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Neurobiology > Synapses and Signalling > Flashcards

Synapses and Signalling Flashcards

1
Q

electrolytic theory (Watter Nernst)

A

explains existence of membrane potential in living cells

net movement of solute is comb. of electrical potential and chemical across membrane

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2
Q

membrane ions on either side at resting potential

A

high conc. sodium outside, low inside

high potassium inside, low outside (potassium poores open without stimulation)

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3
Q

excitable cells

non excitable cells

A

can generate AP

do not generate action potentials but exhibit dynamic changes in resting membrane potential - glial, immune, epithelial, tumour

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4
Q

history of nerve discoveries

A

lecture 6 bottom of page

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5
Q

patch clamp

& equipment

A

cell in bath chamber surrounded by extracellular medium
glass pipette contact cell body
record activity in patch of membrane
(can record single channels)
sodium into cell measured as -ve current, potassium out is +ve

need micromanipulators to position pipette, faraday cage to reduce electrical noise, air table reduce vibration, clean solutions, smooth pipette tip

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6
Q

excised patches

A

take out bit of membrane and expose outer/inner to extracellular liquid which can change rapidly
can control voltage and change inner/outer solutions
but can change channel properties so not good

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7
Q

whole cell patch clamp

A

records from all ion channels
control potential and current
can change inside/out solutions
but leakage current can damage membrane

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8
Q

command voltage

A

set membrane potential in patch clamp

if change from -60mV to 30mV then currect response changes and peak increases

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9
Q

transient current (shortlived)

A

the big AP dip can see is mediated by sodium because still see effect if block potassium, rapidly inactivates
if block sodium - isolate outward SLOW current

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10
Q

Hodgkin-Huxley model significance

A

introduced concepts of ionic channels as separate molecular structures
confirmed by molecular bio
provide good numerical description by experimental data, foundation for computational neuroscience

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11
Q

open probability

A

of sodium channels - v high initially then almost 0 when inactivation (similar as predicted by H-H)
potassium probability doesn’t change with time because don’t inactivate

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12
Q

potassium channel types

A 
delayed rectifier
A-type/transient
inward rectifier
BK calcium dependent (large conductance)
SK calcium dependent (small conductance)
K-ATP (ATP dependent)
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13
Q

delayed rectifier (K channel)

A

strong dependence on membrane voltage

slow kinetics

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14
Q

sodium channel types (and why they’re diff/similar)

A 
I
II
IIA
III
VI

more similar to each other, diff sesitivity to antagonists and diff thresholds

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15
Q

voltage activated calcium channels

A

if block sodium and potassium channels, the current measured resembles inward sodium but smaller amplitude
so this calcium activity is normally masked by sodium activity

mostly in pre-synaptic terminal for calcium entry for NT release

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16
Q

calcium channel types

A

LVA/T-type (low voltage activated, below -30mV) - rapid

HVA (high) - above -30mV, split into more types depending on pharmacology/location/threshold/kinetics

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17
Q

structure of ion channels

all same except inward rectifies and K-leaks

A

6 subunits
4 homologous subunits forms transmembrane pore
each 4 subunits contains 6 transmembrane segments S1-S6
all 4 S5 and S6 segments form internal pore of channel with ion selectivity filter
S4 sensitive to voltage - responsible for gating

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18
Q

S4

A

12 +ve AAs move in response to voltage, relax pressure on S5 and S6 so open channel
so 4 gates but 3 enough to open channel and 1 inactivation gate

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19
Q

how do ion channels close?

A

polypeptide structure at bottom closes channel
inactivation gate
1 per channel
between S6 of subunit III and S1 of subunit IV

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20
Q

gating and opening of Na vs K

A

Na - rotation sliding movement of subunits and +ve residues move outward so widen pore

K - more like paddle movement of S1-S4 alpha helices

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21
Q

inactivation and activation of Na

A

need to be open and activated before inactivating gate can go inside pore

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22
Q

why is ion selectivity filter a thing?

A

if were not selective, AP wouldn’t work

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23
Q

ion selectivity filter

A

small no. AAs in p-loop chains of S5-P-S6 (ring of selectivity filter)
inner filter rings are -ve so repels -ve attracts +ve

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24
Q

Na is slightly smaller than Ca so….

A

can pass Ca channels in absence of Ca

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25
K ion selectivity filter
narrow pore of neutral AAs so no net charge | filters out large ions
26
what do K ions have to lose to pass small pores?
hydration shells of water molecules | oxygen atoms of AAs in filter region help strip shells of ions
27
hydration shell of Na?
Na too small so can't strip shell so effectively larger in respect to channel
28
why is correct resting potential important?
AP requires depolarisation from certain level because if shift, it can change firing rate, change patterns, change ease of reaching threshold higher depolarisation --> higher firing frequency hyperpolarisation makes cell less excitable depolarise too far inactivates AP
29
how does the circadian rhythm change excitability of SCN neurones?
master clock in SCN of hypothalamus AP firing freq changes with cycle from changes of melatonin secretion from pineal gland in daytime increase Ca so affect K conductance
30
gating-pore channelopathies
diseases with ion channel malfunction current leak through displacement of S4 affected - leaves space for water non-selective, fast activating, non-inactivating, low conductance leads to permanent depolarisation
31
diseases associated with altered resting potential and ions in NS
end of lecture 7
32
electrical synapses
gap junction no delay, 2-way, little flexibility and plasticity, not great role connexins in vertebrates innexins in invertebrates are ion channels (6 subunits) which form gap junctions, allow current flow between 2 neurones
33
chemical synaptic transmission
neurones isolated from each other, across cleft, short delay (0.5-1ms), 1-way, great flexibility and plasticity, main role in brain ``` driven by conc gradient 2 responses (dep./excitation or hyperp./inhibition) ``` synapses everywhere but mostly on dendrite/axon spine/synapse shaft on dendritic process
34
snap
SNARE-associated protein
35
SNARE
v-SNARE (vesicle) t-SNARE (target membrane) v and t needed for docking docking can be blocked by tetanus and botulinum toxin
36
vesicles fusion
calcium increases, changes conformation so SNARE twisted (energy from ATP), cause vesicles to fuse calcium dependence not linear (3-4 needed to release 1 vesicle)
37
stochastic
Ca increases probability of NT release but not guarantee
38
measuring synaptic transmission
HPLC, amperometry, muscle contraction, electrophysiology, biosensors, FM -dyes (direct visualisation of vesicles)
39
NT release without AP
miniature synaptic current/potential | by single vesicle
40
vesicular release of NT is, and therefore synaptic response should be....
quantal | size of response should depend on amount of NT
41
quantal content
no. vesicles released by response to single AP quantal content of miniature response - typically 1 vesicle of evoked response - over 1 quantal content = amplitude evoked divided by amplitude miniature amplitude = no. vesicles x quantal size
42
probability of release and docking
not constant but depends on last event and affects recycle
43
vesicles retrieval (endocytosis)
full fusion - vesicle fusion and then get whole back kiss + run - small amount NT released then vesicles closes and stays inside bulk retrieval - many vesicles fused in at same time
44
vesicles recycling (to reserve pool)
proteins form coat on membrane then around vesicles as fuses in so can bud off membrane, then coated with clathrin cage
45
synaptic strength
is the average response triggered by single AP varies large scale among diff synapses (changes during development, plasticity) depends on presynaptic no. vesicles, release probability and post-synaptic receptor density to NT and efficiency (phosphorylation by kinases can affect onductance and open time) (amount of NT in vesicles - not strong influence)
46
Ribbon synapse
mainly in receptor cells conveyor belt of vesicles persistent high f synaptic transmission e.g. cone cells of retina, inner hair cells of ear
47
Calyx of Held synapse
big synapse in mammalian auditory central nervous system many active zones large vesicle pool large quantal content fire high f for long time
48
vesicles filling
2 kinds of transporter in vesicles 1. vH+ - ATPase : creates high gradient of protons for NT transport 2. transporter for specific NT, use proton gradient (H out and NT in)
49
cationic NTs vs glutamate (/other -ve)
monoamines, ACh, depend on change in pH use electrical components
50
vesicle transporter proteins | and examples
is a criteria for a substance to be a NT | examples lecture 9 top (e.g. vAChT)
51
NT criteria
present in presynaptic with synthesis machinery (should be made in cell body) and specialised vesicular transporter released and con. increases when presy. stimulation mimic affects of presy. stimulation when added to extracellular fluid mechanism of removal exist
52
NT types
classical - small, some AAs (ACh, dopamine, serotonin, adrenaline, histamine) neuropeptides - larger, 3-20 AAs (endorphins, oxytocin) other - NO, ATP, adenosine
53
co-localisation
each synapse has main classical NT but also some release co-transmitter in same/diff vesicles so can't always classify synapse w/ NT e.g. (lecture 9 bottom)
54
synapse specialisation
specific neurone make specific NT but short-lived event because can change what NT make
55
ACh synthesis
acetyl coenzyme A + choline by choline acetyltransferase (ChAT) cholinergic synapse
56
action of NT determined by.....
receptor | speed, facilitation, depression of firing, modulation of activity
57
temporal characteristics
speed/duration depends on kinetics of receptor (ligand binding and receptor properties e.g. don't desensitise so always active when ligand bound)
58
why can't we divide NTs into excitatory/inhibitory
action depends on receptors | so can have diff roles in diff tissues
59
types of receptors
``` ionotropic metabotropic (ion channel separate from receptor) ``` many NTs have both
60
ionotropic
``` ligand-gated channels important in direct electrical to chemical signal 3 families (trimeric, tetrameric, pentameric) e.g. lecture 9 2nd page ```
61
metabotropic
G-protein coupled uncoupling of receptor (a from b y) when activated alpha interacts with effector protein increase CAMP and Ca conc. (learning, memory)
62
acetylcholine receptors
nicotinic (ionotropic) | muscarinic (metabotropic)
63
nicotinic (ACh) | properties, structure, mechanism, selectivity, types
``` ionotropic increase cations (Na), fast excite ``` hetero-pentamer of 4 subunits (2a,b,y,d) each w/ transmembrane alpha-helix (M2) and the 5 M2 helices form the pore 2 alpha bind ACh so rotation of alpha subunits cause rotation of all and open receptor twisting so smaller polar residues line channel instead of bulky hydrophobic Leu side chains in closed channel 3 rings of -ve residues so attract +ve a2,b,y,d skeletal muscles a2,b3 neurones but always 2a
64
muscarinic | (properties, subtypes
metabotropic K permeability, slow excite/inhibit 5 subtypes M1,3,5 (Galphaq) activate protein kinase C/phospholipase C so produce IP3 and release Ca M2,4 (Galphai) inhibit adenylate cyclase so inhibit cAMP/regulate K channels
65
ACh pathways in brain
axons releasing ACh in brainstem to hypothalamus to modulating activity of neurones in brain but in PNS is an excitatory NT
66
glutamate receptors (types, glutamate)
ionotropic: fast AMPA - increase Na, main excitatory in most brain neurones, high glut to activate slow NMDA - increase Ca, not active at resting pot. because Mg block, excess Glu means cell damage (excitoxicity) metabotropic: increase IP3, modulatory glutamate: side effect of Krebs cycle, coupled with synthesis of glutamic acid glutamic acid converts to GABA which antagonises action of glutamate
67
GABA receptors (types, structure, allosteric)
inhibitory (excite in embryo) GABAa is ionotropic, increase Cl, fast, hyperpolarise GABAb metabotropic, increase K, decrease Ca, slow 5 subunits, 2 bind GABA allosteric modulation - increase open time so increase inhibitory current (sedation by benzodiazepine, barbiturate)
68
Serotonin (origin, types)
from tryptophan AA in brainstem nuclei widespread 3 types: 5-HT1 GPCR in brain, 5-HT2 GPCR in periphery + brain (LSD), 5-HT3 ion channel in sensory neurones and brain (vomit)
69
Dopamine/adrenaline (origin, adrenergic synapses, receptors)
from tyrosine AA, released from 2 brainstem nuclei mostly from substantia nigra noradrenaline from nucleus locu coeruleus, widespread to cerebellum/neocortex no adrenergic synapses in brain - instead, adrenaline released from noradrenergic presynptic terminals and diffuse towards target all GPCR receptors, diverse effects
70
drugs
agonists/antagonists for receptors e.g. nicotine agonist for AChR tubocuraine poison antagonist for AChR
71
NT uptake pathways
degradation (ACh) | re-uptake by glial cells (glutamate)
72
important things regarding integration of the NS
signalling is via AP amount of info = AP fired AP don't decrement (all or none) so record frequency when investigating
73
input integrative conductive output
from env. to sensory, from other neurones to motor/other at dendrites but some at soma AP, myelinated or passive propagation in small neurones presynaptic terminals
74
frequency encoding
convert amplitude of stimulus to freq of AP
75
factors determine firing
``` synaptic input (temporal/spatial summation) position of synapses proportion of inh/exc synapses modulation facilitation/depression ``` depend on ion channel properties and electrical properties of cellular membrane
76
membrane properties
insulated (separate charges) acts like capacitor plates (larger neurone bigger capacitance because more charge store but greater time constant takes longer to charge) greater resistance = bigger voltage change because less charge leaking
77
capacitance of membrane equations
lecture 10 top 2nd page
78
summation
combine info before deciding to fire temporal/spatial high chance pass threshold if w/o inhibition (IPSPs stop APs)
79
temporal summation
membrane has time constant and holds charge, previous AP don't disappear so build higher f means shorter time between and larger change of AP
80
synapse position affects synaptic potential
where dendrites are dendrites depolarisation spreads passively down to soma and potentials will decrement (distance a signal decrements is 1/e = lambda length constant) synapse on soma/near dendrites increase inhibiting
81
diameter of dendrites
thicker means longer lambda (length constant, distance a signal decrements) thin means large SA for more synapses and more info
82
integration process in nerve terminal
AP activates Ca channels in presynaptic amplify Ca from ER/IP3 more AP means Ca is more elevated and prolonged higher Ca means increased NT (more vesicles) presynaptic receptors influence Ca level and release probability NT released affected by depletion and replenishment of vesicles
83
facilitate
freq firing converted to more NT release
84
depress
decrease NT, by depletion of vesicles is small pool/modulation
85
modulation of glutamate release in neocortical and hippocampal nerver terminals
AP excite, GABAb receptors inhibit calcium still elevate ATP co-transmitter activate Ca channels so increase Ca but also ATP to adenosine so inhibit
86
neurones are organised in... | spiny vs non-spiny
networks - activity expressed as overall firing rate of APs principle neurones - excitatory, pyramidal shape, long range inputs, local inputs from interneurones, send axons to other networks interneurones - inhibitory, inputs from local principle neurones, outputs locally
87
dendritic spines
protrusion from stalk of dendrite, synapses with single axon bulbous head and thin neck connects spine to stalk of dendrite principle neurones multiple synapses on spines principle/inter synapse on dendritic stalk
88
interneurones inhibitory effects
feed-forward - enhances by inhibit opposing feed-back - self-regulating, excitatory act on inhibitory to act on primary excitatory neurones to dampen activity, prevent over-excitation
89
bottom-up pathway top-down pathway
sensory N input to relay N (several levels) motor cortex to muscles (output)
90
parallel processing distributed processing
sensory info sent to specific zones in cortex which consists of columns innervated by parallel streams cortical columns/local network may be part of diff pathways of analysis
91
neurone-glia communication
astrocytes enwrap synaptic terminals and monitor 90% brain tissue astrocyte Ca signal transducer - spill over glutamate/ATP activates electrical/Ca signalling that spill out synapses

Neurobiology (4 decks)

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