Exam 2 Flashcards
(156 cards)
1
Q
what are the two main functions of a neuron?
A
regulate bx (keep things in optimal range)
info processing (transmit, integrate, store)
2
Q
what are the five categories of neurons?
A
inhibitory: local & distant
excitatory: local & distant
neuromodulatory (diffuse area, mainly distant)
3
Q
where on the neuron is the input zone located at? what does it do?
A
dendrites & soma
- electrical signal due to ligand/receptor that causes a rxn (channel open / close)
- passive current (no AP)
4
Q
where on the neuron is the integration zone located at? what does it do?
A
axon hillock
- several messages coming in are summed (EPSP, IPSP) and if they are strong enough, they generate an AP
5
Q
where on the neuron is the conduction zone location at? what does it do?
A
axon, myelin
- regenerates current that moves along axon so it stays at a consistent strength
6
Q
where on the neuron is the output zone located at? what does it do?
A
axon terminal
- releases chemical signal (NT) to the next neuron
7
Q
what are the five ways neurons are classified?
A
- function / connection
- morphology
- axon diameter
- axon length
- chemistry (NT released = cholinergic, dopaminergic)
8
Q
what are the three names of the neurons classified by neuron function / connection?
A
sensory (recieves input) -> interneuron -> motor (to effector)
9
Q
what are the three ways neurons can be classified by their morphology?
A
- number of neurites (processes from soma)
- dendritic tree structure
- dendritic spines
10
Q
what are the three types of neurons named for the number of neurites? describe their differences and one example
A
bipolar = 2 processes, RETINA
unipolar = 1 process that splits, 1st ORDER SENS. NEURON
multipolar = 3+ processes, RGC & PYRAMIDAL
11
Q
what is the difference between pyramidal and stellate dendritic tree structure?
A
pyramidal = triangular, long (40% is dendritic spines)
stellate = round, star shape (local & distant signaling)
12
Q
what is the difference between spiny and aspinous dendritic spines? (excit or inhib?)
A
spiny = asymmetric synapses, excitatory (pyrm. & stellate)
aspinous = smooth, inhibitory
13
Q
what is the purpose of having dendritic spines? what are they?
A
small protrusions from dendritites
- increase surface area so it’s easier to receive the signal
- high plasticity (ability to adapt)
- reduced in diseases such as dementia
- exhibit LTP to increase activation
14
Q
what are the four types of neurons classified by their axon diameter (biggest -> smallest)? what are each of the used for?
A
A-alpha = proprioceptors in muscle (body position)
A-beta = mechanoreceptors
A-delta = pain, temp (fast than C)
C = pain, temp
15
Q
which axon diameters have the fastest and slowest conduction?
A
A-alpha = FASTEST, largest diameter
C = slowest, small diameter & unmyelinated
16
Q
what are the two types of neurons based on axon length? describe them
A
Golgi Type 1 = long axons, projection neurons
Golgi Type 2 = short / no axons, interneurons for local signaling
17
Q
what is another name for the presynaptic element of the synapse? describe what is located there
A
active zone (AZ)
- vesicles, fusion proteins, exocytosis machinery (docking, priming)
18
Q
what is another name for the postsynaptic element of the synapse? describe what is located there
A
postsynaptic density (PSD)
- receptors, channels
19
Q
what is the cleft of the synapse? what important molecule sites laterally in the cleft?
A
space b/w neurons
- CAMs sit on the sides of the neuron
20
Q
what do the presynapse, postsynapse, and astrocytes make?
A
tripartite synpase
21
Q
why do the astrocytes surround the cleft?
A
helps make diffusion more localized
- we don’t want molecules floating away
22
Q
what are the two types of synapses?
A
Gray Type 1
Gray Type 2
23
Q
what is the difference between gray type 1 synapse and gray type 2?
A
type 1 = asymmetric synapse (PSD thicker), EXCITATORY
type 2 = symmetric synapse, INHIBITORY
24
Q
what are 9 functions of astrocytes?
A
- role in synaptogenesis
- provide physical support thru tight junctions
- regulates microenvironment
- regulates and monitors glucose
- synaptic communication
- takes in glutamate
- circadian rhythm
- NS repair
- regulates BBB
25
what do astrocytes do in synaptogenesis?
secrete trophic & tropic factors involved in final stages
- TGF, Sem3a, EphrinA3, BDNF
26
how do astrocytes regulate the microenvironment?
localizes NT, and maintains proper K+ conc.
- absorbs K+ to allow for repolarization, RMP
27
how do astrocytes regulate glucose?
stores glycogen
- glycogen is converted to glucose = energy
28
how to astrocytes help with synaptic communication?
TRIPARTITE SYNAPSE
- metabolism of NT
- releases gliotransmitters (Ca2+ dependent, chemical signal)
29
where is circadian rhythm controlled?
suprachiasmatic nucleus (SCN)
- above optic chiasm
30
how do astrocytes help with NS repair?
when injury occurs to SC or brain, the cells form glial scars
31
how do astrocytes regulate the BBB?
- blocks toxins, NTs, lymphocytes from entering brain
- wraps around capillaries to prevet diffusion of molecules out by forming tight junctions around CNS capillaries, no fenstra!
- prevents glucose from entering unless its needed (active trans.)
- keeps brain environ. stable form lg. peripheral fluctuations
32
what does the myelin sheath do?
wraps around axon for saltatory conduction (faster)
- neurotrophic support
- injury responses
33
what are the two types of myelin sheath cells? describe the differences between them
oligodendrocytes = CNS, multiple myelin seg
schwann cells = PNS, single myelin seg.
34
for what reason do oligodendrocytes and schwann cells differ in their myelin segments?
in the CNS, we want to decrease CNS volume because we need way more neurons in the brain vs PNS
35
what are microglia?
CNS immune cells (since lymphocytes aren't allowed past the BBB)
- derived from yolk sac (prior to gastrulation)
- cleans out CNS debris
- role in development, plasticity (LTP, TD), and cognition
- highly plastic (reactive)!!
36
why are microglia highly plastic?
we need quick responses to injury in the brain
- several states of reactivity (resting state most reactive)
37
what activates a microglia response?
increased K+, inflammation, necrosis (cell death)
- extra K+ fluid outside of cell is damaging to neurons
38
what are ependymal cells?
glial cells that develop from radial glia to produce, circulate and reabsorb CSF
- line walls of ventricles (lots of neurogenesis)
39
what is the bioelectric potential?
electrical signal generated in a biological system
40
what does potential mean?
ability of a current to flow
41
what are the three types of bioelectical potentials?
- receptor potentials
- synaptic potentials
- action potentials
42
what are receptor potentials?
sensory cells
-mechanoreceptors = pressure by touch causes release of NT
43
what are synaptic potentials?
dendrites, soma
- act locally, chemically gated
44
what are action potentials?
axon
- activation of motor neuron, can travel long distances
45
what is a semipermeable barrier?
in the neural MB and is selectively leaky (some things get thru, some can't)
- fluid mosaic model
46
whats the fluid mosaic model?
hydroPHILIC phosphate heads = love water
hydroPHOBIC lipid tails = hate water
47
what are five MB proteins?
- receptors
- ion channels
- metabolic pumps
- transducers (G-protein)
- enzymes
48
whats the difference between non-gated and gated ion channels?
non-gated = pore always open, anything that fits thru gradient
gated = chemically, voltage, mechanically
49
difference between chemical, voltage, and mechanical gated ion channel?
chemical = postsynaptic side, open by ligand / receptor
voltage = generated & dependent on charge, open by change in MB potential
mechanical = physical movement (cilia bending), open by pressure or stretch
50
whats the difference between ion gated channels and metabolic pumpss such as the Na+ / K+ pump?
ion gated = passive current, no energy needed
metabolic pump = active current, requires energy
51
what are the two forces that move ions?
concentration gradient (C) = conc. of ions
electrostatic gradient (E) = charges of ions
52
what is high outside the cell?
Na+, Cl-
- more POSITIVELY charged
53
what is high inside the cell?
K+, A-
- more NEGATIVELY charged
54
what is the equilibrium / reverse potential? (E-rev)
the voltage when the two gradients are balanced, no ion movement
- distribution of a single ion across MB & it's potential for movement if channels are open
- constant number!!
55
what equation calculated the equilibrium potential?
Nernst Equation
- calculates equilibrium potential for ONE ion
56
in the Nernst equation....
what is Z?
(K+)O vs (K+)I?
R?
Z = valence of ion
O = conc. outside cell
I = conc. inside cell
R = gas constant
57
what does the gas constant account for?
pressure of gas and energy generated
58
what does faraday constant account for?
amount of energy produced from ions
59
what is the resting membrane potential?
net bioelectric potential for ALL ions (balance of both C & E)
-65 mV
60
what equation calculated the membrane potential? (Vm)
Goldman Equation
- allows us to predict movement of ions
- constantly changing
61
what is the permeability of K+, Na+, and Cl-? what is the leakiest
K+ = 1.0 LEAKIEST
Cl- = 0.45
Na+ = 0.04 LEAST LEAKY, good barrier
62
what is the driving force? (Vdf) what is the equation?
movement of ions and gives us direction & strength
Vm - Erev
63
what happens if the Vdf is 0?
no net cation / anions
64
what happens if the Vdf is positive?
cation efflux (OUT)
anion influx (IN)
* more positive OUT*
65
what happens if the Vdf is negative?
cation influx (IN)
anion efflux (OUT)
* more positive IN*
66
what is the Na+ / K+ pump?
3 Na+ OUT
2 K+ IN
- we want inside more negative
- maintains gradient at rest (no role in AP)
67
what are the two types of electrical currents in the neuron?
Postsynaptic Potentials (EPSP, IPSP)
Action Potentials
68
what are postsynaptic potentials?
passive current at the synapse (dendrites, soma)
69
what type of channel do postsynaptic potentials use? where are these located
chemically-gated channels (ionotropic)
- axodendritic, axosomatic, axoaxonic
70
how far to postsynaptc potentials travel?
locally
71
are postsynaptic potentials regenerated?
NO!
- electrotonic (push from one source to a target)
- decremental (decrease strength w/ time & distance)
- 10-100 msec
- moves only 2-3mm
72
which ones are faster, EPSP or IPSP?
EPSP (10 msec)!
- IPSP 100 msec
73
as resistance increases in the axon, what happens to the amount of leakage?
as resistance increases = leakage increases
74
do postsynaptic potentials summate?
YES!
- adds together multiple signals of EPSP & IPSPs
- occurs at axon hillock
75
what do EPSPs do to the membrane potential?
POSITIVE Vm = Na+ influx (depo)
76
what do IPSPs do to the membrane potential?
NEGATIVE Vm = K+ efflux & Cl- influx (hyerpol)
77
what are the two types of summation? describe them
Temporal = one synapse, 2 pulses
Spatial = multiple synapses, many pulses, close in space
78
what must both types of summation have in order to summate?
temporal contiguity
- close together in time
79
what is a postsynaptic potential more likely to produce, EPSP or IPSP?
EPSP
- we want the RMP to become more positive to produce an AP
80
where is an AP generated at?
axon hillock
81
what does an AP cause to happen?
the opening of voltage-gated channels
- detected by voltage sensors on the channel
82
during what part of the AP do voltage-gated channels open?
depolarization
83
during what part of the AP do voltage-gated channels close?
hyperpolarization & RMP
84
what is a selectivity filter?
on the channels to determine which ions can go through
85
what is the selectivity filter of the Na+ pore?
filled w/ negative charges that repel anions & attract cations
- K+ is too big for the pore
86
what is the selectivity filter of the K+ pore?
Na+ forms a strong bond to H2O, so as it tries to go through the pore, it forms a water cloud and becomes too big to pass
- K+ is dehydrated so it can easily pass thru
87
what are the three states of Na+ pore? when do these occur?
Deactivated @ RMP & hyper
Activated @ Depo
Inactivated @ end of Depo
88
what are the two states of the K+ pore? when do these occur?
Deactivated @ RMP & hyper
Activated @ end of depo
89
what causes the undershoot?
the slow closing of K+ channels
90
what are refractory periods?
parts of the AP where signals can no longer sum which allows it to repolarize
91
what is the absolute RP?
no stimulus can trigger an AP, Na+ channels need to reset
- depo curve above threshold
92
what is a relative RP?
need a larger than normal stimulus to trigger AP
- undershoot!
93
are AP's regenerated?
yes!
- allows for the signal to be boosted and travel long distances
- non-decremental = consistent strength w/ time & space (self-propagated)
- 1-2msec to reach axon terminal
94
what does all-or-none threshold potentials for AP's mean?
need the EPSP signal to be strong enough to reach threshold and trigger AP
- number of Na+ channels open is proportional to strength of depo
95
what is the sub-threshold potential?
right before depo reaches threshold (-40)
- increase of K+ efflux offsets Na+ influx
96
what is the frequency code of APs? what determines the duration of the AP?
intensity of stimulus is determined by frequency of APs (rate of APs, not magnitude)
- duration is determined by fast / slow adapting receptors
97
what is the difference between fast and slow adapting receptors?
fast = on or off
slow = continuous signal
98
as diameter of axon increases, what happens to the speed of APs?
faster AP due to less resistance
99
as myelination of axon increases, what happens to the speed of APs?
faster AP by plugging leak channels in axon, allows the passive current to not dissipate as much
100
what is the difference between the active and passive currents?
active = regenerated, but slow
passive = decremental, but fast
*AP uses both types of currents*
101
what is multiple sclerosis?
an autoimmune disorder that affects the inflammatory response
- due to CNS demyelination (loss of myelin segments)
- oligodendrocyte damage causes a slower conduction of APs and since they secrete neurotrophic factors it leads to damage of the axon due to a decreased glial trophic support
102
what are symptoms of multiple sclerosis?
monocular blindness (optic nerve)
motor weakness / paralysis (corticospinal tract)
dizziness (vestibular pathways)
increased inflammation (CSF)
103
what are four main causes of multiple sclerosis?
- persistant infection that increases the inflammatory response for a long period of time
- the cell adhesion molecule, Contactin-2, is similar in composition to a virus, so it will be destroyed when antibodies are present
- the bacteria, anterobacter, is similar to myelin so it will be destroyed when antibodies are present
- vitamin D3
104
what are the two types of signaling b/w neurons?
electrical
chemical
105
what is the difference b/w electrical and chemical synapses?
electrical = fast, synchronize activity (smooth & cardiac muscle), use gap junctions (w/ connexons) to allow for bidirectional signaling and large molecules to pass through
chemical = slow, release NT into synaptic cleft to convert an AP to a neurocrine that binds & activates a pathway
106
what are the six steps of the synaptic transmission model? (chemical synapses)
1. precursor loading
2. NT synthesis (small molecule NT, large molecule NT)
3. Storage in vesicles
4. Release of NT due to AP (Ca2+ exocytosis)
5. Activation due to ligand / receptor binding
6. Termination
107
how are smalll molecule NT (glutamate, GABA, dopamine) synthesized?
enzymes come from the soma and make the NT in the axon terminal
- fast, transient changes
- slow axonal transport to vesicles (lots of stops)
108
how are neuro-peptides (large molecule NT) synthesized?
made in the soma
- fast axonal transport to vesicles (uses kinesin & microtubules)
- activated by ATP to carry vesicles & move
- ADP bind, ATP swing forward
109
describe neuropeptides
chains of AAs undergo neuromodulation (slow, enduring changes)
110
what are vesicles made out of? what do they store? how do they move molecules in and out?
organelle w/ a lipid bilayer
- contain NT, ATP, GTP, Ca2+
- uses metabolic pumps, protein kinases, and docking proteins to transport molecules in
111
what are co-transmitters?
different NT that are released from the same neuron
- can be stored in same or different vesicles
112
what are the two ways co-transmitters are released? describe the main difference between them
simultaneous release = released at same time
differential released = released at different times
- one vesicle requires a stronger depolarization for released
113
what time of frequency stimulation does a small NT need for released? what about large NT?
small = low frequency
large = high frequency, but slow to replenish
114
what are the two types of neurocrine (chemical factor) receptors? describe them
ionotropic = fast, ligand / receptor, short-term changes in MB potential, EPSP & IPSP
metabotropic = slow, G-protein (2nd mes), neuromodulation
115
what are the three NT criteria?
found in axon terminal
released by AP
has postsynaptic receptors available
116
what are the four groups of small NT? give examples of each
ACh
Biogenic-/Mono- Amines (DA, 5HT, NE, Histamine)
Amino Acids (Glut, Aspartate, GABA, Glycine)
Purines (ATP, GTP)
117
what are the two main groups of large (peptide) NT? give examples of each
opioids (enkephalins, endorphins, dynorphins)
substance P = pain signaling in SC
118
what is different about unconventional NT?
still mediated by Ca2+ EXCEPT....
- they are lipid soluble (not stored in vesicles)
- can be retrograde messengers (post -> pre)
119
what are the two main unconventional NT?
endocannabinoids (Anandamide, 2-AG)
Nitric Oxide (NO)
120
what do endocannabinoids do? how are they made?
inhibit GABA released
- synthesized from degrading the MB
121
what are the four main receptors on the post-synaptic MB that are activated through chemical synapses?
ionotropic (channel-linked = receptor & channel in one protein)
metabotropic (G-protein coupled = requires energy)
enzyme-linked
intracellular
122
what are the differences between the four main receptors on the post-synaptic MB that are activated through chemical synapses?
iono = ions move along gradient to make short-term changes in MB potential
meta = G-protein acts as transducer molecule to covert energy into a signal, makes long-term changes in MB potential
enzyme-linked = ligand binds and immediately activates effector (TK receptor, neurotrophin receptor)
intracelluar = only for lipophilic molecules (steroids, NO, endocannabinoids)
123
what are the two subgroups of receptors for ACh?
nACh = nicotinic
mACh = muscarinic
124
what are the subgroups of the nicotinic subgroup receptors?
muscle nACh-R = 2alpha, 1beta, 1 gamma/epslion
neuronal nACh-R = 2alpha, 3beta OR 3alpha, 2beta
125
what are the four methods of termination of a signal?
1. NT disengages & diffuses away
2. Reuptake by transporters
3. Enzymatic Degradation
4. Terminal Autoreceptors
126
how does the NT disengage and diffuse away?
whena. NT binds, it cahnges the receptor which can weaken it's affinity for the molecule, allowing it to diffuse
- NT can then bind to other receptors or be destroyed
127
how is the NT terminated through reuptake by a transporter? two ways! list there molecules
NT pumped back into presynaptic terminal through metabolic pumps (DA, NE, 5HT) or by glial cells (Glut, GABA)
- active transport (ENERGY!)
128
how is the NT terminated through enzymatic degradation?
enzyme specific for that molecules breaks it's bonds (in the synapse or intracellularly)
- ACh = acetylcholinesterasae
- monoamines = MAO
- opioids = peptidases
- GABA = GABA-T
129
how is the NT terminated through terminal autoreceptors?
as NT accumulated in synapse (too full) they bind to NT to decrease the NT signal
- metabotropic receptor!
130
what to glial cells do during neural signaling?
- remove extracellular K+ to help maintain gradient
- reuptake & synthetic cycle (glutamate -> glutamine -> glutamate)
- tripartite synapse
131
how does the tripartite synapse work to regulate neural signaling/
- glia cells have NT receptors that respond when NT is released from axon terminal
- NT binds and produces MB potential changes in glia cells by altering their intracellular Ca2+
- altered Ca2+ acts as a 2nd mes cascade to releases Glu, GABA, ATP (gliotransmitters) through exocytosis
132
what are the 5 types of chemical synapses? what classifies them into each group?
- autocrine (autoreceptors)
- synaptics (structured, short-distance)
- paracrine (cell-to-cell)
- endocrine (hormones thru blood)
- exocrine (pheromones thru air)
133
what are the three signal molecule types of chemical synapses? describe each
- cell-impermeant = won't diffuse, need receptor on post.
- cell-permeant = diffuse into post.
- cell-associated signaling mol. = ligand & receptor embedded (DELTA), non-diffusible
134
signal transduction pathways are a ___fast/slow___ activating system
slow
- require energy & several steps before reaching effector
- very precise and longer lasting effects
- AMPLIFICATION
135
what inactivates G-proteins?
GAP (GTPase-activating protein)
- removes the GTP and binds GDP to the G-protein
136
what is the difference between monomeric and hetertrimeric G-proteins?
mono = one subunit
hetertri = multiple subunits
137
describe the Ras pathway? is it mono- or hetertri- meric?
monomeric
- once activated, GEF replaces GDP w/ GTP and binds to Ras
- Ras-GTP is inactivated by the conversion of GTP -> GDP which goes on to inactivate the G-protein
138
what happens in the hetertrimeric G-protein when GTP is bound?
- activates G-protein subunits and they dissociate
- alpha activates primary effector enzymes
- beta-gamma activates effectors
139
what are the three types of hetertrimeric G-proteins? describe them
Gs = stimulating, increases 2nd mes (cAMP)
Gi = inhibiting, decreases 2nd mes (cAMP)
Gq = activates phospholipase C to degrade MB adn produce DAG & IP3
- increases protein phosphorylation & Ca2+ binding proteins
140
what is the 1st messenger?
NT that binds the extracellular G-protein
141
what is part of the MB components in signal transduction? (3)
receptor
transducer (G-protein)
primary effector (enzymes)
142
what is part of the intracellular components in signal transduction? (2)
2nd messenger
secondary effector (kinase, phosphatases)
143
what are the three types of 2nd messengers?
Ca2+
Cyclic Nucleotides (cAMP, cGMP)
MB derived (DAG, IP3)
144
describe Ca2+ as a 2nd messenger
- come from internal and external stores
- strong gradient INWARDS (high conc out -> low conc in)
145
what maintains the Ca2+ gradient to pump Ca2+ OUT?
Ca2+ pump
Na+ / Ca2+ exchanger
146
what maintains the Ca2+ gradient to pump Ca2+ IN?
voltage-gated channels
ligand-gated channels
147
where do the internal stores of Ca2+ come from?
endoplasmic reticulum (ER)
mitochondria
* released Ca2+ into cytosol to bind to targets *
148
what are Ca2+ targets? (2)
Calmodulin
Calbindin
149
what happens after Calmodulin is activated by Ca2+? name the two receptors!!
activates downstream targets and cause more release of Ca2+ internal stores from ER through....
IP3 gated channels
Ryanodine-gated channels
150
what happens after Calbindin is activated by Ca2+?
TERMINATION
- acts as a buffer protein to bind to Ca2+ and inactiavte the extra Ca2+ in the cytosol
151
describe how cyclic nucleotide 2nd messengers are synthesized? what do they do after they are made?
synthesized through activation of G-pro -> adenylyl cyclase -> cAMP
- binds to protein kinases (PKA) & ligand-gated channels
152
what terminates cAMP and cGMP?
phosphodiesterases
153
describe how MB derived 2nd messengers are synthesized?
PIP2 degrades phospholipase C into DAG & IP3
154
what does DAG do?
stays embedded in MB and activates PKC
155
what does IP3 do?
binds to IP3 intracellular receptors to release internal Ca2+ stores (REMEMBER CALMODULIN??!?!?)
156
what terminates DAG & IP3? (MB derived)
phosphatases
