Neurons Flashcards
1
Q
how is brain activity tracked
A
O2 usage in tissues
2
Q
optogenetics
A
changes in cell function using light gated ion channels
3
Q
blood brain barrier
A
filters most particles out of blood that reaches brain
4
Q
what animal has giant axons
A
squid
5
Q
nerve related diseases
A
MS, alzheimers, huntingtons, epilepsy
6
Q
integration
A
coordination of functions via receiving and then sorting signals out
7
Q
autocrine
A
releases smth to bind to self receptors
8
Q
paracrine
A
signaling to nearby cells in tissue
9
Q
endocrine
A
signaling molecules move thru system via blood. long-term, metabolism, growth, reproductive cycles = coordination of tissues
10
Q
synaptic signaling
A
specialized APs and neurotransmitters, spec to target cell where endocrine is general
11
Q
why are neurons important
A
instant action. needed for being predator or prey
12
Q
signal pathway in neuron
A
synapse > dendrite > cell body > hillock (AP starts) > axon > synapse
13
Q
glial cells in CNS purpose
A
half of brain cells, direct and connect and protect neurons
14
Q
astrocytes
A
glial CNS cells, connect neurons to blood vessels for nutrients
15
Q
microglia
A
glia in CNS, brain immune cells
16
Q
oligodendrocytes
A
insulation in CNS, wrap around cells many times and can wrap many neurons
17
Q
Schwann cells
A
insulation in PNS. only cover 1 neuron and wrap around 200+ times
18
Q
membrane potential
A
Vm , measured in mV
19
Q
resistance
A
Rm (ohms). low resistance inside axon and high membrane resistance is ideal for prop of AP
20
Q
length constant
A
l, or lamba. = the time it takes for 37% of the signal to degrade (related to length the signal travels while strong, we want it to be large)
21
Q
ohms law
A
V=IR
22
Q
voltage
A
separation of + and - charges
23
Q
current
A
movement of ions
24
Q
ohms law in cell terms
A
ion flow = membrane potential/resistance
25
krogh principle application
squid axons use same principles as ours
26
square wave
the blip in current when it is applied
27
depolarization of membrane is..
graded until it reaches AP threshold
28
time constant
the delay btwn peak of stimulus and peak of the response depolarization
29
hyperpolarization
movement of charge further from 0
30
lambda (length constant) eq
k(sqrt(membrane R/internal R))
31
maximizing lambda in verts vs inverts
usually verts minimize int resistance somewhat but focus on maximizing membrane R. inverts minimize int resistance and dont care about membrane
32
Nernst eq
z(61)log(Cext/Cint)
33
the resting Vm is closest to equilibrium for..
whatever species is most permeable
34
goldman eq
shows total membrane potential, 61log(P(Cext)+.../P(Cint)..) or the int/ext for anions. with each species in the cell involved in this eq
35
how many ions cause potential change
literally a few out of thousands
36
action potential magnitude
always the same, but can show diff signal by the freq of APs
37
parts of AP
resting, rising phase, overshoot, falling phase, undershoot, back to resting
38
channels open in resting neuron
just leaky K
39
Hodgkin cycle
Na channels. they open at threshold (-50 mV), cause more depolarization, stay open, more open, at 40 mV the second gate closes but the first stays open until cell gets back under -50.
40
voltage gated K open/close
open around 40 mV, close at -70 or -80
41
channels open during rising phase
leaky K, voltage Na
42
channels open during overshoot
all 3 types
43
channels open during falling
just K (voltage and leaky). same for undershoot
44
tetradotoxin
inhibits voltage gated Na channels
45
absolute refractory period
during high peak, there absolutely cannot be another AP (they cannot amplify one another) because the Na inactivation gate stays closed during falling phase
46
relative refractory period
during undershoot, sometimes another stimulus can activate Na channels before the neuron is back to resting potential. but the purpose of undershoot is to make this more difficult
47
speed of AP prop
55 mph
48
what part of neuron has graded potentials
dendrite
49
when circumference of axon doubles
Rm halves, but Ri dec exponentially
50
saltatory conduction
AP jumps thru insulation and is refreshed at nodes of Ranvier
51
invert myelin
not same thing but crustaceans have their own version
52
7 main neurotransmitters
norepinepherine, acetylcholine, serotonin, dopamine, GABA/glycine, glutamine
53
electrical synapses
neurons connected by gap junction, AP travels directly thru (slows down AP a little but still fast)
54
chemical synapses
neurotransmitters released at end of one neuron stimulate response when picked up by next neuron receptors. can be ionotropic or metabotropic
55
ionotropic synapse steps
faster. AP activates Ca channels at synapse, the Ca activates SNARE and vesicles release NT into synapse. receptors are ion channels, and open or close having some effect (often AP at the next cell)
56
metabotropic synapse steps
slower, AP activates Ca channels at synapse, the Ca activates SNARE and vesicles release NT into synapse. receptors are GCPRs which can have cascading effects, learning, memory, etc.
57
gates at the end of axon
calcium gates activated by voltage at end of AP, Ca comes in and activates proteins for vesicle movement so neurtransmitters released
58
vesicle proteins in axon
SNARE proteins. activated by Ca, deactivated (cleaved) by botulinum and also the tetanus toxin
59
post synaptic potential
graded potential at cell body. can be EPSP (excitatory, depolarization - lets in Na+) or IPSP (inhibitory, hyperpolarization - lets in Cl-)
60
types of neurotransmitter molecules
amino acids (glutamate, GABA/glycine) - usually ionotropic, biogenic amines (acetylcholine, norepinepherine, dopamine, serotonin) - usually longer lasting and metabotropic
61
what determines cell response to neurotransmitters
type of receptors at synapse
62
muscarine receptors
slow the heart rate. activated by acetylcholine but also poison mushrooms
63
how does neuron integrate signals
summation of magnitude of inputs based on magnitude and distance from hillock.
64
presynaptic inhibition
a synapse can exist on an axon to stop the AP from reaching its target cell
65
NMJ
neuromuscular junction, each muscle cell has only one nerve cell controlling it (neurons can control multiple muscle cells). always nicotinic acetylcholine receptors (excitatory). junction is HUGE with LOTS of Ach released. each AP gives a response (relay signal)
66
acetylcholinerase
destroys Ach. and the products go back to og neuron to be recycled. its inhibitors include pesticides and nerve gas (muscles stay constantly flexed). also can treat alzheimers by helping the nt stay in junction longer so a normal amount can build up
67
alcohol effects
disrupts cell membranes so many processes are changed
68
nicotinic receptors
acetylcholine, ionotropic EPSPs
69
muscarinic receptors
acetylcholine, metabotropic IPSPs
70
agonist
increases the effect of smth
71
curare
used in poison arrows, antagonist of nicotinic receptors, leads to respiratory arrest. can be counteracted by acetylcholinerase inhibitors
72
synaptic plasticity
mechanism of learning and memory, synapses change based on inputs
73
habituation
decrease in response upon repeated exposure
74
sensitization
having a reaction again and the reaction increases to something that it was accustomed to when a different stimulus is given (resets pathway)
75
facilitation
successive PSPs increase in amplitude when presynaptic APs have a higher freq
76
antifacilitation
successive PSPs decrease in size as freq of APs from the neuron increases
77
how do facilitation and antifacilitation occur
change in NT release or receptors at synapse
78
aplysia
sea hare/slug. syphon withdrawal demonstrated habituation and could be reset by an electric shock
79
aplysia experiment mechanism
NMJ monitored with electrode when touch stimulus was given (electrode activated sensory neuron and the corresponding nmj magnitude was recorded), activation dec but unsure if it is due to receptors or NTs. when pain neuron is activated, it triggers serotonin receptors before the sensory neuron synapses and these are metabotropic GPCRs, activate vesicle proteins to put out more NT and cAMP activates a kinase that mobilizes vesicles, inactivates the K a bit, allowing Ca channels to stay open longer (more NT released). this is sensitization
80
LTP
long term potentiation. shown in rat brain. enhancement of synaptic transmission after intense stimulation at some past time.
81
hippocampus
part of the brain for long term memory and spatial learning.
82
tetanus
a bombardment of APs
83
nerves in the rat experiment
CA3 stimulates, PS is CA1
84
CA1 neuron setup
starts with NMDA receptors blocked by Mg, and AMPA (both activated by glutamate and should let in Na). extreme stimulus (tetanus) causes depolarization, Mg leaves NMDA, NMDA lets Ca in, which activates more implantation of AMPA and other cell processes via calmodulin inc expanding the synapse. after stimulus, NMDA is blocked again but the permeability and therefore PSP has changed
85
how can LTP happen
large stimulus like strong emotion, or repetition
86
what feedback does LTP demonstrate
positive
87
proof NMDA helps with hippocampus
mice (Doogie) with more NMDA were more curious and had improved spatial memory
88
nervous system
cells designed for repeated conduction of electrical signals
89
CNS
brain, spinal cord
90
PNS
sensory and motor neurons
91
nerve
bundle of neurons in PNS (afferent and efferent)
92
ganglia
PNS grouping of cell bodies and synapses
93
diff btwn CNS and PNS neurons
there is none
94
path of info in spinal cord
goes in dorsal root and out ventral
95
white matter
glial cells
96
grey matter
neurons
97
what does autonomic NS control
smooth muscles, exocrine glands, cardiac muscles, some endocrine glands (adrenal)
98
somatic NS
skeletal muscles
99
involuntary reflex
signal goes to spinal cord, must contract one muscle and relax its pair, and tell brain to be alert for this stimulus
100
parasympathetic impacts
rest and digest - inc bile, digestion, blood vessel dilation, dec bp
101
sympathetic impacts
fight or flight - activates adrenal, blood to muscles and lungs, bp up, vasoconstriction, pupils contract
102
autonomic ganglion
where the signal from NS switches neurons to go to effectors, all pos and fast, nicotinic with Ach
103
catecholomines
epinepherine, norepinepherine
104
somatic synapses
more myelin, travels body with no synapse until destination, always Ach and nicotinic
105
norepinepherine receptors in autonomic ns type
metabotropic with GCPRs. alpha1, alpha2, beta1 = adrenergic receptors
106
beta blockers
block beta receptors for norepinephrine in the heart, brings down heart rate
107
dopamine reuptake inhibitors
cocaine, meth, adderall (receptors are saturated with dopamine (usually metabotropic)>reward response/excitatory)
108
serotonin reuptake inhibitors
depression meds (receptors are saturated with serotonin (usually metabotropic)>inhibitory)
109
ketamine
inhibits NMDA receptor for for glutamate (excitatory)
110
typical glutamate receptors
AMPA, NMDA
