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BIOM2011 > MODULE 2: neurons > Flashcards

MODULE 2: neurons Flashcards

1
Q

4 electrical properties of ion movement

A
  1. current (I)
    - measured in amperes, A
    - rate of movement of electrically charged particles
    - biological I ~ picoA = 10^-12 A
  2. voltage (V)
    - measured in volts, V
    - force acting on charged particles to cause movement,
    - due to an imbalance in charge distribution = a battery
    - biological V ~ milliV = 10^-3 V
  3. conductance (g)
    - measured in siemens (S)
    - ease with which charged particles can move
    - biological g ~ nanoS = 10^-9 S
  4. resistance (R)
    - measured in ohms (Ω)
    - resistance to movement of charged particles
    - inverse of g (R = 1/g)
    - biological R ~ mega W = 10^6 Ω
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2
Q

ohm’s law

A

The rate of movement of a charged particle (I) depends on
the force moving it (V) and the ease with which it can move (g)

I = gV

I = V/R

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3
Q

ionic equilibrium potential

A

ionic equilibrium occurs when forces exerted on an ion by concentration and electrical differences across membrane are equal and opposite –> NO NET ION FLOW

ionic equilibrium potention (Eion) is electrical potential which counter-balances force of ionic concentration gradient
calculated using Nernst equation

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4
Q

how potassium controls the resting membrane potential

A

K+ permeability is high and ratio of K+ across membrane is high —> RMP predominantly determined by K+

increasing extracellular K+ will strongly depolarise membrane (vice versa)

glial cells buffer changes in potassium concentration by taking K+ up and distributing it elsewhere through gap junctions between glial cells

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5
Q

whole cell patch clamping

A

method of recording electrical signals in neurones

  • to measure potential, conductive pathway must be established across membrane
  • glass pipette of salt water placed against membrane
  • measure difference in potential between electrode tip and extracellular space via suction
  • break membrane via suction, insert electrode, measure potential
  • compare potential on inside and outside of cell
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6
Q

action potentials - firing mechanism

A

decision to fire occurs in axon hillock

needs depolarisation of MP from resting (-60mV) to threshold (-40mV)

this depolarisation is due to integrated sum of responses to all active synaptic inputs to neurone

this depolarisation activates VG ion channels - Na+ or K+

at threshold, Na+ VG ion channels rapidly open
positive feedback loop:
–> Na+ channels rapidly open due to positive MP
–> Na+ enters cell down gradients
–> positive charge accumulates on inside of cell mrmbrane
–> MP becomes more positive
–> repeat

this loop creates overshoot

VG K+ channels also slowly begin to open during rising phase, preventing MP from reaching E(Na)

at AP peak, open Na+ channels inactivate and no more open, more K+ channels open

As g(Na) decreases and g(K) increases, AP enters repolarisation

eventually, all Na+ channels close and open K+ channels hyperpolarise the membrane below RMP –> undershoot

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7
Q

electrical synapses

A

direct flow of electrical current between cells
–> fast, bidirectional, fail safe

current flows through connexons
–> protein ion channels which directly connect two cells via a gap junction

connexons have large pores which allow passage of ions and small molecules

opening of connexons regulated by intracellular calcium concentration

  • -> high Ca2+ = closed
  • -> low Ca2+ = open

electrical synapses important in cardiac muscle, smooth muscle, glial cells and in the embryonic brain

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8
Q

amino acids –> “the big 2 G’s”

A

glutamate (glu)

glycine (gly)

gamma-amino-butyric acid (GABA)

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9
Q

amines –> “the sidekick 6”

A

acetylcholine (ach)

dopamine

adrenaline

noradrenaline

serotonin

histamine

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10
Q

basic neurotransmitter functions

A

amino acids mediate fast excitatory (glu) and inhibitory (GABA, gly) synaptic transmission at most CNS synapses

ach mediates fast excitatory synaptic transmission at all neuromuscular junctions and some peripheral/central synapses via nicotonic ach receptors

amino acids, aines and peptides also mediate slow synaptic transmission at centra/peripheral synapses

many synpases contain both peptides (in large dense core vesicles) and aa’s or amines (in small clear synaptic vesicles) and can co-release both

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11
Q

neurotransmitter release mechanism

A
  1. AP invades presynaptic terminal from axon and depolarises
  2. depolarisation opens VG ion channels on presynaptic terminal and calcium enters
  3. calcium triggers exocytosis of neurotransmitter vesicle, diffusion across synaptic cleft
  4. neurotransmitter binds to postsynaptic receptors, opens ion channel
  5. postsynaptic potential is generated
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12
Q

synaptic vesicle cycle (recycling)

A

exocytosis of synaptic vesicle contents part of continuous recycling process

vesicle membrane is endocytosed and refilled with transmitter

refilled vesicles dock near active zone

docked vesicles primed for release through ATP-dependent process

Ca2+ entering through close VG ion channels triggers fusion of vesicle membranes with presynaptic membrane
–> Ca2+ channel thought to be synaptic protein in vesicle membrane which may bind 4 calcium ions at a time

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13
Q

neurotransmitter synthesis (amino acids, amines and peptides)

A

amino acids and amines:

  • synthetic enzymes and precursors transported into NERVE TERMINAL
  • these are subject to feedback inhibition from recycled neurotransmitters
  • can be stimulated to increase activity via Ca2+ stimulated phosphorylation

peptides:
- peptide transmitters made from precursor proteins in the CELL BODY

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14
Q

neurotransmitter storage (amino acids, amines and peptides)

A

amino acids and amines:

  • uptake from terminal to cytoplasm into vesicle involves transporter protein
  • protein in vesicle membrane
  • powered by pH gradient between outside and inside of vesicle

peptides:

  • packaged into vesicles which bud off golgi apparatus in cell body
  • then transported along axon terminals = anterograde transport
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15
Q

neurotransmitter recovery / degredation

A

neurotransmitters must be removed from synaptic cleft because postsynaptic receptors will desensitise if stimulated too much

diffusion:
- diffused away from synaptic cleft in extracellular space

re-uptake:
- re-uptake into nerve terminal via transporters (vesicles)

glial cells:
- uptake into glial cells by transporters

enzymes:

  • enzymatic breakdown in synaptic cleft
  • acetylcholinesterases rapidy break down ACh
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16
Q

inotropic glutamate receptors

A

main excitatory neurotransmitter in CNS (~90% of synapses)

4 protein subunits around central ion pore
–> permeable to sodium, potassium and sometimes calcium

three types:

1) AMPA –> fast rising and falling, generally not permeable to calcium
2) NMDA –> slower rising and falling, always calcium permeable, voltage dependent block of ion pore of Mg2+ ion (prevents other ions moving through at -70mV)
3) kinate –> similar to AMPA but function not understood

17
Q

nicotinic, GABA and glycine receptors

A

common channel structure

  • -> 5 protein subunits in each receptor
  • -> arranged in ring around ion pore
  • -> positively charged to attract anions

GABA receptor:

  • inhibitory structure in forebrain
  • numerous subunits
  • subunits have many sites for binding drugs and endogenous factors which modulate receptor activity
  • major target for sedative drugs- several intracellular phosphorylation sites influenced by 2nd messenger systems
  • drugs modulate activity of ion channel so it becomes easier to open and stays open for longer

glycine receptor:

  • important in brain stem and spinal cord
  • glycine composed of alpha and beta subunits
  • mutation leads to “startle disease”
  • –> reduces Cl- flow
  • –> thus reduces synaptic inhibition
  • –> tetanic muscle spasms in response to stimulation
18
Q

GPCRs and neurotransmitters

A
  • slow synaptic transmission due to delayed activation and long time course
  • don;t have integrated ion channel in protein structure –> response not immediate
  • can directly GP gated ion channels or modulate activity via phosphorylation

GLUTAMATE
ligand-gated ion channel –> AMPA, NMDA, kainate
GPRC –> metabotropic glutamate

GABA
ligand-gated ion channel –> GABA(A)
GPRC –> GABA(B)

ACh
ligand-gated ion channel –> nicotinic
GPRC –> muscarinic

19
Q

mechanisms of postsynaptic inhibition

A

1) hyperpolarisation
- if resting MP more positive than ionic equilibrium potential for Cl- ions, MP will hyperpolarise when Cl- channels open
- MP becomes further away from threshold

2) shunting inhibition
- if resting MP is ~ionic equilibrium potential for CL- ions, MP will not change significantly because there is no driving force
- Cl- channels still opened
- this lowers MP resistance at synapse and allows current to leak out across membrane
- shunts other synaptic inputs to neurone

20
Q

mechanisms of presynaptic inhibition

A
  • neurotransmitter released by first synapse
  • binds to receptor on second synapse
  • this reduces neurotransmitter release by second synaptic terminal
  • —> decrease in excitability in second presynaptic terminal due to activation of K+/Cl- channels
  • —> reduced opening of Ca2+ channels in second presynaptic terminal
21
Q

spacial and temporal summation

A

spatial –> summation of simultaneously active synapses at different locations on dendritic tree

temporal –> summation of asynchronously active synapses, either different or same synapses

22
Q

short-term synaptic plasticity

A

when presynaptic neurones dire at rapid rates, synaptic responses can change with each successive AP

changes are transient –> synaptic responses will return to original amplitude within sec/min after firing rates slow

responses can become larger (facilitation) or smaller (depression)

synaptic facilitation –> produces greater than normal summation, enabling excitatory inputs to reach AP threshold quicker

synaptic depression –> produces less than normal summation, increasing time taken for EPSPs to summate to AP threshold

23
Q

hebbain model of synaptic plasticity

A

“when an axon of cell A is near enough to excite cell B and persistently takes part in firing it, some growth process or metabolic change takes place such that A’s efficiency as one of the cells firing B is increased”

i.e. cells that fire together wire together

this underlines human learning and memory

24
Q

long-term synaptic plasticity in the hippocampus

A

long-term potentiation (LTP) –> persistent increase in synaptic responses induced by high-frequent stimulation
long-term depression (LTD) –> persistent decrease induced by infrequent stimulation

removal or damage to hippocampus impair memory formation but no effect on memory already formed

25
Q

signalling in the hippocampus

A

signals enter from entorhinal cortex
–> perforant path (excitatory synapse)
dentate gyrus, axons, mossy fibres
–> excitatory synapse release glutamate
CA3 region, parental cells (schaffer collateral, SC)
–> excitatory synase on other side of hippocampus
CA1 region, paramental cells

to induce LTP at CA3 and CA1, SCs are stimulated with high frequency tetanus –> significant membrane depolarisation –> summation of EPSPs

26
Q

mechanism of LTP induction

A

transmitter at CA3 and CA1 is glutamate –> activates postsynaptic AMPA and NMDA receptors

NMDA only allows Ca2+ into postsynaptic cell is MP is sufficiently depolarised (removes Mg2+ block) by summation of AMPA EPSPs

influx of Ca2+ through NMDA chanels essential for LTP

increase in postsynaptic Ca2+ enhances eactivity of many protein kinases

blocking NMDA receptors or postsynaptic kinase prevents LTP

BIOM2011 (6 decks)

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