g protein which sends enzyme to nucleus to change DNA
72
dna change by metatropic receptor
results in structural changes in neurons
73
examples of plastic changes in neuron
- increased axonal transport - increase in number of synaptic vesicles - changes in size of synaptic cleft - change in stem length and width - increase in protein transport for spine construction - increase in size or area of spine - increase in density of contact zones - increase in size or area of terminal - more dendrites goes both ways - increase/decrease changes dont stay
74
neurotransmitter activating systems
a series of connected neural pathways in which one specific neurotransmitter dominates
75
main neurotransmitters
acetylecholine dopamine norepinphrine serotonin
76
acetylcholine function
in cholinergic system - midbrain and basal forebrain learning, memory with attention and waking us up primary NT of the PNS goes to muscle fibers and depolarizes
77
norepinephrine function
in the noradrenergic system provides energy to sympathetoc nervous system to kickstart with acetylcholine
78
two main pathways of dopamine
nigrostriatal and mesolimbic pathway
79
nigrostriatal pathway for dopamine
repetitive and moderated movements in the substantia nigra
80
mesolimbic pathway for dopamine
in the basal ganglia - nucleus accumbens - reward center
81
overactivity of dopamine leads
schizophrenia
82
seratonin function
in brainstem and digestin - mood and emotion schizophrenia + lsd - HALLUCINATONS controls appetitive since its lined with seratonin neurons major NT in sleep cycles
83
glutamate
excitory in the CNS most numerous
84
GABA
inhibitory in the CNS
85
neuroinflammatory response
defense mechanisms that intially protect the brain against pathogens carried out by microglia and assisted by atsrocytes glutamate and GAB modulate
86
too much glutamate
excitoprosisity - overexitability - overinflammation - damage aka stroke astrocytes supposed to help with reuptake of glutamate
87
role of microglia and astrocytes in neurodegenerative diseases
both can switch from neuroptoective role to neurotoxic one - may differ with the severity and stage of disease
88
neuropeptide NTs
opiods and endorphins natural painkillers - drugs
89
agonist
substance that enhances the function of neurtransmitters at a synapse
90
antagonist
substance that inhibits the function of neurotransmitters at a synapse
91
Ach agonist - diet
choline rish diet increases acetylcholine - not produced naturally in CNS
92
agonist ACh - black widow
starts as agonist - increases acetylcholine - muscle switches - exahusts - rigid muscle - stop breathing - not usually in humans
93
botulin antagonist Ach
boutlin toxin blocks release - type of food poisioning
94
agonist Ach nicotine
nicotine stimulates Ach with sensitivyt increase for nicotine - increases focus
95
anatognist in Ach - curare
blocks and crowds receptors
96
agonsit - Ach enzymes
physostigmine and organophosphates block enzyme degradation
97
agonist MAO inhibior seratonin
inhibits breakdown of seratonin so there is more for release
98
selective seratonin reuptake - agonist
block transporter protein for serotonin reuptake so that serotonin stays in the syanpse longer