Nervous System

Question 1

What are axodendritic, axosomatic, and axoaxonic synapses?

Answer 1

-Axodendritic: connecting w the dendrites
-Axosomatic: connecting w the soma/cell body
-Axaoxonic: connecting w the synapse btw two other neurones, often inhibitory, it can block/ cancel out signal

Question 2

What is Dales law?

Answer 2

Neurons will use the SAME neurotransmitter at all of its synapses

Question 3

What is the difference between Type I and II synapses?

Answer 3

Type I has asymmetrical membranes and is excitatory
Type II has symmetrical membranes and is inhibitory

Question 4

What is labelled line code?

Answer 4

each sensory neuron encodes only one stimulus modality

Question 5

What is rate code?

Answer 5

stimulus intensity encoded by firing rate

Question 6

What is population code?

Answer 6

stimulus intensity encoded by rate and population code

.# of axons activated can also encode information abt stimulus strength

Question 7

What is timing code?

Answer 7

central neurons may use spike timing codes as well as spike rate codes for representing information

Question 8

What is temporal summation?

Answer 8

• A typical input on its own is not enough to activate AP
• If memebrane A is active just once, there is 1 depolarization and it does reach threshold
• If you activate A in quick sucession before it can go to rest then the inputs ‘add up’ or ‘sum’ and may be enough to trigger AP

Detects high frequency firing by upstream neurons

Question 9

What is spacial summation?

Answer 9

• Activation of A on its own is not enough for AP, and same for B (not enough on its own)
  But if A and B are together, happens at same time, then they are enough

Detects coincident firing of upstream neurons

Question 10

What is inhibition summation?

Answer 10

• activity in synapse C prevents simultaneous activity in A & B from generating an impulse

Enables upstream neurons to prevent downstream firing

Question 11

What are some main differences between NMJ and central synapses

Answer 11

• NMJ has 1 presynaptic neuron per muscle fibre, vs central has many converging onto one post-syanptic neuron
• NMJ has a ‘safety factor’ vs central has integration
• NMJ’s main NT is ACh, vs central uses lots of different NT
• NMJ EPP is excitatory, vs central can be excitatory or inhibitory
• NMJ AP frequency and the number of recruited fibers determine contraction strength, vs central AP frequency, AP timing, and neuronal identity are important for central representation of information

Question 12

Where is glutamate synthesised?

Answer 12

• Synthesised in the presynaptic terminal

Question 13

How is glutamate released?

Answer 13

• Loaded into vesicles in the presynaptic terminal and then released during AP
• Its taken back up by transporters or glilal cells that convert glutamate into glutamine then back to glutamate

Question 14

How is glutamate/glutamine broken down?

Answer 14

Glutamate turned into glutamine by glutamate synthase in glilal cell
Glutamine broken by phosphate activated glutaminase (turns glutamine to glutamate) in presynaptic terminal

Question 15

How do ionotrophic glutamate receptors cause excitation?

Answer 15

• Needs spacial summation
• When glutamate binds it triggers Na and K channels to open

(influx of Na and efflux of K)
At typical resting potential, membrane potential is driven towards eq potential= suggests excitatory response

Question 16

What do AMPA receptors mediate?

Answer 16

The fast component of glutamatergic synaptic current

Question 17

What do NMDA receptors mediate?

Answer 17

The slow component of glutamatergic synaptic current
AP5 is an antagonist of NMDA receptor and blocks slow component

Question 18

What are the effects of glutamate on AMPA and NMDA receptors?

Answer 18

AMPA: when glutamate binds, channel opens
NMDA: when glutamate binds, channel opens but Mg2+ blocks channel and only leaves during depolarization

Question 19

What is the difference between ionotrophic glutamate receptors and metabotrophic glutamate receptors?

Answer 19

• Ionotropic glutamate receptors (iGluRs): membrane ion channels that are gated by glutamate
• Metabotropic glutamte receptors (mGluRs): seven transmembrane domain proteins that couple to G proteins

Question 20

What evidence suggests that glutamate is important in membrane and plasticity?

Answer 20

• High densities of channels activated by glutamate are found in brain regions associated with learning and memory function
• Mg2+-dependent block enables NMDA receptors to act as coincidence detectors for associative memory
• Block of NMDA receptors by intraventricular infusion of AP-V prevents learning

• Drugs that block the action of glutamate inhibit learning and memory
• Drugs that potentiate the actions of glutamate enhance learning and memory

Question 21

Whats the difference between cholinergic and glutamatergic synaptic transmission?

Answer 21

Cholingeric: uses nicotinic (Na/K) and muscarinic (G-protein) receptors
Glutamatgeric: uses AMPA (Na/K), NMDA (Na/K/Ca), and mGluR (G-protein) receptors

Question 22

What are the two main inhibitory neurotransmitters?

Answer 22

GABA
Glycine

GABA and glycine both mediate fast synaptic inhibition through activation of ionotropic receptors.

Question 23

How is GABA synthesised?

Answer 23

Synthesised from glutamate by glutamic acid decarboxylase in the presynaptic terminal

Released via vesicles into the post-synaptic terminal and then into glilal cells and recycled in the presynaptic terminal

Question 24

How is GABA broken down?

Answer 24

Broken down in the TCA cycle to glutamate then glycine

Question 25

What would happen if too much or too little GABA regulation were to occur?

Answer 25

Too much regulation would cause seizures Too little regulation would cause brain dead ## Footnote GABA is inhibitory, regulation of inhibition is important

Question 26

How do GABA receptors cause inhibition?

Answer 26

When GABA binds, Cl- channels open

Question 27

What is the difference between GABAa and GABAb?

Answer 27

GABAa: ionotrophic (fast), mediates Cl channels GABAb: metabotrophic (slow), mediates Ca channel closure and K channel opening ## Footnote Ca2+ channel closure - inhibition of transmitter release. K+ channel opening- slow IPSP. Baclofen is a selective GABAB receptor agonist, while 2-hydroxy-saclofen is a selective GABAB receptor antagonist

Question 28

What does strychnine do?

Answer 28

- competitive antagonist that binds to the α subunit of GABAa receptor (posion if swallowed) - causes convulsions and asphyxia

Question 29

What drugs target GABAa receptor and what effects do they have?

Answer 29

Benzos: anxiolytics, anti-convulsants Ethanol: Barbiturates: Neurosteroids: ## Footnote Benzodiazepines potentiate the action of GABA at GABAA receptors by increasing the probability that the channel opens following the binding of GABA. Only GABAA receptors that contain a γ subunit (in addition to α and β subunits) show potentiation by benzodiazepines. Make amplitude of synaptic current larger, and makes the duration of the synaptic conducters change longer as well

Question 30

Whats the difference between glycine and GABA synaptic transmission?

Answer 30

Glycine: Cl- channels GABA: GABAa (Cl-) and GABAb (G-protein)

Question 31

Whats the difference between glycine and GABA synaptic transmission?

Answer 31

Glycine: Cl- channels GABA: GABAa (Cl-) and GABAb (G-protein)