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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
Q

K ion selectivity filter

A

narrow pore of neutral AAs so no net charge

filters out large ions

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26
Q

what do K ions have to lose to pass small pores?

A

hydration shells of water molecules

oxygen atoms of AAs in filter region help strip shells of ions

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27
Q

hydration shell of Na?

A

Na too small so can’t strip shell so effectively larger in respect to channel

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28
Q

why is correct resting potential important?

A

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

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29
Q

how does the circadian rhythm change excitability of SCN neurones?

A

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

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30
Q

gating-pore channelopathies

A

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

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31
Q

diseases associated with altered resting potential and ions in NS

A

end of lecture 7

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32
Q

electrical synapses

A

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

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33
Q

chemical synaptic transmission

A

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

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34
Q

snap

A

SNARE-associated protein

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35
Q

SNARE

A

v-SNARE (vesicle)
t-SNARE (target membrane)
v and t needed for docking
docking can be blocked by tetanus and botulinum toxin

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36
Q

vesicles fusion

A

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)

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37
Q

stochastic

A

Ca increases probability of NT release but not guarantee

38
Q

measuring synaptic transmission

A

HPLC, amperometry, muscle contraction, electrophysiology, biosensors, FM -dyes (direct visualisation of vesicles)

39
Q

NT release without AP

A

miniature synaptic current/potential

by single vesicle

40
Q

vesicular release of NT is, and therefore synaptic response should be….

A

quantal

size of response should depend on amount of NT

41
Q

quantal content

A

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
Q

probability of release and docking

A

not constant but depends on last event and affects recycle

43
Q

vesicles retrieval (endocytosis)

A

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
Q

vesicles recycling (to reserve pool)

A

proteins form coat on membrane then around vesicles as fuses in so can bud off membrane, then coated with clathrin cage

45
Q

synaptic strength

A

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
Q

Ribbon synapse

A

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
Q

Calyx of Held synapse

A

big synapse in mammalian auditory central nervous system

many active zones
large vesicle pool
large quantal content
fire high f for long time

48
Q

vesicles filling

A

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
Q

cationic NTs vs glutamate (/other -ve)

A

monoamines, ACh, depend on change in pH

use electrical components

50
Q

vesicle transporter proteins

and examples

A

is a criteria for a substance to be a NT

examples lecture 9 top (e.g. vAChT)

51
Q

NT criteria

A

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
Q

NT types

A

classical - small, some AAs (ACh, dopamine, serotonin, adrenaline, histamine)
neuropeptides - larger, 3-20 AAs (endorphins, oxytocin)
other - NO, ATP, adenosine

53
Q

co-localisation

A

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
Q

synapse specialisation

A

specific neurone make specific NT but short-lived event because can change what NT make

55
Q

ACh synthesis

A

acetyl coenzyme A + choline by choline acetyltransferase (ChAT)
cholinergic synapse

56
Q

action of NT determined by…..

A

receptor

speed, facilitation, depression of firing, modulation of activity

57
Q

temporal characteristics

A

speed/duration depends on kinetics of receptor (ligand binding and receptor properties e.g. don’t desensitise so always active when ligand bound)

58
Q

why can’t we divide NTs into excitatory/inhibitory

A

action depends on receptors

so can have diff roles in diff tissues

59
Q

types of receptors

A 
ionotropic
metabotropic (ion channel separate from receptor)

many NTs have both

60
Q

ionotropic

A 
ligand-gated channels
important in direct electrical to chemical signal
3 families (trimeric, tetrameric, pentameric) e.g. lecture 9 2nd page
61
Q

metabotropic

A

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
Q

acetylcholine receptors

A

nicotinic (ionotropic)

muscarinic (metabotropic)

63
Q

nicotinic (ACh)

properties, structure, mechanism, selectivity, types

A 
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
Q

muscarinic

(properties, subtypes

A

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
Q

ACh pathways in brain

A

axons releasing ACh in brainstem to hypothalamus to modulating activity of neurones in brain but in PNS is an excitatory NT

66
Q

glutamate receptors (types, glutamate)

A

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
Q

GABA receptors (types, structure, allosteric)

A

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
Q

Serotonin (origin, types)

A

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
Q

Dopamine/adrenaline (origin, adrenergic synapses, receptors)

A

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
Q

drugs

A

agonists/antagonists for receptors
e.g. nicotine agonist for AChR
tubocuraine poison antagonist for AChR

71
Q

NT uptake pathways

A

degradation (ACh)

re-uptake by glial cells (glutamate)

72
Q

important things regarding integration of the NS

A

signalling is via AP
amount of info = AP fired
AP don’t decrement (all or none) so record frequency when investigating

73
Q

input
integrative
conductive
output

A

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
Q

frequency encoding

A

convert amplitude of stimulus to freq of AP

75
Q

factors determine firing

A 
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
Q

membrane properties

A

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
Q

capacitance of membrane equations

A

lecture 10 top 2nd page

78
Q

summation

A

combine info before deciding to fire
temporal/spatial
high chance pass threshold if w/o inhibition (IPSPs stop APs)

79
Q

temporal summation

A

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
Q

synapse position affects synaptic potential

A

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
Q

diameter of dendrites

A

thicker means longer lambda (length constant, distance a signal decrements)
thin means large SA for more synapses and more info

82
Q

integration process in nerve terminal

A

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
Q

facilitate

A

freq firing converted to more NT release

84
Q

depress

A

decrease NT, by depletion of vesicles is small pool/modulation

85
Q

modulation of glutamate release in neocortical and hippocampal nerver terminals

A

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
Q

neurones are organised in…

spiny vs non-spiny

A

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
Q

dendritic spines

A

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
Q

interneurones inhibitory effects

A

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
Q

bottom-up pathway

top-down pathway

A

sensory N input to relay N (several levels)

motor cortex to muscles (output)

90
Q

parallel processing

distributed processing

A

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
Q

neurone-glia communication

A

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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